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Tim Noakes: we need you back for a moment
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don't leave so soon! we have some unfinished business.

as i understand it, your views on in-race hydration stem from a two-part thesis:

1. that the human body is wonderfully adaptive to weather and conditions; is great at thermo regulation, and in maintaining great equanimity in the face of harsh conditions; and has an advanced ability to self-meter the need for water and salt based on craving; and that, during races, we ignore our craving instinct at our own peril.

2. when we consider causation: getting the human to this present advanced state is due to evolutionary pressures (and indeed why would it not, since evolutionary pressures are solely responsible for species variation and specialization prior to the advent of farming and animal husbandry).

let's leave part-2 alone for now, because i think that this allows certain folk to segue off, and to hijack the discussion. i don't care how i got to be the organism i now am. i just want to talk about how to comport myself during upcoming races.

i'm 100 percent with you on the folly of hyper-hydration, pre-hydration, and so on. but salt: that's another matter.

simply put, i don't crave salt until it's too late. i crave salt the night following the race, not so much during the race. so unless my cramping is due to something other than electrolyte depletion, i'm blindsided by salt depletion during the race.

why don't we / can't we treat salt the way we treat carbs? we have -- what? -- 2000 kcals floating around in the form of blood glucose and liver/muscle glycogen? so, we have an olympic distance triathlon in us, more or less, but longer than that and we must start taking in carbs at a rate that we absorb carbs (maybe 350 kcal/hr, more or less? that's a reasonable rate of carbohydrate intake?). we don't have to wait until we crave carbs before we start ingesting, true?

why not the same with salt? i don't think i know a successful male pro ironman triathlete who does not supplement fairly significantly with salt (maybe a half-gram an hour or more). why is it folly for me to supplement with salt prior to the onset of salt craving? my own race history argues that it's folly to eschew salt intake until the onset of craving.

Dan Empfield
aka Slowman
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Re: Tim Noakes: we need you back for a moment [Slowman] [ In reply to ]
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From years of racing, I found that if I hit 3-4% dehydration (157lb on my current 162lb average weight) then I am literally at the "walking not jogging" level. I have a horrible thirst sense, as I can easily get to 3% without feeling thirsty...so in my case if I followed Noakes' drinking suggestions then I would be a DNF at most races rather than finishing IMs and 50 milers at mid-to-front of pack. My only option is to drink a lot more than I think I need, because I always sweat it out. I have NEVER finished a race overhydrated, and usually (if I'm lucky) am 2-3lb down at the end. Is this a form of "central governor" where my performance is directly related to my hydration or sweat rate? Or maybe more obviously directly related to my internal body temp? I.e. when I am significantly dehydrated (3-4% in my case) I tend to stop sweating and my body overheats and shuts down. These responses don't seem to support a central governor theory, just simple direct response to physical conditions.

Regardless of the mechanism, what is the best racing solution? Over years of experimenting I started adding a bit more salt (and other electrolytes) and found that I responded the best in terms of ability to digest water with an intake around 1g per hour. For a 11hr IM race my measured average sweat rate is about 1.9L/hr (hot, humid FL conditions) with a salt concentration in the general public of 1-1.8g/liter...that means I'll lose close to 20g of salt over the above race. With the ~12g stores the body keeps available, this means I'll need to supplement with around 1g/hour...surprisingly close to what I found worked the best experimentally. Anything much more than 1g/hr ended up with puffy hands or indigestion issues, and substantially less meant I couldn't digest in enough water to keep hydrated (sloshing stomach while getting dehydrated).


Mad
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Re: Tim Noakes: we need you back for a moment [triguy42] [ In reply to ]
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Another question is: what is the disadvantage of consuming salt in proportion to its loss? You lose x grams per hour, you supplement with the same amount. This, of course, must be tested in terms of the gut's ability to assimilate. And this isn't about buying product. I did the whole of last season drinking homemade drink with a pinch of table salt.

I am the same with regards to salt craving; I eat a relatively low sodium diet but still very rarely crave salt, even after long hot workouts workouts. I must be intentional in my races as far as salt intake goes as trusting my craving would be folly.

http://www.triathloncoach.ca
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Re: Tim Noakes: we need you back for a moment [Slowman] [ In reply to ]
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Hey Dan, read this - http://www.bartleby.com/65/al/aldoster.html
The body is very good at regulating sodium levels. We can trick it to a degree by going very low on sodium for a while and then pumping it in in concentrated doses just prior to the start of a race but that's kinda risky.
I've found that sodium phosphate is the easiest to assimilate in quantity (1 gram/hour or more) either before or during a race. Hammer Nutrition makes a good inexpensive sodium phosphate product called Race Day Boost. Try it out.
Cheers,
Scott
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Re: Tim Noakes: we need you back for a moment [Slowman] [ In reply to ]
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Interesting post.

I've been craving salt like CRAZY lately during the day after workouts. Normally I am a sugar-craving creature so this salt thing, I cannot figure out. LOL.

maybe she's born with it, maybe it's chlorine
If you're injured and need some sympathy, PM me and I'm very happy to write back.
disclaimer: PhD not MD
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Re: Tim Noakes: we need you back for a moment [Slowman] [ In reply to ]
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Basic Physiology 1.

The textbooks say that sodium is the principal electrolyte in the extracellular fluid (ECF) which is a volume of 10-14 L depending on body mass. There is apparently little sodium inside cells. The measured concentration inside cells is about 5mmol/L versus 140mmol/L in the ECF. Indeed 40% of the energy we expend at rest is spent on pumping sodium to the outside of our cells. The amount of sodium in the ECF determines the ECF volume. This is because the body homeostatically regulates the osmolality of the body fluids so that there is a constant osmolality which produces a blood sodium concentration of about 140mmol/L in an ECF volume of 10-14 L. What the usual textbooks do not say is that whilst this relationship can well explain the ECF osmolality, it cannot explain the whole body osmolality. Thus in 1957 Edelman discovered that to explain the osmolality of the total body water (TBW - a volume of 35-42 L) there has to be substantially more sodium in the body than that measured in the ECF. But where is it since we “know” it is not in the cells (which are actively pumping sodium from the cells into the ECF to insure that the measureable intracellular sodium (Na+) concentration is very low)? Edelman used a radioactive sodium tracer and showed that the “sodium space” into which the tracer dilutes is much greater than the ECF sodium “space”. He called this new, previously undiscovered amount of sodium the “exchangeable sodium”. It constitutes about 50% more sodium than that present only in the ECF.

The next interesting observation is that in the 1950’s McCance produced a true state of sodium deficiency in humans. To my knowledge this is the only study in the published literature showing that a true sodium deficit can be produced in humans under experimental conditions. He had to go to inordinate lengths to achieve this. Three of the four subjects for his study had to live in his house whilst Mrs McCance fed them a sodium-free diet. Each day they sat in a hot room which produced prodigious sweating for 2 hours a day. By the fifth day they began to show evidence for a salt deficiency. The fourth subject a medical student at Oxford, a Miss Edwards, chose not to live in the McCance residence. A state of sodium deficiency could not be produced in her. Probably she was sneaking some extra salt in her diet.

The evidence for the salt deficiency was a set of symptoms that the subjects developed – absolute lethargy was a key factor – and a fall in blood sodium concentrations (hyponatremia). But the interesting observation was that to recover, the subjects needed to ingest far more sodium than the amount that would have been predicted on the grounds of the fall in their blood (and ECF) sodium concentrations. Thus it were as if something was preventing the fall in ECF sodium concentrations which should have fallen to much lower values based on how much salt the subjects had lost in their urine and sweat during the experiment. It were as if there was a store of sodium that had been called upon to maintain the ECF sodium at a higher concentration than in should have been if all the sodium in the body was only in the the ECF.

(For the purposes of this discussion we can ignore the fact that in the first few days of the experiment the blood sodium concentration was protected by the usual contraction of the ECF that occurs whenever there is an acute sodium loss from the ECF. But after day 4 the ECF began to expand despite an ongoing whole body sodium loss. This caused the blood sodium concentration to fall more sharply thereafter).

More recently there has been increased interest in this “hidden” sodium store. Balance studies of humans fed a very high salt diet showed that they were storing sodium in a site other than the ECF. Thus they did not simply excrete (in urine and sweat) the excess sodium in the diet; nor was it stored in the ECF causing an expansion of the ECF. It had gone somewhere else.

The authors proposed that the extra sodium is stored in the body in an “osmotically-inactive but exchangeable” form (Na) in which it is not measureable as ionic sodium (Na+) but where its presence can be detected by radioactive dilution techniques of the type undertaken by Edelman.

According to this theory there is a store of osmotically-inactive sodium (Na) in the body which can produce osmotically-active sodium (Na+) when it is required. Alternatively when the ECF Na+ concentration rises too high, there can theoretically be osmotic-inactivation of circulating Na+ which is then stored inside cells in the osmotically-inactive form (Na) to be returned to the ECF when it is required.

There are a number of modern observations that support McCance and Edelman’s findings that there must be more sodium in the body than is accounted for by the measured Na+ in the ECF.

For example, if subjects ingest less sodium and water than they lose in sweat during exercise, their blood sodium concentrations ALWAYS rise. This of course is not a fact that the sports drink industry wants you to know. Instead over the past 15 years that industry and its funded scientists have consistently argued that if you don’t replace all the sodium and water that you lose during exercise you will develop exercise-associated hyponatremia (EAH) (which can therefore only be prevented by ingesting a sports drink containing sodium (at low concentrations)). But this is simply not true. The blood sodium concentration ALWAYS rises under these conditions because sweat contains less sodium than does blood (and as I hope we will discuss in due course can contain essentially NO sodium in people living on a very low salt diet) so that more water is lost that salt. As a result the ECF contracts causing the blood sodium concentration to rise. Of course in a perfectly homeostatically regulated system this rise should not be more than a few mmoles/L but in some athletes in competition it can be up to 10-12mmol/L which is surprising and presently unexplained (although it might be explained by individual differences in the ability to osmotically-inactivate ECF Na+ as discussed below).

However we have shown that the change in blood sodium concentrations during exercise is highly individualized and cannot (probably) be explained purely by sodium losses in sweat and urine and changes in the ECF volume. Rather in our paper published in the Proceedings of the National Academy of Sciences in 2005 (and available for free from their website) we proposed that some of this variation must be explained by individual differences in the movement of sodium between the osmotically-active and inactive stores during and after exercise.

Interestingly the ability to deactivate Na+ during prolonged exercise and store it would delay the onset of thirst (which is stimulated by a rising ECF sodium concentration). Thus the presence of this store could have been a way in which our hominin ancestors were able to delay their thirst during long, hot, water-less hunts (see the thread on Why cannot scientists ever agree on anything?).

A tragic case supports this contention that there must be this internal sodium store. When Cynthia Lucero died after the 2002 Boston marathon because she had drunk too much of a sports drink (and retained that fluid excess within her body because she was also excreting too much anti-diuretic hormone – ADH), our calculations show that she simply could not have drunk sufficient to drop her blood sodium concentration as low as the value measured when she was admitted to hospital. Instead something else must have happened and one possibility is that she had also osmotically-inactivated some of her ECF Na+ at the same time transporting it into her cells causing her hyponatremia to be exacerbated. When we performed calculations on the data of fluid and sodium balance on patients treated by either ourselves or Dr Speedy in New Zealand for EAH, we came to the conclusion that some may have inactivated Na+ during the races in which they developed EAH with subsequent osmotic re-activation during recovery. But since we did not actually measure the process we cannot be sure.

What might this all mean. To return to the evolutionary perspective. It would make sense for humans evolving in a relatively salt-free environment to have an internal sodium store that could be filled in times of plenty and depleted in times of scarcity. Since salt is the most important regulator of the ECF volume and since if we cannot regulate the ECF volume accurately we die very quickly it makes sense to de-link regulation of the ECF volume from the daily sodium intake. How could we have survived if our lives depended on finding just enough salt each day in an environment in which salt was in scarce supply? Those who developed an internal sodium store under these conditions would be the most likely to survive.

If this store exists it might explain, in part, why it is so difficult to cause a true state of sodium deficiency in humans.

But more importantly, how does one measure a state of sodium deficiency in athletic humans? This is important since many contributors to this forum as do you yourself, believe that you develop cramps (or impaired performance) because of a sodium-deficit caused by large sodium losses in sweat. (Note that the model you use to explain this is catastrophic and non-homeostatic. It is based on the belief that the body has no ability to homeostatically regulate its losses and so will just continue to exercise until there is a catastrophic failure of function, in this case muscle cramps. But does it not make more sense to believe that evolution would have weeded out all these obvious system failures so that your problem is not likely caused by a system that is known to be homeostatically regulated and essential for life not just during exercise and the failure of which would have killed you long before you developed muscle cramps? Should we not look elsewhere for a better explanation than in a system that if it did not work perfectly we would not survive? Of course this is not how industry sees it. They want us all to believe that humans are weak and on the verge of a catastrophic biological failure that can only be prevented by the ingestion of their products, be they pharmaceutical products, sports drinks or other nutritional supplements).

The usual way to measure a sodium deficiency is by measuring the blood sodium concentration. But this is not fool proof since we know that the main cause of a low sodium concentration is a large increase in the ECF (and TBW) volume as occurs in EAH. Thus to prove a sodium deficiency you need to measure a low blood sodium concentration WITHOUT any increase in ECF volume. But this would not necessarily tell you what is the state of your internal sodium stores. The problem might be in the ability to activate intracellular osmotically-inactive Na.

But we can prove when a sodium-deficit does NOT explain your symptoms. Thus if you have symptoms and your blood sodium concentration is normal then BY DEFINITION your symptoms cannot be due to a sodium-deficit. Of course this is not something that you will hear from the sports scientists who acts as spokespersons for the sports drink industry. I recall hearing one well know (notorious?) such speaker for the industry say at a meeting in Australia that the presence of muscle cramps proved that the athlete had a sodium deficit even though the blood sodium concentration was normal. Of course this is not what we were taught in medical school. But then why cannot industry develop its own brand of physiology? Especially if it can find sufficient “scientists” to promote this novel brand of knowledge.

So the short answer to your question is the following: What was your blood sodium concentration at the time you developed your muscle cramps? If it was normal then the ingestion of salt either before or during exercise does not cure or prevent the condition by preventing the development of a sodium deficit. Rather it is acting in some other way that we currently do not understand.

That is enough for today. More on anther occasion.
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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Dr. Noakes, Thank you for your response. I have found that when drinking sports drink (gatorade) even at extremely high rates in high heat and humidity I lose a lot of weight and performance greatly suffers.

However, when I take a concentrated sports drink like infinit or a gel and mostly drink plain water I can retain my weight much better.

Does this fit in with your findings? Could it also be that the sodium (and possibly small amounts of protein ) cause us to be able to retain enough water rather than functioning to keep our sodium levels high enough?

Thanks,
Dan
http://www.aiatriathlon.com

http://www.aiatriathlon.com
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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Dr. Noakes -
Thank you for taking the time to respond - and thanks Slowman for asking him back :-)

I'm enjoying your Lore or Running (don't laugh that it took me to desperate measures to really start reading). As a quickie background - I do have a DC degree (not using it) so I am able to understand basic Physiology, which is why I don't get what is happening. I begged several physiologists at several Universities to help, but they all had too much on their plate to take on the solo project. Maybe you can spread some light. I do not cramp. The only time I have ever cramped is the first time back in the pool (always left calf and sometime foot if its a special day) after a hiatus, and typically the first 400 mile ride of the season (around May every year) - always left vastus lateralis - previously torn muscle there. I do not sweat excessively at all. My body has plenty of reserves and I end up not really eating on rides, only once I start going past maybe mile 90 do I start to get hungry and a bit of a thirst. Yes, I am aware that is not 'normal' but its just how it is. I hear of people loading their bikes down for halves and olympics and typcially for a century bike ride I might go through one water bottle - and that is because I am forcing it down. It is truly a chore for me to eat food - especially during racing. Infinit is my fluid of choice and maybe an entire container is used during the race (the deca is a 14 day race - 24 mile swim/1120 mile bike/262 mile run). Outside of food intake and Infinit extra supplementation with salt is NOT used (used to use it and the bloating problem was sooner and more fierce and bp was way too high - heart would actually hurt). The Euros I race with always ask me for Magnesium, never Sodium. Yes aware of the sodium, magnesium, calcium, potassium importance. Blood tests are drawn pre-event by both their Dr. and mine in the States, nothing is ever out of whack. If anything one of the values they look at for doping is supposed to be in the low 40s and I am always in the high 30s (can't think of the name right now - argh - iron/blood ratio?).

The problem I am in search of a solution for is the bloating - the endless water weight gain. The horrid water belly. The look is seriously like a big huge pregnant woman include jaw line completely disappearing. Although no cankles - so I got that going for me.

I do ultras. In particular the deca iron (have done the double/triple/and quintuple irons too). I just finished up my third deca falling shy at mile 217 on the run - had plenty of energy, had wicked blisters and quite frankly just wanted to sleep. Every single ultra from the triple on up at day two I throw my period, day 2.5-6days I start gaining measurable fluid weight (35 lbs was the max on this last venture) and then immediately dump it with intervention. Intervention has been: running (getting my ass off the bike seat), taking Lasix in the quintuple, and hydroxycuts as a last ditch effort in this last race. Heart rate values get scary (for me) and taking in more fluid is obviously not the answer. Sugar values can fluctuate pretty high sometimes (again for me). Without fail, for the decas around day 7-9 kidney stones get passed, for the quintuple it happened at day 5, and for the triple it happens right at the end of the race (all the events its when running). Most amount of kidney stones was this last venture at number 5 - that was quite enjoyable.

There is no one to ask about this stuff - only 4 other women (the hormone thing) and with that barely getting input. So I'm back to theories. Taking this season off and getting the body semi regulated and probably doing another go next season (maybe at the end of this year). Will be trying stuff out on my own personal camps again this year - so open to ideas, since I'm my own guinea pig and I really really really want to finish one of the decas again, just tired of the bloating and weight gain. Very concerned about long term damage. All my values have been very healthy thus far, in fact have gotten stronger in all test measures. Only other thing you might find intriguing - everything grows excessively during the decas - hair, nails. Have to physically cut my toe nails on the bike and again on the run (usual is maybe once every 6 weeks for toes) and the hair physically grows out a solid 2"s during the event (as evident with the highlights). Post race - I heal freaky quick. New toe nail growth is insane, and anything ripped/torn typically heals right up. Oh, and there is the start of the weight gain in the pool - my theory submerged for 17 hrs in water you're going to bloat. There is also a very nasty cough (usually producing blood - quite a bit, although the color makes me think its just irritation of the aggressive heaving cough) from the pool and heavy by day 3 on the bike. Attribute this to the chlorine inhalation and the heavy dust that is prevelant. Antibiotics/inhalers typically clear this stuff up - just usually really stubborn over putting drugs into the system with the level of abuse. Pain killers I only used 2 in this last event (infection in my pinky toe and heal was unbearable), all others, nothing was used.

I know there is muscle memory/adaptation - as this was single handed the easiest deca to date - second best attempt.

Give me whatcha got - as the lore of running has truly only told me what I already knew plus threw in some interesting data never read before.
thanks in advance for any crazy insight. I will not be offended if you have nothing as I always run into brick walls. If you'd rather not share this stuff here, I can be reached at eileensteilATaol.com as I really would like to hammer this race sometime soon, not waddle my way through.
~eileen
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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At ironguides we have a very simple indicator for our athletes to determine if they should seek more sodium/salt or more water during a race -- it aligns closely with your stance on the body's ability to dictate needs to the consciousness via cravings:
  • If your drink "tastes" too "watery" you need to increase your salt intake. For example, most athletes have had the experience that "the volunteers at that last aid station aren't mixing the Gatorade strong enough, it's way too dilute!" Well -- usually the drink's mixed right and that is your body's way of telling you that you're in fact diluting your own electrolytes, internally.

    NOTE: There is no "salt craving" associated with this "watery taste." In fact, it's more a feeling of "water aversion."

  • If your drink tastes too "sweet" or concentrated you need to increase your water intake -- this i your body's way of telling you that you're dehydrated. Same example holds true: You come away from an aid station thinking the drink's been mixed too strong, or things simply taste too sweet, syrupy, or concentrated. Your body is telling you it needs water.
We find that athletes who train by heart rate, power or other external reference points (such as exclusive reliance on a metronome for stride rate, strict adherence to a speedometer, and so on) by and large fail to learn or heed these small but powerful signs. Quite literally, they have trained themselves to ignore their body and rely on other guidelines.

For this reason we intentionally structure our training around perceived exertion and use HR or power only as anecdotal reference points from time to time. Never is the training structured to these quantitative approaches, however, because we find that the less skilled the athlete, or the longer the event, the more important it becomes to develop self-awareness, intuitive understanding and qualitative reference points. We train the athletes to "go within."

In particular, beginners can quickly learn to interpret their body's signals by following a repetitive routine rather than a set of instructions to follow certain "zones" or to achieve certain power outputs. More advanced athletes who have conditioned themselves to train by a quantitative protocol tend to take longer to decondition and relearn an intuitive approach. In this day and age of hyper-gadgetry unfortunately that's the majority of athletes.

As a rule, we find that our athletes do better the tougher conditions get. For example, in 2009 already we had disproportional results at the Ironmans held in the most extreme conditions -- Ironman Malaysia and Ironman China. "When the going gets tough, the tough get going."

At IM Malaysian all our athletes who went set personal bests and we placed four AG athletes in the top twenty, each placing 2nd in their AG (out of 5 athletes).

At IM China, ironguides athletes won the overall race in both the women's Ironman event (Charlotte Paul, 5th overall and with the fastest overall run split of all men and women, beating Olympian Rasmus Henning) and the women's 70.3 (Amanda Balding), and came in 3rd overall in both the men's Ironman (Joszef Major - on a borrowed bike!), and the 70.3 race (Mark Jansen, AG athlete from Singapore).

We teach our athletes to rely on internal indicators on race day by training them that way. When race conditions get extreme ironguides athletes seem to be showing that they are better able to monitor and pace themselves and persevere through extreme conditions by virtue of a reliance on internal indicators and a trained intuitive response to their body's signals. This takes time to develop and there is no secret means by which we do this: Just "wax on, wax off", week in, week out -- without the gadgets.

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Last edited by: ironguide: Apr 22, 09 5:22
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Re: Tim Noakes: we need you back for a moment [Slowman] [ In reply to ]
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In Reply To:
To return to the evolutionary perspective. It would make sense for humans evolving in a relatively salt-free environment to have an internal sodium store that could be filled in times of plenty and depleted in times of scarcity. ... How could we have survived if our lives depended on finding just enough salt each day in an environment in which salt was in scarce supply?[/quote]
BINGO.

finally, someone with the guts and smarts to point out to us the obvious fact that 95% of the stuff that "nutritional" drink and supplement makers tell us is simply a bunch of crock.





Where would you want to swim ?
Last edited by: GregX: Apr 22, 09 5:25
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Re: Tim Noakes: we need you back for a moment [ironguide] [ In reply to ]
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Dr. Noakes, thanks for long and detailed explanation. Again, thanks for the help in 2003 in setting me straight after the big hypervolemic hyponatremia day at IMLP in the cold.

Mark, those guidelines are absolutely brilliant!
ur
Eileen.....35 lbs...that's nuts. If you use Mark Becker's guidelines, are you holding down 30 lbs of excess weight and still filling thirsty? Ever since I went "exclusively on the thirst indicator", I don't drink unless I am thirsty, and thuse I have not gained fluid mass in racing in 5 years. Then again, my races are only 20 minutes to 11 hours in duration.

Dr. Noakes....one more question.

After long airline flights (like 12 hours, Vancouver to Beijing last week), it seems for the next day I am peeing constantly. I don't really overhydrate on the flight. On this last flt, I drank 6 small cups of green tea, 2 sprites, and 2 small cans of Clamato juice. Seems quite reasonable for a sum total of 12 hours in the air, and I was drinking cause I was thirsty, not just pounding down liquid....it seems it is barely ~ 1L of liquid over those 12 hours. I believe I went to the washroom around twice in the flight, but then a few hours after hitting the ground, after going for a swim (45 min, 2500m), it seemed like I had to go to the washroom every hour. Then the following day, I feel thirsty all day, but have to pee frequently. And this seems to happen whenever I go up to 6000-10000 ft in a semi pressurized cabin for >10 hours. I can't really explain what the long flight does, but I'm all messed up for a while afterwards on the fluids front.

Dev
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Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
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being a veteran of many long flights and a student of the body, i think your urination issue is likely caused by interstitial edema from sitting so long during the flight. when you sit so long, the body is "losing" water into the interstitial space, mostly in your legs, during the flight.

then, when you start moving again or lay down or do both, the fluid begins to return back into the circulating blood, so your now have an excess of fluid in the blood which is quickly removed by the kidneys. hence the urination for hours after the flight.





Where would you want to swim ?
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Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
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Hi Paul - use with care! :-) Borne out by hundreds of tests and confirmations, it is simply being attuned to the age-old wisdom that lies within.

We're getting great satisfaction watching the same common sense (which happens to be "out of the box" thinking in triathlon these days) generate great results via our training plans and not just our coached programs.

A lot of what passes through this forum clouds the issues and buries very simple, very effective techniques with too much data, too much analysis, and too much doubt.

We like to refer to the following quote to illustrate the point better:

Obsession with measurement is an expression of self doubt. Many of the things that matter the most defy measurement. When we enter the realm of human nature and human actions, we are on shaky ground when we require measurable results as a condition of action.

- Peter Block, in The Answer to How is Yes

What's revealed in endurance sport is human nature and our ability to confront ourselves. By avoiding the temptation to always resort to quantitative approaches, we strengthen our athletes' resolve and sense of purpose, and give them more powerful tools to work with to achieve their goals.

Our PDF training plans already prove that the training approach works all by itself without the intervention of a coach. The plans are delivering many top ten results, including sub 8:30 Ironmans, and we are getting from Age Groupers reports of 2-hour Personal Best's, first-time finishes far exceeding expectations, and short-course races much faster than anticipated. A top-three at Kona uses our Plan in his revamped training, and each week a new report of someone achieving better times on less training volume, better sleep, more energy - even better sex has been reported back to us.

There's no mystery in it from my vantage point. Our approach turns training on its head. When you add one of our coaches to the mix, we are able to work on the athlete's ability to rely more confidently on their intuition and internal indicators.

The little tip about drink concentration is something I learned first-hand when I started paying attention to my racing and my body, and came only after I threw away the HR monitor and power meter many years ago and started the process of forgetting what I'd been "taught" by one of the other big name coaching outfits we compete against. :-)


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ironguides.net : Home of The Method
Join the New Generation of Champions!

--- Your best is our business. ---
Last edited by: ironguide: Apr 22, 09 6:16
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Re: Tim Noakes: we need you back for a moment [ironguide] [ In reply to ]
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In Reply To:


Obsession with measurement is an expression of self doubt.



Thanks for the quote! And your outstanding advice for IM hydration!

I am a bad swimmer. The swim is by far the worst part of triathlon for me, but I am always obsessed with the clock in the pool. I bike without computer, I don't have a heart rate monitor, and I use the watch only for some interval running. Rest of the training is all on feel, but I can't stop watching the clock in the pool. Now I understand, it is self doubt.
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Re: Tim Noakes: we need you back for a moment [GregX] [ In reply to ]
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This is actually fairly common (and the way my grandfather died...blood clot in the calves after a 12 hour flight) especially in fairly long flights. This happens to me on usually anything more than a 3-4 hour total airflight distance. HOWEVER, it's not entirely caused by just being inactive, or we would all have this sort of problem after spending Sunday sitting on the couch watching TV. Massaging your calves during flight is a good preventative measure, as is drinking beer (as if we needed another reason...) because it dehydrates you a bit and lessens the water weight gain. Smile


Mad
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Re: Tim Noakes: we need you back for a moment [GregX] [ In reply to ]
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By the way, I did take your previous advice and no longer run immediately after long flights. I either walk, or go for a swim if there is a pool at hand. I assume this is OK. Also started wearing compression socks on long flights and as a bare minimum, legs feel lighter when I deplane....hoping to get an upgrade on the Tokyo Toronto leg tomorrow and I can have my legs up for 12 hours :-)

Dev
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Re: Tim Noakes: we need you back for a moment [big slow mover] [ In reply to ]
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I only use the pace clock around 1x per week in the pool and the only time when I use it when running is at the track or in the winter from time to time on a couple of measured loops of 500m and 1000m that I have near home and work just to make sure my pace is what I think it is. On the bike, it is all by feel, unless I am indoors on the trainer or roller in which case the quantified output is is staring your right back in the face (unless of course I tape over the display).

The best sport for this is XC skiing...there is only interval pace, race/TT pace, moderate and easy. The conditions change so much that the only way to quantify anything is by one's perceived exertion meter :-)

Dev
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Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
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In Reply To:
By the way, I did take your previous advice and no longer run immediately after long flights.[/quote] very smart move.

In Reply To:
I either walk, or go for a swim if there is a pool at hand. I assume this is OK.[/quote] unfortunately, not a lot of data (that i'm aware of) that says this is safe either. hopefully it is safe. but there is no doubt at all that running after a very long flight is not just unsafe, it can be fatal.





Where would you want to swim ?
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Re: Tim Noakes: we need you back for a moment [GregX] [ In reply to ]
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Greg,

By the way, after a long flight can you end up with SIADH, thus affecting the subsequent urination during the next hours and day? I am wondering if the sudden altitude shift from sea level up to 10000 foot cabin pressure and back the other way has the some effect. For example, on Easter weekend, I drove from Ottawa to NYC and back, pretty well 8 hours each way with one short 30 min stop. No issues with leg swelling etc in car...just an aircraft and technically I move around more in the airplane.

Dev
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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According to this theory there is a store of osmotically-inactive sodium (Na) in the body which can produce osmotically-active sodium (Na+) when it is required. Alternatively when the ECF Na+ concentration rises too high, there can theoretically be osmotic-inactivation of circulating Na+ which is then stored inside cells in the osmotically-inactive form (Na) to be returned to the ECF when it is required.

This makes perfect sense and brings about the observation that perhaps this entire argument comes down to the individual variability of the activation rate of the stored sodium. While the study on true sodium depletion was useful to prove the existence of the stored sodium, it perhaps had little bearing on the athletic usage question since the depletion & demand are in the order of minutes and hours as opposed to days. I can see the real possibility that on an individual basis, the activation rate and timing could easily be delayed enough to require supplementation because the demands of an event such as a half or full ironman, can easily exceed any genetically evolved human demands. While certainly individuals may have faced occasional demands such as this, I wouldn't think it would be enough of a norm to force a genetic change for the whole of the human/pre human population. It's just as likely that a fast Na activation rate lies on the far end of the bell curve of activation ability leaving as many on the other end and the bulk of us in the middle. In my mind, your research on
hyponatremia only strengthens this hypothesis as I would argue that your female doctor that died in the marathon, died because she was on the other end of the activation rate scale and her body wasn't equiped to recruit enough Na to balance the extreme amount of fluids she drank in a timely matter. Another similar athlete, under similar conditions may have survived with no ill effects if they happened to be at the other end of the curve of activation rates. The fact that your research showed a sexual disparity could be explained from an evolutionary standpoint if we assume that males were more likely to be under evolutionary pressure to develop a faster activation rate due to a more likely hunting role as opposed to staying back at the cave and watching the kids. In conclusion, both sides of the sodium supplementation argument could be right depending on the individual, which certainly seems to be the general experience.


JJ


Every night that I run, the thought crosses my mind that there's no way in hell I'll still be running a month from now.
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Re: Tim Noakes: we need you back for a moment [Slowman] [ In reply to ]
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2. when we consider causation: getting the human to this present advanced state is due to evolutionary pressures (and indeed why would it not, since evolutionary pressures are solely responsible for species variation and specialization prior to the advent of farming and animal husbandry).

l

Adaptation yes. Evolution, no. Given the time frame...
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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....(For the purposes of this discussion we can ignore the fact that in the first few days of the experiment the blood sodium concentration was protected by the usual contraction of the ECF that occurs whenever there is an acute sodium loss from the ECF. But after day 4 the ECF began to expand despite an ongoing whole body sodium loss. This caused the blood sodium concentration to fall more sharply thereafter)...

Perhaps I'm showing my ignorance here, but isn't this exactly what an exercising athlete is trying to avoid by ingesting salt during exercise? In other words, keeping the blood sodium levels closer to "normal" helps to lessen or prevent the contraction of ECF in the first place? My assumption is that it's the variation in ECF that leads to problems such as cramps, etc.

Sure, there may be an "internal Na store" that the body can tap into in an "emergency"...but, I think the point is to try to avoid forcing the body to go to "emergency measures", no?

http://bikeblather.blogspot.com/
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Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
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Dev,
i am not sure if it is all due to a diuretic hormone imbalance, i think it is mostly due to gravity and inactivity. but it is certainly possible that perhaps the cabin altitude of the aircraft is a factor as well.

that said, you do realize, though, that an economy-class airliner seat is FAR more restrictive to movement than nearly any auto seat i have ever been in. also, with the edema, to me, the condition seems to accelerate with extended duration, i.e., 5 or 8 hours is significant, but the real kick comes with 10, 12, 14+ hour flights. also, normal airliners don't go to 10,000 ft. cabin altitude, they all top out at about 8,000 ft. cabin altitude (but corporate jets are another matter, they will go higher and often approach 10,000 ft. when the jet is flying very high).





Where would you want to swim ?
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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Basic Physiology 1.

The textbooks say that sodium is the principal electrolyte in the extracellular fluid (ECF) which is a volume of 10-14 L depending on body mass. There is apparently little sodium inside cells. The measured concentration inside cells is about 5mmol/L versus 140mmol/L in the ECF. Indeed 40% of the energy we expend at rest is spent on pumping sodium to the outside of our cells. The amount of sodium in the ECF determines the ECF volume. This is because the body homeostatically regulates the osmolality of the body fluids so that there is a constant osmolality which produces a blood sodium concentration of about 140mmol/L in an ECF volume of 10-14 L. What the usual textbooks do not say is that whilst this relationship can well explain the ECF osmolality, it cannot explain the whole body osmolality. Thus in 1957 Edelman discovered that to explain the osmolality of the total body water (TBW - a volume of 35-42 L) there has to be substantially more sodium in the body than that measured in the ECF. But where is it since we “know” it is not in the cells (which are actively pumping sodium from the cells into the ECF to insure that the measureable intracellular sodium (Na+) concentration is very low)? Edelman used a radioactive sodium tracer and showed that the “sodium space” into which the tracer dilutes is much greater than the ECF sodium “space”. He called this new, previously undiscovered amount of sodium the “exchangeable sodium”. It constitutes about 50% more sodium than that present only in the ECF.

The next interesting observation is that in the 1950’s McCance produced a true state of sodium deficiency in humans. To my knowledge this is the only study in the published literature showing that a true sodium deficit can be produced in humans under experimental conditions. He had to go to inordinate lengths to achieve this. Three of the four subjects for his study had to live in his house whilst Mrs McCance fed them a sodium-free diet. Each day they sat in a hot room which produced prodigious sweating for 2 hours a day. By the fifth day they began to show evidence for a salt deficiency. The fourth subject a medical student at Oxford, a Miss Edwards, chose not to live in the McCance residence. A state of sodium deficiency could not be produced in her. Probably she was sneaking some extra salt in her diet.

The evidence for the salt deficiency was a set of symptoms that the subjects developed – absolute lethargy was a key factor – and a fall in blood sodium concentrations (hyponatremia). But the interesting observation was that to recover, the subjects needed to ingest far more sodium than the amount that would have been predicted on the grounds of the fall in their blood (and ECF) sodium concentrations. Thus it were as if something was preventing the fall in ECF sodium concentrations which should have fallen to much lower values based on how much salt the subjects had lost in their urine and sweat during the experiment. It were as if there was a store of sodium that had been called upon to maintain the ECF sodium at a higher concentration than in should have been if all the sodium in the body was only in the the ECF.

(For the purposes of this discussion we can ignore the fact that in the first few days of the experiment the blood sodium concentration was protected by the usual contraction of the ECF that occurs whenever there is an acute sodium loss from the ECF. But after day 4 the ECF began to expand despite an ongoing whole body sodium loss. This caused the blood sodium concentration to fall more sharply thereafter).

More recently there has been increased interest in this “hidden” sodium store. Balance studies of humans fed a very high salt diet showed that they were storing sodium in a site other than the ECF. Thus they did not simply excrete (in urine and sweat) the excess sodium in the diet; nor was it stored in the ECF causing an expansion of the ECF. It had gone somewhere else.

The authors proposed that the extra sodium is stored in the body in an “osmotically-inactive but exchangeable” form (Na) in which it is not measureable as ionic sodium (Na+) but where its presence can be detected by radioactive dilution techniques of the type undertaken by Edelman.

According to this theory there is a store of osmotically-inactive sodium (Na) in the body which can produce osmotically-active sodium (Na+) when it is required. Alternatively when the ECF Na+ concentration rises too high, there can theoretically be osmotic-inactivation of circulating Na+ which is then stored inside cells in the osmotically-inactive form (Na) to be returned to the ECF when it is required.

There are a number of modern observations that support McCance and Edelman’s findings that there must be more sodium in the body than is accounted for by the measured Na+ in the ECF.

For example, if subjects ingest less sodium and water than they lose in sweat during exercise, their blood sodium concentrations ALWAYS rise. This of course is not a fact that the sports drink industry wants you to know. Instead over the past 15 years that industry and its funded scientists have consistently argued that if you don’t replace all the sodium and water that you lose during exercise you will develop exercise-associated hyponatremia (EAH) (which can therefore only be prevented by ingesting a sports drink containing sodium (at low concentrations)). But this is simply not true. The blood sodium concentration ALWAYS rises under these conditions because sweat contains less sodium than does blood (and as I hope we will discuss in due course can contain essentially NO sodium in people living on a very low salt diet) so that more water is lost that salt. As a result the ECF contracts causing the blood sodium concentration to rise. Of course in a perfectly homeostatically regulated system this rise should not be more than a few mmoles/L but in some athletes in competition it can be up to 10-12mmol/L which is surprising and presently unexplained (although it might be explained by individual differences in the ability to osmotically-inactivate ECF Na+ as discussed below).

However we have shown that the change in blood sodium concentrations during exercise is highly individualized and cannot (probably) be explained purely by sodium losses in sweat and urine and changes in the ECF volume. Rather in our paper published in the Proceedings of the National Academy of Sciences in 2005 (and available for free from their website) we proposed that some of this variation must be explained by individual differences in the movement of sodium between the osmotically-active and inactive stores during and after exercise.

Interestingly the ability to deactivate Na+ during prolonged exercise and store it would delay the onset of thirst (which is stimulated by a rising ECF sodium concentration). Thus the presence of this store could have been a way in which our hominin ancestors were able to delay their thirst during long, hot, water-less hunts (see the thread on Why cannot scientists ever agree on anything?).

A tragic case supports this contention that there must be this internal sodium store. When Cynthia Lucero died after the 2002 Boston marathon because she had drunk too much of a sports drink (and retained that fluid excess within her body because she was also excreting too much anti-diuretic hormone – ADH), our calculations show that she simply could not have drunk sufficient to drop her blood sodium concentration as low as the value measured when she was admitted to hospital. Instead something else must have happened and one possibility is that she had also osmotically-inactivated some of her ECF Na+ at the same time transporting it into her cells causing her hyponatremia to be exacerbated. When we performed calculations on the data of fluid and sodium balance on patients treated by either ourselves or Dr Speedy in New Zealand for EAH, we came to the conclusion that some may have inactivated Na+ during the races in which they developed EAH with subsequent osmotic re-activation during recovery. But since we did not actually measure the process we cannot be sure.

What might this all mean. To return to the evolutionary perspective. It would make sense for humans evolving in a relatively salt-free environment to have an internal sodium store that could be filled in times of plenty and depleted in times of scarcity. Since salt is the most important regulator of the ECF volume and since if we cannot regulate the ECF volume accurately we die very quickly it makes sense to de-link regulation of the ECF volume from the daily sodium intake. How could we have survived if our lives depended on finding just enough salt each day in an environment in which salt was in scarce supply? Those who developed an internal sodium store under these conditions would be the most likely to survive.

If this store exists it might explain, in part, why it is so difficult to cause a true state of sodium deficiency in humans.

But more importantly, how does one measure a state of sodium deficiency in athletic humans? This is important since many contributors to this forum as do you yourself, believe that you develop cramps (or impaired performance) because of a sodium-deficit caused by large sodium losses in sweat. (Note that the model you use to explain this is catastrophic and non-homeostatic. It is based on the belief that the body has no ability to homeostatically regulate its losses and so will just continue to exercise until there is a catastrophic failure of function, in this case muscle cramps. But does it not make more sense to believe that evolution would have weeded out all these obvious system failures so that your problem is not likely caused by a system that is known to be homeostatically regulated and essential for life not just during exercise and the failure of which would have killed you long before you developed muscle cramps? Should we not look elsewhere for a better explanation than in a system that if it did not work perfectly we would not survive? Of course this is not how industry sees it. They want us all to believe that humans are weak and on the verge of a catastrophic biological failure that can only be prevented by the ingestion of their products, be they pharmaceutical products, sports drinks or other nutritional supplements).

The usual way to measure a sodium deficiency is by measuring the blood sodium concentration. But this is not fool proof since we know that the main cause of a low sodium concentration is a large increase in the ECF (and TBW) volume as occurs in EAH. Thus to prove a sodium deficiency you need to measure a low blood sodium concentration WITHOUT any increase in ECF volume. But this would not necessarily tell you what is the state of your internal sodium stores. The problem might be in the ability to activate intracellular osmotically-inactive Na.

But we can prove when a sodium-deficit does NOT explain your symptoms. Thus if you have symptoms and your blood sodium concentration is normal then BY DEFINITION your symptoms cannot be due to a sodium-deficit. Of course this is not something that you will hear from the sports scientists who acts as spokespersons for the sports drink industry. I recall hearing one well know (notorious?) such speaker for the industry say at a meeting in Australia that the presence of muscle cramps proved that the athlete had a sodium deficit even though the blood sodium concentration was normal. Of course this is not what we were taught in medical school. But then why cannot industry develop its own brand of physiology? Especially if it can find sufficient “scientists” to promote this novel brand of knowledge.

So the short answer to your question is the following: What was your blood sodium concentration at the time you developed your muscle cramps? If it was normal then the ingestion of salt either before or during exercise does not cure or prevent the condition by preventing the development of a sodium deficit. Rather it is acting in some other way that we currently do not understand.

That is enough for today. More on anther occasion.
A few comments.

So, where is this sodium reservoir, in your opinion. It must be in contact with the ECF but not readily exchangeable. The only areas that might fit this description I can think of are 1. the eyeball, 2. the bones, 3. the gut.

The gut is the only part that of the body that makes any sense to me, off the top of my head, that might serve this purpose.

Next, why are you so fixated on sodium alone. The change in any one electrolyte has an impact on every other one. Arguably the most difficult electrolyte to discern total body deficiency is potassium, because it is by far the most common one yet, the most inaccessible for testing because it is in high concentration only in the ICF. But, it is the balance of na/k that primarily determines "optimum" cell function, especially for electrically active cells such as nerves and muscles. During exercise potassium tends to come out of the cells which would further mask a potassium deficiency, should one be present, and it cannot be corrected with potassium supplementation because such would only make the situation worse because the problem is getting the potassium into the cells, not into the body. Sodium deficiency is relatively easy to measure compared to potassium deficiency.

The other electrolytes are also important, especially if one is discussing cramping. This is a much more complicated problem than simply water and sodium.

Regarding bloating and failure to absorb fluids we must remember this is a passive process. If the body is dehydrated and shunting blood from the gut to support other demands it will be pretty much impossible to rehydrate until the "other demands" stop and "bloating" and "sloshing" is going to occur.

Seems to me, if you want to understand this stuff, it is necessary to put people on the treadmill for 4-6 hours and try to cause it (there is also, probably, more than one mechanism) while monitoring a whole bunch of parameters to try to understand where the water and sodium is and is going when these problems occur. If one can reliably cause these problems then one should be able to figure out how to reliably prevent them.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Tom A.] [ In reply to ]
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No. What you are trying to do is to maximize your performance. All the published evidence shows that if you drink to thirst you will maximize that performance. If you want to maintain your ECF volume during exercise you have to drink way beyond thirst and ingest a large amount of salt, much more than is present in sports drinks. So you can't do it by just drinking a sports drink. We showed this years ago - published in the European Journal of Applied Physiology (B. Sanders et al).

So clearly the body does not need to maintain its ECF volume in order to maximize performance. Again the evidence is that the very best athletes are able to sustain large fluid losses during exercise (presumably with quite large drops in ECF volume) without any apparent impact on their performances.

More later.
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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All the published evidence shows that if you drink to thirst you will maximize that performance.
To what study or studies are you referring?
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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This is important since many contributors to this forum as do you yourself, believe that you develop cramps (or impaired performance) because of a sodium-deficit caused by large sodium losses in sweat. (Note that the model you use to explain this is catastrophic and non-homeostatic. It is based on the belief that the body has no ability to homeostatically regulate its losses and so will just continue to exercise until there is a catastrophic failure of function, in this case muscle cramps. But does it not make more sense to believe that evolution would have weeded out all these obvious system failures so that your problem is not likely caused by a system that is known to be homeostatically regulated and essential for life not just during exercise and the failure of which would have killed you long before you developed muscle cramps? Should we not look elsewhere for a better explanation than in a system that if it did not work perfectly we would not survive? Of course this is not how industry sees it. They want us all to believe that humans are weak and on the verge of a catastrophic biological failure that can only be prevented by the ingestion of their products, be they pharmaceutical products, sports drinks or other nutritional supplements).

Regarding cramping: I had some pretty serious cramping at the end of a long rugby practice back in the '90s. Later, I discussed that with a girl who was working as an athletic trainer at the time. She asked me, "Are you drinking milk?" I said, "No, not at all." (At that point, I wasn't drinking any.) She told me then it was likely related to a calcium deficiency.

I started drinking milk again, and I haven't had cramps since.

I had the same discussion with a marathoner (my dad) a few years ago: "I had this awful cramping around mile 20." "Are you drinking milk?" "Not at all." "Maybe you should."

So, Dr Noakes, or anyone else who wants to respond, is calcium deficiency perhaps a more primary cause of cramping? How about other electrolytes like potassium? What's their relationship to all of this?
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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Seems to me, if you want to understand this stuff, it is necessary to put people on the treadmill for 4-6 hours and try to cause it (there is also, probably, more than one mechanism) while monitoring a whole bunch of parameters to try to understand where the water and sodium is and is going when these problems occur.

So you don't think that observational studies in the field are the best way to answer such questions?
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Re: Tim Noakes: we need you back for a moment [Slowman] [ In reply to ]
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Dan,
At a recent fund-raiser 5k in Glendale, I met a duathlete who is proficient enough to have been to the world champs and he said that any sodium intake by him during races makes him nauseous. I, on the otherhand, do the opposite. I get nauseous and feel drained on hard efforts over an hour without a salty fluid. When I played tennis in my teens, in El Paso, we did pretty well with just water, but I did begin to bloated and sluggish after a few hours. I always went home after a few hours of playing with big white lines all over my body. (the dog loved it.)

As an undergraduate in New Orleans, where sweating took on a whole new meaning, after a set or two, even with plenty of water I felt very sluggish and bloated. A playing partner introduced my to Gatorade. This was in the 70's, and, if I recall correctly, the formula was closer to Pedialyte (2.5% glucose and ~0.3Normal Saline--less sugar and more sodium. It also tasted pretty lousy). After that, I could down a quart after each set and play for much longer period without losing performance.

When using cytomax, I just couldn't get over the bloated feeling and nausea until I began to add salt to make a mixture of around 25mg/oz of fluid. So, this is proportion that I use, except of shorter workouts, where water seems to suffice.

I suspect that some individual variation is at work here and might explain why some athletes, like the duathlete above and Fleck (if I recall correctly) do not use or like sodium in races and others don't seem to do well without it. Maybe those of us needing more have ancestors that evolved in areas where the was no shortage of sodium and others in more inland valleys and highlands where sodium is less available. Or, we are just 'weak sauce.'

_________________
Dick

Take everything I say with a grain of salt. I know nothing.
Last edited by: docfuel: Apr 22, 09 8:22
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Re: Tim Noakes: we need you back for a moment [jsquared] [ In reply to ]
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... a sexual disparity could be explained from an evolutionary standpoint if we assume that males were more likely ...

fine. except that there really isn't a lot of compelling evidence for gender-based roles in early human or pre-human populations. so maybe we could just skip the usual hand waving "men hunted, women raised children" simplifications, and move right along?


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Re: Tim Noakes: we need you back for a moment [Andrew Coggan] [ In reply to ]
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In Reply To:
Seems to me, if you want to understand this stuff, it is necessary to put people on the treadmill for 4-6 hours and try to cause it (there is also, probably, more than one mechanism) while monitoring a whole bunch of parameters to try to understand where the water and sodium is and is going when these problems occur.

So you don't think that observational studies in the field are the best way to answer such questions?
No, because you are only seeing the end result and you don't know if there is one or several mechanisms that might lead to a similar end. And, it is difficult to do the specialized testing necessary to understand what is going where.

Not every person has this problem. Unless you understand the characteristics of those who do and what it requires to avoid such problems in those people you cannot say you understand the problem. If we could figure this out from simple "observational studies in the field" this would have been solved a long time ago as this issue has been around and observed by many very smart people for a long time.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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In Reply To:
No. What you are trying to do is to maximize your performance. All the published evidence shows that if you drink to thirst you will maximize that performance. If you want to maintain your ECF volume during exercise you have to drink way beyond thirst and ingest a large amount of salt, much more than is present in sports drinks. So you can't do it by just drinking a sports drink. We showed this years ago - published in the European Journal of Applied Physiology (B. Sanders et al).

So clearly the body does not need to maintain its ECF volume in order to maximize performance. Again the evidence is that the very best athletes are able to sustain large fluid losses during exercise (presumably with quite large drops in ECF volume) without any apparent impact on their performances.

More later.
It makes perfect sense that performance could be maximized with a slightly smaller than resting ECF volume, since this reduces the diffusion distance of oxygen from the capillary to the mitochondria, at least as long as enough blood volume is maintained to maintain cardiac filling pressures to maintain cardiac output.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [dawhead] [ In reply to ]
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... a sexual disparity could be explained from an evolutionary standpoint if we assume that males were more likely ...

fine. except that there really isn't a lot of compelling evidence for gender-based roles in early human or pre-human populations. so maybe we could just skip the usual hand waving "men hunted, women raised children" simplifications, and move right along?

If it makes you happy, but it's funny how many primitive societies still follow this pattern. It also seems funny that gross uniformity of activity & environment appears to be what drives adaptation & evolution but if you want to think the women hunted and the men stayed back and did their nails power to you.

JJ

Every night that I run, the thought crosses my mind that there's no way in hell I'll still be running a month from now.
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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thank you for taking the time to comprehensively confront this for us.

your explanation notwithstanding, i am still left with the question of what causes my muscle cramps. further, i also suffer from an occasional heart arrhythmia at moderately high heart rates, specifically a-fib above HRs of 135 or 140 bpm. this is short lived, just 3 or 4 beats at a time, and self-resolves, but it seems persistent after several days of intensive training, esp if a large component of that training is high-HR.

i can only guess at the mechanisms, but since both heart function and muscle contraction are electrical functions, i'm left to wonder whether it's a cation i'm low on.

as frank day pointed out, while sodium stores (except for the hidden sodium treasure) are readily measurable because the cells' active pumping of sodium into the ECF, potassium exists largely in the ICF and is therefore hard to measure. i'm quite eager to hear that my problem is not with sodium, but with K+, Ca+, Mg+.

that established, i'm still not convinced that Na+ supplementation is a bad thing. let's liken it to petroleum. what you're saying is that the body maintains the sodium analog of what in america is called our "strategic petroleum reserve," which for lack of a better term consists of a "valve" our government turns on and off to moderate the effects of acute petroleum shortages. if the body, during exercise, excretes large amounts of sodium through sweat, and calls on its "strategic sodium reserve," then that sodium will have to be replenished eventually anyway. why not during the race instead of after the race?

but let's leave that aside. to bottom-line it, i'm guessing (and it's just a guess) that my a-fib and my cramping might have etiologies in some way connected. i don't personally care whether gatorade makes billions or goes broke. if all my muscles (heart and skeletal) rhythmically fire, i'm a happy guy. i'm open to hearing that it's not due to a lack of Na+, but what about the other cations? my occasional exercise-induced a-fib is nothing compared to heart problems associated with hyperkalaemia, and i don't know when and if i might be in danger of intaking too much potassium.

if i was to hazard a guess, it would be that my Mg+ is the one cation i might be missing, only because of my occasional and stress-induced arrhythmia. but my cardiologist is so busy shuffling 85 year olds in and out of his office he's got no time for a thoughtful discussion.

whether it's on this thread or elsewhere, i would eventually like to drill down to:

1. what relieves or delays cramping?
2. what bad thing can happen if i take salt pills during a race, during a workout, after a workout, assuming i'm not hypertensive?
3. what do we do with the very high incidence of salt pills taken by top triathletes? are they all indulging in mass cation hysteria?
4. and finally, anecdotal cases of hyponatremia in my experience pale in contrast to anecdotal cases of heart arrhythmias in otherwise very healthy athletes; can prolongued exercise in the absence of a certain factor be the proximate cause?

Dan Empfield
aka Slowman
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Re: Tim Noakes: we need you back for a moment [Slowman] [ In reply to ]
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Wendy Ingram spoke at a local Tri Club meeting a few years back and was asked about the "Crawl-Fest" in Kona. She said that she typically wore a pouch around her wrist to store her salt tabs and that she accidentally left the zipper open and lost all of the salt. She seemed certain that's what caused her meltdown.

Maybe that was the problem, maybe it was something else but it seems like "Wing Nut" paid very close attention to detail and her salt intake was the only element that was not executed accoring to her plan. Slowman noted some real-world experiences that seem to support his claims that taking on salt has helped him. At Oceanside this month, I felt a cramp coming on at Mile 1 of the run. I forgot my salt on my bike so I grabbed some pretzels and bananas at the first two aid stations. The cramp went away.

I guess my point is that while all that science looks impressive...and sorry, is as boring as whale shit...I think it's possible that something is missing. I think it goes without saying that everyone should experiment during training, figure out what works for them, and do that on race day.
Last edited by: cjbruin: Apr 22, 09 9:42
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Re: Tim Noakes: we need you back for a moment [jsquared] [ In reply to ]
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1) "primitive" societies are human societies that are generally at least 5-10,000 years old. there is some evidence that they have undergone their own kinds of societal transformation during that time, and although they can serve as useful indicators of how very early humans may have lived, they are certainly not examples of very early human life.

2) early humans didn't hunt much anyway, so the notion that one set of them stayed home and did X while another group went out hunting appears (based on current archeology) to be a bit of a distortion.

3) if you take a look at non-human primate societies, which have also likely changed in significant ways since the fork that gave rise to us, you will find some gender based roles but they appear to have a lot more to do with mating and dominance behavior than with the kinds of physical tasks that might lead to gender disparities in relation to "endurance athletics". male, non-human primates simply do not spend much time doing things that would lead to to strong evolutionary benefits for those adapted to endurance tasks.

4) studies of both chimpanzee and orang-utan clans suggest that both males and females appreciate doing their nails to about the same extent.

5) anytime an animal lives in a predominantly social context, evolutionary pressures change dramatically. what leads to genetic continuance in even a small tribe of hunter-gatherers is very very different from the traits that lead to success as a lone predator. there are some hypotheses that suggest that traits like empathy (in the broadest sense of having some clue what another individual is thinking), communication (verbal, body, other) and planning are probably more critical to genetic continuance in even early human societies than the ability to run towards or away from potential food sources and predators. its not likely that we're going to know the relative significance of these kinds of traits for a very long time, if ever.
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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Again the evidence is that the very best athletes are able to sustain large fluid losses during exercise (presumably with quite large drops in ECF volume) without any apparent impact on their performances.

More later.
That is a huge presumption that large fluid losses during exercise are mostly accounted for my drops in ECF volume. I suspect that large fluid losses do not see large ECF volume losses because of the buffering effect from fluid shifts from the ICF just like large shifts in acids in the body do not cause large shifts in pH because of the buffering system in place. Unless these different compartment volumes are actually measured during these conditions one is just guessing as to what is going on.

Your arguments seem to imply that it doesn't matter how much fluid the athlete loses, they will be ok, perhaps even perform superiorly - as long as they "listen to their thirst". In my opinion, such an approach may work for some but will fail many.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [dawhead] [ In reply to ]
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1) "primitive" societies are human societies that are generally at least 5-10,000 years old. there is some evidence that they have undergone their own kinds of societal transformation during that time, and although they can serve as useful indicators of how very early humans may have lived, they are certainly not examples of very early human life.

Perhaps not very early human & pre human life, but evolution and adaptation happens more quickly than most people suspect. Although the underlying mechanisms may have evolved over millions of years, the specific level of things such as the rate of Na transfer from some existing storage capacity could adapt to much higher or lower levels very quickly in the order of thousands of years or at worst 10's of thousands of years, if there is sufficient environmental pressure and the underlying mechanism is already in place. So the hypothesis of the male hunter fueling this adaptation is as valid as any.

2) early humans didn't hunt much anyway, so the notion that one set of them stayed home and did X while another group went out hunting appears (based on current archeology) to be a bit of a distortion.

It depends on what we're calling "early", pre humans a million years ago or early homo sapian 30K years ago.

3) if you take a look at non-human primate societies, which have also likely changed in significant ways since the fork that gave rise to us, you will find some gender based roles but they appear to have a lot more to do with mating and dominance behavior than with the kinds of physical tasks that might lead to gender disparities in relation to "endurance athletics". male, non-human primates simply do not spend much time doing things that would lead to to strong evolutionary benefits for those adapted to endurance tasks.

I don't consider the non-human primates to be relevant as they have had different evolutionary pressures for the order of millions of years.

4) studies of both chimpanzee and orang-utan clans suggest that both males and females appreciate doing their nails to about the same extent.

Some males of the human species too but I'll stick with sexual diversity on the percentages.

5) anytime an animal lives in a predominantly social context, evolutionary pressures change dramatically. what leads to genetic continuance in even a small tribe of hunter-gatherers is very very different from the traits that lead to success as a lone predator. there are some hypotheses that suggest that traits like empathy (in the broadest sense of having some clue what another individual is thinking), communication (verbal, body, other) and planning are probably more critical to genetic continuance in even early human societies than the ability to run towards or away from potential food sources and predators. its not likely that we're going to know the relative significance of these kinds of traits for a very long time, if ever.

The social context only strengthens the argument for sexual diversity of tasks within the society. Even today, members of the society gravitate toward the tasks that they are best suited for and most proficient at (mostly anyway because it seems some individuals are proficient at nothing). It would make sense that the tasks most males performed would differ from the tasks most females performed, and the perceived fitness as a mate would select for mates better adapted for these tasks. It may not exactly have been spending 4 hours running down an antelope but likely it was more physically demanding tasks fueling the adaptation that human males, on average, are stronger & faster than females even though the range is so vast that many females can outperform all but the best of males.

JJ

Every night that I run, the thought crosses my mind that there's no way in hell I'll still be running a month from now.
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Re: Tim Noakes: we need you back for a moment [docfuel] [ In reply to ]
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I suspect that some individual variation is at work here and might explain why some athletes, like the duathlete above and Fleck (if I recall correctly) do not use or like sodium in races and others don't seem to do well without it. \\

This is exactly right. And when you study certain groups of people, you very well may get a skewed result. If you only look at elite runners, you are looking at mostly super low body fat folks of mainly African descent. If you study Ironman champions, most have been pre selected for heat tolerance from their genetics. That is a big reason they are at the top of Hawaii, so to test them only would not be a fair sampling..

In Noakes talking about the house study, I don't doubt the results, but Ironman is not sitting in a house for days on end with no salt. What I think happens is a vastly accelerated version of the study. I feel that in a 9 hour race in Hawaii, it could quite possibly be like a week in that house, as far as depletion is concerned. And in that house, the body has time to regulate and compensate for the stress put on it. I believe in racing, the bodies compensation triggers, do not have time to click in so to speak, and thus cannot be relied on for good information. That is why almost all sucessful Ironman athletes stay ahead of those, and begin drinking, eating, and electrolyte supplements before the felt need for them.

Basically I'm with Frank on this(who would have thought? (-;, you need to study the entire situation, before, during, and after, and you need a representative sample group. I guarantee you that if you take me, Molina, Pigg, and a few others, and you just test us, then the result is going to be waaay different that if you take Paula, Dave, Chrissie, Erin Baker, and all the others that have done well at Hawaii, and seem impervious to the heat there....
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Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
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By the way, I did take your previous advice and no longer run immediately after long flights. I either walk, or go for a swim if there is a pool at hand. I assume this is OK. Also started wearing compression socks on long flights and as a bare minimum, legs feel lighter when I deplane....hoping to get an upgrade on the Tokyo Toronto leg tomorrow and I can have my legs up for 12 hours :-)

Dev

Dev, I'm curious as to why no long runs after long flights. I'm doing more international travel these days (LA to Buenos Aires this week) and upon arrival in BA did an easy 10-mile run. Was this a mistake? I'd be curious what guidance GregX or others have provided in the past to lead you to not run long off the flight.

Thanks.

Fred
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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I am catching this thread a little late so please forgive me if these issues have been addressed. If I am reading your post correctly, you imply that we do not need to ingest sodium during a race because our bodies have internal stores of sodium and it makes sense that evolutionarily we have evolved to not need to take it in.
My question then is, do you suggest athletes not ingest calories? It seems to make sense given the logic on sodium. Our bodies have vast stores of calories which they can access during prolonged (multi-day) periods of calorie restriction/starvation. It also makes sense that evolutionarily we would evolve to be able to access these calorie stores. Bonking in a race is bad, bonking while being chased by a predator is death. Yet I hope you would not argue we do not need to consume calories in a race. Yes, we have vast stores of fat which could be used. However we can not access them as quickly as we are using them. Perhaps it is the same with sodium? Yes, it makes sense evolutionarily that we would have evolved to not need to take in calories. Perhaps evolution is not perfect. Perhaps the demands placed on our bodies during exercise are such that evolution has not been able to fully tweak these systems.
It makes sense that we can outrun our bodies ability to regulate itself. You make a comment about, "
the belief that the body has no ability to homeostatically regulate its losses and so will just continue to exercise until there is a catastrophic failure of function, in this case muscle cramps." That is my believe. It makes sense our bodies evolved to be able to run until we die because exercise meant survival. You ran to eat or not be eaten. Anything which hindered your ability to run meant death. So yes, we can run to catastrophic failure. And evolution worked to try to put off this failure as long as possible. But it is not perfect.
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Re: Tim Noakes: we need you back for a moment [GregX] [ In reply to ]
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Basic Physiology 3.

As presented by the Sports Drink Industry and its funded scientists and sports medicine and athletic coaching associations.

1. Humans are a divine creation with a biology that is unique and unrelated to that of all other creatures on earth.

Thus whereas all other creatures on earth are able to regulate their body temperatures and body water and sodium balance by responding to internal cues, all humans must be told exactly when, how much and what to eat and drink before, during and after exercise.

2. Because they are unique creatures, humans have no capacity to homeostatically-regulate their bodily functions particularly their body temperatures, their levels of dehydration and their body salt levels during exercise.

Instead when they exercise their body temperatures rise precipitously leading ultimately to heat stroke or “heat illness” or heat cramps; they develop “dangerous dehydration” causing heat stroke and “heat illness”; and they continue to sweat a “salty sweat” leading to salt-deficiency “heat illness”, salt-deficiency muscle cramps and salt-deficiency hyponatremia. Many of these conditions are potentially fatal.

As a result it is very dangerous for humans to exercise unless (i) they follow the cautionary guidelines provided by influential sports medicine and athletic coaching associations (many of which are generously supported by the sports drink industry to insure that all humans – at least those in the developed world who perhaps have a larger disposable income – appreciate these specific biological weaknesses) and (ii) they ingest novel products designed exclusively for their use and which provide exactly the right amounts of water, salt and other necessary ingredients to insure that they do not develop any of these catastrophic conditions during exercise.

3. Since all other creatures on earth are different, they do not need this information. Thus Veterinary Associations caring for all other creatures do not need to produce detailed guidelines advising dogs, cats, lions, camels, large antelope etc how much, when and what they need to drink before, during and after exercise. Since they have a different and much superior biology (perhaps designed by evolution) that accurately provides this information on a moment to moment basis, they do not need other dogs, cats, lions, camels, large antelope etc to form associations advising each separate species how much, when and what they need to drink before, during and after exercise.

4. There is no limit to the amount of fluid that can be absorbed by the human intestine. Thus a 50kg world-class runner able to sweat at a rate of 3L/hr has the capacity to replace all that fluid and must drink at a rate of 3L/hr (1L every 20 minutes).

5. Anyone who disagrees with any part of this analysis is by common consent an idiot and must be publicly humiliated at every opportunity (see the thread: Why can’t experts agree etc).

Comment: Surprisingly humans have had great difficulty deciding exactly how much and what athletes should drink before, during and after exercise. Before we knew better (ie before the development of the sports drink industry and its funded scientists who worked out 1 and 2 above) humans were advised NOT to drink at all during exercise but that they could ingest salt tablets. Water was considered anathema since it would cause a “stitch” and a sudden impairment in performance known as “weakness”.

Then almost out of nowhere in 1996 the industry-funded American College of Sports Medicine (ACSM) decreed that from now on it was only safe for humans to exercise if they drank either 600-1200ml per hour or “as much as tolerable” during exercise. The ingestion of sodium during exercise was also essential to prevent hyponatremia. Failure of humans to follow these guidelines precisely would cause all exercising humans to develop all the conditions described in 2 above. (This despite an absence of any evidence that these conditions had occurred commonly in athletes who had competed in athletic events including marathons and ultra-marathons between about 1880 and 1970 and had drunk little if at all during those competitions). A global pandemic of cases of exercise-associated hyponatremia (EAH) was unleashed when these guidelines were adopted.

In 2007 the ACSM significantly modified these guidelines which now state that athletes should drink according to the dictates of thirst but should not lose more than 2-3% of their body weight during exercise. Now appropriate fluid intake rates are between 400-800ml/hour. The ACSM continues to advise that sodium must be ingested during exercise in order to prevent EAH.

In contrast US Track and Field and the International Marathon Medical Directors Association have adopted guidelines which propose that the optimum drinking guideline is to drink to thirst regardless of the extent of weight loss that develops during exercise. These guidelines are based on the theory that the brain uses thirst to drive appropriate drinking behaviour and that if the athlete chooses to ignore thirst eventually the brain will cause the body to slow down until fluid is ingested so that the symptoms of thirst disappear. The guidelines do not propose that sodium needs to be ingested during exercise to prevent EAH.

The International Consensus Statement on EAH also agrees that sodium ingestion is not required to prevent EAH.
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Re: Tim Noakes: we need you back for a moment [Slowman] [ In reply to ]
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Basic Physiology 2.

Humans are designed to homeostatically-regulate with exquisite accuracy the amount of sodium that is present in their bodies. They do this by matching to the nearest few milligrams the amount of sodium that they ingest and lose each day. Without this exquisite regulation, human life would not be possible.

It is my argument (based on the work of Dr Dan Lieberman of Harvard University amongst many others) that we evolved as sweaty, long distance runners in a relatively salt-free environment and so evolved mechanisms that would allow us to exercise in heat whilst losing some salt in sweat but still maintaining whole body sodium balance even on this relatively salt-poor diet. I presented some of the evidence for this in the thread: Why can scientists never agree etc.

First is the evidence that it is extra-ordinarily difficult to produce a sodium deficit in free-living humans. In fact the condition may not exist in free-living humans. One of the only studies of which I am aware in which a true sodium deficit was produced was the study of McCance described in Basic Physiology 1. But this could only be produced by subjecting the subjects to Mrs McCance’s sodium-free diet and then forcing them to sweat heavily by exposing them to severe heat on a daily basis.

Second were the studies of iconic US physician JW Conn of the University of Michigan Medical School at Ann Arbor. He noticed that subjects undergoing a period of heat acclimatization reduced their sweat and urine sodium concentrations. He then wondered what causes this and what was the effect of reducing the amount of salt in the diet. He showed that almost immediately on exposure to a reduced sodium intake subjects reduced the amount of sodium they lost in their urine. Within 2 days they also reduced the amount of sodium lost in their sweat. As a result within a day or two subjects had adapted their sodium losses exactly to match their (reduced) sodium intakes. This occurred even on a sodium intake as low as 3g per day; he did not test lower salt intakes. He also showed that sweat sodium concentrations could drop to 1-10mmol/L (compared to the reported values of 50-70mmol/L in the so-called “salty sweaters” beloved of the US sports drink industry).

In time he discovered that the hormone aldosterone was responsible for this adaptation and subsequently described a condition termed Conn’s syndrome in which a tumour of the adrenal cortex secretes excessive amounts of aldosterone causing high blood pressure (and very low sweat sodium concentrations amongst many other features).

Interestingly studies of elite Kenyan runners living and training in Eldoret, Kenya show that they train up to two hours a day whilst eating a diet containing just 3 grams of salt per day. This compares to the typical average salt intake of 7-10 grams per day of sedentary individuals living in developed countries. Since the sweat of the Kenyans was still not as low as 1-10mmol/L it seems probable that they could have adapted successfully to an even lower daily salt intake.

In summary, it is clear that human athletes can adapt to much lower daily sodium intakes than they will ever wilfully choose to ingest. When the intake is higher than this minimum the excess will appear in the urine and sweat. The point is that the presence of salt in the urine and sweat in high concentrations does not mean that the athlete is at risk of becoming salt deficient as is the popular distortion of the sports drink industry. Instead the reality is that the appearance of salt in the urine and sweat in high concentrations indicates a desperate attempt by the body to adapt to an unnecessarily high salt intake. Ingesting even more salt is clearly not the correct choice.
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Re: Tim Noakes: we need you back for a moment [dtreeps] [ In reply to ]
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Dear Dan,

I can't explain your observation. The value of taking gels is that they provide carbohydrate which can improve performance by correcting a low or a developing low blood glucose concentration. Puting carbohydrate in the mouth is enough to improve performance as recently reported in a British study also reported on the Time website. The brain interprets the presence of glucose in the mouth as a good sign and allows the body to exercise more vigorously as a result even before the carbohydrate is absorbed and metabolised.

My own experience in ultradistance running events was that the provision of lots of carbohydrate (25-40 grams per hour) during the second half of races longer than 42km has a much greater impact on my performance than did drinking fluids (hence my bias I suspect). We did not ingest salt in those days.

But I cannot explain how taking more carbohydrate or protein affects your fluid balance. It is not something I have thought about.
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Re: Tim Noakes: we need you back for a moment [Slowman] [ In reply to ]
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This thread is a sketch of human nature. When faced with a problem, we naturally look for a solution, hoping that more is under our control than is often the case.

There are many factors that could cause cramping that are completely beyond our control. The temperature or ph of the tissues might be sufficiently different on hot and humid days to tip the scales toward early failure. The ability of the muscle to remove by-products may be impaired. Venous blood flow may take a more superficial path from the legs to help cool the body, thereby causing several potential changes deep in the muscle.

While it certainly makes sense to control everything as best we can, delivering sufficient fluid, electrolytes, nutrients, etc. to the working muscle, it isn't always enough.

Consider from the perspective of the antelope, whose life is at stake. If given Gu, Gatorade, Endurolytes, would his end result be any different? Or would his fate be the same, being an antelope, after all?


Coach at KonaCoach Multisport
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Re: Tim Noakes: we need you back for a moment [Eileen Steil] [ In reply to ]
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Dear Eileen,

You are developing the syndrome of inappropriate ADH secretion (SIADH). ADH is the hormone that regulates water re-absorption by the kidneys. Once you over-secrete ADH you are unable to excrete any water that you take in excess of your requirement.

The treatment is to exactly match your daily water intake with your requirement. This can only be done by weighing yourself every few hours during these events to insure that you do not gain any weight. Because you will be travelling quite slowly in these events your sweat rate will be much lower than perhaps you suspect. Thus your fluid intake requirement will also be much lower.

There are ADH blockers that are being developed but you do not need a pharmaceutical solution. Using a scale effectively is all you need.
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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I cannot explain how taking more carbohydrate or protein affects your fluid balance. It is not something I have thought about.
I'm...speechless.
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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In Reply To:
Again the evidence is that the very best athletes are able to sustain large fluid losses during exercise (presumably with quite large drops in ECF volume) without any apparent impact on their performances.

More later.
That is a huge presumption that large fluid losses during exercise are mostly accounted for my drops in ECF volume. I suspect that large fluid losses do not see large ECF volume losses because of the buffering effect from fluid shifts from the ICF just like large shifts in acids in the body do not cause large shifts in pH because of the buffering system in place. Unless these different compartment volumes are actually measured during these conditions one is just guessing as to what is going on.

Your arguments seem to imply that it doesn't matter how much fluid the athlete loses, they will be ok, perhaps even perform superiorly - as long as they "listen to their thirst". In my opinion, such an approach may work for some but will fail many.
It clearly fails me (as I mentioned in post #2 in the thread) because my weight loss limits are in the 4% range for onset of extreme fatigue and cramping. My body typically doesn't say "DRINK NOW" until at least 3% loss, at which point I am already deep in the hole. I'm sorry, but the experiments showing that "the very best athletes are able to sustain large fluid losses" does absolutely nothing to help those who cannot sustain large losses. To that extent, Yknot and others make a very good point...to wit...just because humans may have a wide store of slowly-or-variably-slowly-accessible Na stores does not mean it's a good idea to try to use them during a race. The same goes with calories..bonking due to hitting the readily-available glycogen store limits.

Regarding Calcium and Magnesium, I have found two consistent effects of deficiencies. Calcium deficiency is absolutely a big contributor to cramping muscles for me, partially because I'm allergic to milk and likely don't get enough. I supplement with Calcets during excersize (1 per hour roughly) and it's a big help for reducing the chances of cramping. Magnesium deficiencies always show up as "twitchy muscles," usually in the calves. This can definitely be a cramp-causer as the twitchiness expands to cramps. I found this one by searching for information on twitchy calves and RLS (restless leg syndrome).

Regarding the kind of weird animal analogy...most animals aren't INTENTIONALLY going out and racing Ironman...which is arguably well beyond the normal limits based on human evolution. You find animals like dogs, lions, giraffes, etc. sitting in the shade in the middle of the hot summer day...while us idiots are out there attempting to run beyond our limits. Smile


Mad
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Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
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Dear Dev,

Good to hear from you again. Your hyponatremia in the Ironman was due to SIADH so clearly you are prone to conserve water under stressful condtions. Perhaps the low oxygen concentration in the airplane or simply sitting for prolonged periods are enough to activate your systems of water conservation again.
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Re: Tim Noakes: we need you back for a moment [triguy42] [ In reply to ]
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In Reply To:
In Reply To:
In Reply To:
Again the evidence is that the very best athletes are able to sustain large fluid losses during exercise (presumably with quite large drops in ECF volume) without any apparent impact on their performances.

More later.
That is a huge presumption that large fluid losses during exercise are mostly accounted for my drops in ECF volume. I suspect that large fluid losses do not see large ECF volume losses because of the buffering effect from fluid shifts from the ICF just like large shifts in acids in the body do not cause large shifts in pH because of the buffering system in place. Unless these different compartment volumes are actually measured during these conditions one is just guessing as to what is going on.

Your arguments seem to imply that it doesn't matter how much fluid the athlete loses, they will be ok, perhaps even perform superiorly - as long as they "listen to their thirst". In my opinion, such an approach may work for some but will fail many.
It clearly fails me (as I mentioned in post #2 in the thread) because my weight loss limits are in the 4% range for onset of extreme fatigue and cramping. My body typically doesn't say "DRINK NOW" until at least 3% loss, at which point I am already deep in the hole. I'm sorry, but the experiments showing that "the very best athletes are able to sustain large fluid losses" does absolutely nothing to help those who cannot sustain large losses. To that extent, Yknot and others make a very good point...to wit...just because humans may have a wide store of slowly-or-variably-slowly-accessible Na stores does not mean it's a good idea to try to use them during a race. The same goes with calories..bonking due to hitting the readily-available glycogen store limits.

Regarding Calcium and Magnesium, I have found two consistent effects of deficiencies. Calcium deficiency is absolutely a big contributor to cramping muscles for me, partially because I'm allergic to milk and likely don't get enough. I supplement with Calcets during excersize (1 per hour roughly) and it's a big help for reducing the chances of cramping. Magnesium deficiencies always show up as "twitchy muscles," usually in the calves. This can definitely be a cramp-causer as the twitchiness expands to cramps. I found this one by searching for information on twitchy calves and RLS (restless leg syndrome).

Regarding the kind of weird animal analogy...most animals aren't INTENTIONALLY going out and racing Ironman...which is arguably well beyond the normal limits based on human evolution. You find animals like dogs, lions, giraffes, etc. sitting in the shade in the middle of the hot summer day...while us idiots are out there attempting to run beyond our limits. Smile
I was thinking about this on my ride today. What should one preload. Not what they can replenish on the course, the sodium and water. That stuff is easy. But the stuff that is inside the cell, like the potassium and calcium. I would make sure I was supplementing those before the race and not trying to take that stuff in during the race (since it will not get into the cell while racing).

The best and easiest recommendation for most is probably to eat a well-balanced diet and stay hydrated before the race.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [jsquared] [ In reply to ]
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Dear JJ,

I agree with you completely. Our study reported in the Proceedings of the National Academy of Sciences showed that 60% of athletes who gained weight during ultradistance events did not develop EAH. Thus to develop EAH it seemed that there were three important factors: overdrinking; SIADH and inability to osmotically-activate intracellular Na or conversely osmotic inactivation of Na+ in the ECF.
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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The sodium reservoir is thought to be in skin, bone and cartilage.

Potassium losses from the body are very small in both urine and sweat. Potassium deficiency certainly does not occur in healthy athletes under whatever conditions you might impose. This was shown by David Costill in the 1970's. Patients who develop potassium deficiency are those with high blood pressure or heart failure who use specific drugs, one effect of which is to increase potassium losses in the urine. We don't need to invoke "dehydration" to explain this effect.

I am not aware of clear evidence showing that "dehydration" affects blood flow to the gut and so effects fluid absorption. I suspect that there are quite large differences in rates of intestinal fluid absorption amongst individuals. I am aware of some individuals who develop intestinal bloating when they ingest fluid at rates as low as 400ml per hour during prolonged exercise suggesting that that is their peak rate of fluid absorption. Those who develop bloating during prolonged exercise are those who ingest fluid at rates greater than their individual rates of intestinal fluid absorption.

There is no need to evoke "dehydration" to explain this effect.
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Re: Tim Noakes: we need you back for a moment [MikeSprint] [ In reply to ]
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The evidence is that muscle cramping is due to abnormalities in the neural control of the muscle not to individual electrolyte deficiencies. There is so much calcium in blood compared to the amount inside the cells that it is impossible to develop a calcium deficiency that would effect muscle performance. Calcium is the ion that ultimately causes the muscle contraction in muscle cramping. Thus by logical conclusion, cramping is a sign of the action of calcium, not of its absence.

Potassium deficiency does not occur in human athletes unless they are being treated for high blood pressure or heart failure (or perhaps other obscure conditions).
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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I am not aware of clear evidence showing that "dehydration" affects blood flow to the gut
It clearly does when the dehydration is the result of consumption of a low carbohydrate for a few days.
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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What is the evidence that performance during prolonged exercise is related to the cardiac output and blood flow to the muscles? Surely if the exercise is submaximal and occurs at submaximal cardiac output and submaximal blood flow to the muscles, there is no reason to believe that it is limited by (submaximal) rates of oxygen delivery?

So although I would like to accept your explanation i am not certain it is likely to be correct.
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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What is the evidence that performance during prolonged exercise is related to the cardiac output and blood flow to the muscles? Surely if the exercise is submaximal and occurs at submaximal cardiac output and submaximal blood flow to the muscles, there is no reason to believe that it is limited by (submaximal) rates of oxygen delivery?

So although I would like to accept your explanation i am not certain it is likely to be correct.
He gets that a lot....
Last edited by: JustCurious: Apr 22, 09 13:15
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Re: Tim Noakes: we need you back for a moment [Andrew Coggan] [ In reply to ]
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In Reply To
I cannot explain how taking more carbohydrate or protein affects your fluid balance. It is not something I have thought about.[/reply] I'm...speechless.

Again!!!! By my count, that's twice in two years. What is this world coming to?

I must admit, I did a double take as well.


Steve

http://www.PeaksCoachingGroup.com
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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What is the evidence that performance during prolonged exercise is related to the cardiac output and blood flow to the muscles? Surely if the exercise is submaximal and occurs at submaximal cardiac output and submaximal blood flow to the muscles, there is no reason to believe that it is limited by (submaximal) rates of oxygen delivery?

So although I would like to accept your explanation i am not certain it is likely to be correct.

Here we go, HOLD ON!!!

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Re: Tim Noakes: we need you back for a moment [S McGregor] [ In reply to ]
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I'm...speechless.[/quote]
Again!!!! By my count, that's twice in two years. What is this world coming to?
I'm slowing down in my old age.
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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Correct. The site from which the fluid is lost depends on the amount of sodium and potassium that are lost with the water. The more sodium that is lost, the more of the fluid loss will come from the ECF.

Sporting performance is strongly belief centred. If you believe that becoming "dehydrated" will effect your performance, then it will. Similarly if you believe that drinking ahead of thirst will improve your performance it probably will. But there is a point at which fluid retention will lead to an impaired performance perhaps as a result as much of brain swelling as of changes in the muscles caused by an increase in their water content.

The interesting point is that it seems to depend where you come from as to your view of how much you should be drinking during exercise. If you are an elite distance runner from Africa you will very likely drink to thirst during training and competition. If you come from Europe or North America, it seems to me that you would be more likely to believe that you must drink to "stay ahead of thirst". Is this because of differences in biology? Or of pre-programming?
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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Tim,
I appreciate your spending time to defend your research on this board. I read a lot of these articles on sodium supplementation and it has more meaning when somebody that has actually done the research will go toe to toe with critics of the research in an open forum like this. One of the things I've taken from this discussion is the possibility that in some cases it could be the component ingredients of a given product that produces the net positive effect that some athletes experience instead of the sodium. As each product has it's own distinct formulation, the observance by some athletes that certain products work better for them than others demonstrates that supplementation can be useful, but knowing what component is actually producing the positive effect would be far more useful and gets us back to the common adage on this board that we are each an experiment of N=1. The most effective strategy I see from a racing perspective is to use the available research to systematically and experimentally determine our own individual needs and not treat any particular study as gospel.

JJ

Every night that I run, the thought crosses my mind that there's no way in hell I'll still be running a month from now.
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Re: Tim Noakes: we need you back for a moment [Yknot] [ In reply to ]
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Your question is relevant. Why for example are humans of a particular height and weight (and subject to large geographical differences)? Why are all humans not 3m tall and weighing 200kg? Because evolutionary pressures chose that as humans of 40-120kg would be the most likely to survive. In a 70kg human the carbohydrate reserves are enough to sustain high intensity running for about 2-3 hours after which carbohydrate needs to be ingested. If we had been 140kg we would have had larger stores and could have exercised for longer (although at that weight we would not have been great distance runners).

There is no evidence that humans can run themselves into a catastrophic failure. Even the winners of the Ironman Triathlon do not die at the finish. They walk over to the medical tent etc showing that they finish with reserve. When death does occur it is almost always due to a pathological condition.
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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Basic Physiology 3.

As presented by the Sports Drink Industry and its funded scientists and sports medicine and athletic coaching associations...

Hmmm...as I read that whole entry, why did the words "Straw Man" keep popping into my head?

http://bikeblather.blogspot.com/
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Re: Tim Noakes: we need you back for a moment [Slowman] [ In reply to ]
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Dear Slowman,

One of the best predictors of risk of developing atrial fibrillation is years of athletic training. Magnesium supplementation has some specific cardio-protective effects. You would be better off trying that as a supplement for your heart condition. Also reduce caffeine intake. But in the end it is continued endurance training that is perhaps the major deterninant of whether or not the condition will or will not settle. So it is a tough decision.

Answers to your questions:

1. Fifteen minutes stretching each day. Stretch during the event.
2. None.
3. In my opinion yes. Fads come and go. Let us see if this one is still around in 5-10 years time. Has there been a dramatic improvement in performance since triathletes began to ingest salt tablets? Also how much are they actually ingesting - grams, tens of grams or hundreds of grams? And how do the amounts they are ingesting relate to how much they are losing and how much is present in their bodies?

BUT: What if the ingestion of sodium acts like that of carbohydrate by acting through the brain to improve performance (and not by altering whole body sodium balance)? We need the group in Birmingham who showed this effect for carbohydrate perhaps to study salt ingestion in the same way.

So I have not been absolutely dogmatic. But my bias is to believe that salt intake will not pass the test of time.
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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The sodium reservoir is thought to be in skin, bone and cartilage.

Potassium losses from the body are very small in both urine and sweat. Potassium deficiency certainly does not occur in healthy athletes under whatever conditions you might impose. This was shown by David Costill in the 1970's. Patients who develop potassium deficiency are those with high blood pressure or heart failure who use specific drugs, one effect of which is to increase potassium losses in the urine. We don't need to invoke "dehydration" to explain this effect.

I am not aware of clear evidence showing that "dehydration" affects blood flow to the gut and so effects fluid absorption. I suspect that there are quite large differences in rates of intestinal fluid absorption amongst individuals. I am aware of some individuals who develop intestinal bloating when they ingest fluid at rates as low as 400ml per hour during prolonged exercise suggesting that that is their peak rate of fluid absorption. Those who develop bloating during prolonged exercise are those who ingest fluid at rates greater than their individual rates of intestinal fluid absorption.

There is no need to evoke "dehydration" to explain this effect.
Fluid absorbtion from the gut is passive and solely dependent upon blood flow to where the fluid is, as far as I know. When a person becomes dehydrated the body selectively routes blood away from organs that are not critical to those that are. Not critical organs would include the kidneys, gut, and skin. To say you are not aware of any "clear evidence" that dehydration affects blood flow to the gut and so effects fluid absorbtions suggest you need to go back and reread a basic physiology text or talk to Chris Lieto.

Potassium deficiency is not a "dehydration" phenomenon. Under normal circumstances daily potassium losses are small. But, sweating will increase that daily loss and many athletes are on potassium depleting drugs and many athletes have particularly poor diets from a balance diet perspective or have had recent diarrheal episodes within a few days of any race. To say that an athlete could not suffer from chronic potassium depletion is ignoring real life possibilites. It is easy to diagnose sodium depletion. It is difficult to diagnose potassium depletion. If you want your nerves and muscles to work properly you need the proper balance of both sodium and potassium across the cell membrane.

I would be surprised if the skin were the sodium reservoir in an athlete as the increased skin flow during activity would cause the sodium to equilibrate quickly. I guess cartilage and bone could act that way but they don't seem to have enough mass (edit: cartilage) to be much of a reservoir (edit: or have too much blood flow to be a delayed reservoir, bone). To my mind, the gut is a better candidate as the sodium concentration should be in pretty good equilibrium with the ECF so it would be a large reservoir and it seems to me the diffusion back into the blood would be slow. Regardless of the mechanism, this is pretty much a non-issue to the athlete.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
Last edited by: Frank Day: Apr 22, 09 14:21
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Re: Tim Noakes: we need you back for a moment [Tom A.] [ In reply to ]
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I doubt that the families of Cynthia Lucero, Hillary Bellamy, Kelley Barrett and the other 9 or so US citizens (and probably many other unrecorded individuals) who died needlessly from EAH think that this is a Straw Man.
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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I doubt that the families of Cynthia Lucero, Hillary Bellamy, Kelley Barrett and the other 9 or so US citizens (and probably many other unrecorded individuals) who died needlessly from EAH think that this is a Straw Man.
Your concern is valid. However, you seem to be ignoring the many others who have died from inadequate fluid intake and dehydration during exercise from either kidney failure or heat stroke.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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In Reply To:
I doubt that the families of Cynthia Lucero, Hillary Bellamy, Kelley Barrett and the other 9 or so US citizens (and probably many other unrecorded individuals) who died needlessly from EAH think that this is a Straw Man.

Wow...now I'm nearly speechless...

http://bikeblather.blogspot.com/
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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Fortunately there is not one case in the literature of heat stroke or kidney failure in an endurance athlete that can be linked directly to 'dehydration'.

The point as you know is that because two events occurs simultaneously, this does not mean that they are causally related.

In those studies that have been properly conducted there is no evidence that dehydration effects the body temperature response during exercise to an extent that would suggest that further dehydration would cause heat stroke. Again the key is that the brain is there to insure that the exercise intensity is reduced if the body temperature rises too high.

The most interesting recent work is by Dr Chris Byrne from the UK and reported in Medicine and Science in Sports and Exercise. His work shows that the body temperature response to exercise is determined by the exercise intensity (metabolic rate) not by the level of dehydration that develops during exercise.

My guess is that both conditions are related to abnormalities in skeletal muscle function and that is where we should seek the real causes of exercise-associated heat stroke and kidney failure.
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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The point as you know is that because two events occurs simultaneously, this does not mean that they are causally related.



It has been established before that Frank does not know that.

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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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Fortunately there is not one case in the literature of heat stroke or kidney failure in an endurance athlete that can be linked directly to 'dehydration'.

The point as you know is that because two events occurs simultaneously, this does not mean that they are causally related.

In those studies that have been properly conducted there is no evidence that dehydration effects the body temperature response during exercise to an extent that would suggest that further dehydration would cause heat stroke. Again the key is that the brain is there to insure that the exercise intensity is reduced if the body temperature rises too high.

The most interesting recent work is by Dr Chris Byrne from the UK and reported in Medicine and Science in Sports and Exercise. His work shows that the body temperature response to exercise is determined by the exercise intensity (metabolic rate) not by the level of dehydration that develops during exercise.

My guess is that both conditions are related to abnormalities in skeletal muscle function and that is where we should seek the real causes of exercise-associated heat stroke and kidney failure.
Wow, I have never heard someone so manipulate the interpretation of data to support their theory.

Perhaps you could elucidate for those of us who have been so misguided to think that dehydration might possibly result in eventual hyperthermia as to what the literature shows the cause of these many instances to be? One of the elite females at Sea Otter came across the finish line and collapsed. Medical personnel were seen "packing" her in ice before putting her in the ambulance. I understand she took 3 liters of fluid in the tent and is fine now. To what would you attribute this incident to, if not dehydration?

I participated in an experiment once, running on the treadmill for an hour with it being 90 degrees and 90% humidity because a colleague collapsed 100 yds from the finish line of a 10k with a temp of 107. I got through it fine I suspect because it wasn't enough to dehydrate me. How long do you suspect I could have gone and continued to maintain a normal temperature. According to you, forever. It seems to me that for one to know if dehydration is or is not associated with increased temperature one needs to run these experiments to the point where the subject stops sweating and see what happens to the temperature. Love to see someone getting that experiment through the human uses committee.

While conditons such as malignant hyperthermia most assuredly accounts for some of these instances, it cannot account for all of them. It seems you cannot accept that there are legitimate reasons people are concerned about your recommendations. Life threatening heat stroke seems like a lot more common occurance in athletes than life threatening EAH.

The fact that two events occur simultaneously is not evidence they are not related. Unless I am shown convincing evidence that dehydration and hyperthermia in the athlete are never related I will trust my knowledge of basic physiology and answer that question, true, true, related. I am just blown away.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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Has there been a dramatic improvement in performance since triathletes began to ingest salt tablets?

Dr Noakes,

That would be a key question to ask.

It's funny, go back 10 years or so and this was not that big an issue in triathlon. Drink some Gatorade, eat a few bananas along the way and thousands of people every year were finishing 1/2 and full IM triathlons. Now the entire triathlon population has, for lack of better wording become salt obsessed. Of course the sports drink and sport nutritional companies have all jumped on board with this and now it's hard to find a sport drink, sport bar or gel that does not have salt in it, and almost every coach is admonishing triathletes to pop salt pills like candy! All of this happened in the last 5 years. What happened? How could we go from one extreme to the other in such a short period of time?

To answer your question, my feeling at a high level is that, "no" their has not been a dramatic improvement in performance with the massive across the board ingestion of salt by the triathlon masses.
In fact, when you look at average finish times and most big triathlons, of all distances, the average finish times are getting slower!



Steve Fleck @stevefleck | Blog
Last edited by: Fleck: Apr 22, 09 15:28
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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In Reply To:

Wow, I have never heard someone so manipulate the interpretation of data to support their theory.

Oh, the irony...

In Reply To:

Perhaps you could elucidate for those of us who have been so misguided to think that dehydration might possibly result in eventual hyperthermia as to what the literature shows the cause of these many instances to be? One of the elite females at Sea Otter came across the finish line and collapsed. Medical personnel were seen "packing" her in ice before putting her in the ambulance. I understand she took 3 liters of fluid in the tent and is fine now. To what would you attribute this incident to, if not dehydration?

I don't know Frank... That woman was exercising pretty hard for hours, could it be that her core temp was up and she was exausted? Going out on a limb here...

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Re: Tim Noakes: we need you back for a moment [Fleck] [ In reply to ]
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In fact, when you look at average finish times and most big triathlons, of all distances, the average finish times are getting slower!

Why does that matter? Averages will go down because you have more slow, crappy athletes (like me for instance)
involved.

-Jot

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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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Hey Tim, Thanks for taking so much time for this discussion as its a big issue for all of us.
With your reply here I think you are closest to answering Dan's original question which to paraphrase was "why do I cramp and how can I prevent it?"
In examining further the idea that "abnormalities in the neural control of the muscle" are the cause of cramping, is it plausible that due to sodium lost through sweat and due to sodium moved into the blood that cramping is at least partially caused by normal cell chemisty being altered due to the change in ratios of the ions normally available?
Cheers, Scott Molina
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Re: Tim Noakes: we need you back for a moment [Paulo Sousa] [ In reply to ]
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Well, at least up to a certain precentage they are not directly related:


Core temperature and hydration status during an Ironman triathlon
[/b]P B Laursen1, R Suriano2, M J Quod3, H Lee3, C R Abbiss1, K Nosaka1, D T Martin3 and D Bishop2
1 School of Exercise, Biomedical and Health Sciences, Edith Cowan University, Joondalup, WA, Australia
2 School of Human Movement and Exercise Science, University of Western Australia, Perth, WA, Australia
3 Department of Physiology, Australian Institute of Sport, Canberra, ACT, Australia
Correspondence to:
Correspondence to:
Dr Laursen
School of Exercise, Biomedical and Health Sciences, Edith Cowan University, Building 19, Room 162, 100 Joondalup Drive, Joondalup, WA, Australia 6027; p.laursen@ecu.edu.au

British Journal of Sports Medicine 2006;40:320-325; doi:10.1136/bjsm.2005.022426

"Conclusion: In contrast with previous laboratory based studies examining the influence of hypohydration on performance, a body mass loss of up to 3% was found to be tolerated by well trained triathletes during an Ironman competition in warm conditions without any evidence of thermoregulatory failure."


You guys are aware how and why thermoregulation in the human body works on a cellular/molecular level, right?

Sometimes I doubt you even consider some basic science in your discussions.

And please, drop the drama!












___________________________________________
Ego numquam pronuncio mendacium,
sed sum homo salvaticus
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Re: Tim Noakes: we need you back for a moment [Paulo Sousa] [ In reply to ]
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In Reply To:
In Reply To:

Wow, I have never heard someone so manipulate the interpretation of data to support their theory.

Oh, the irony...

In Reply To:

Perhaps you could elucidate for those of us who have been so misguided to think that dehydration might possibly result in eventual hyperthermia as to what the literature shows the cause of these many instances to be? One of the elite females at Sea Otter came across the finish line and collapsed. Medical personnel were seen "packing" her in ice before putting her in the ambulance. I understand she took 3 liters of fluid in the tent and is fine now. To what would you attribute this incident to, if not dehydration?

I don't know Frank... That woman was exercising pretty hard for hours, could it be that her core temp was up and she was exausted? Going out on a limb here...
That is what I like about you Paulo, always willing to go out on a limb. So, just give me an mechanism to explain her elevated core temperature. Exercising hard for hours (I think she exercised for about 90 minutes) and being exhausted doesn't quite cut it for me as a mechanism.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [de-tri-mental] [ In reply to ]
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In Reply To:
Well, at least up to a certain precentage they are not directly related:


Core temperature and hydration status during an Ironman triathlon
P B Laursen1, R Suriano2, M J Quod3, H Lee3, C R Abbiss1, K Nosaka1, D T Martin3 and D Bishop2
1 School of Exercise, Biomedical and Health Sciences, Edith Cowan University, Joondalup, WA, Australia
2 School of Human Movement and Exercise Science, University of Western Australia, Perth, WA, Australia
3 Department of Physiology, Australian Institute of Sport, Canberra, ACT, Australia
Correspondence to:
Correspondence to:
Dr Laursen
School of Exercise, Biomedical and Health Sciences, Edith Cowan University, Building 19, Room 162, 100 Joondalup Drive, Joondalup, WA, Australia 6027; p.laursen@ecu.edu.au

British Journal of Sports Medicine 2006;40:320-325; doi:10.1136/bjsm.2005.022426

"Conclusion: In contrast with previous laboratory based studies examining the influence of hypohydration on performance, a body mass loss of up to 3% was found to be tolerated by well trained triathletes during an Ironman competition in warm conditions without any evidence of thermoregulatory failure."


You guys are aware how and why thermoregulation in the human body works on a cellular/molecular level, right?

Sometimes I doubt you even consider some basic science in your discussions.

And please, drop the drama!
Up to a certain percentage, water intoxication is not a problem either. Can't we all agree that serious problems occur at both ends of the hydration spectrum. Apparently Dr. Noakes cannot bring himself to admit that dehydration can be a problem.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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Dear Slowman,

One of the best predictors of risk of developing atrial fibrillation is years of athletic training. Magnesium supplementation has some specific cardio-protective effects. You would be better off trying that as a supplement for your heart condition. Also reduce caffeine intake. But in the end it is continued endurance training that is perhaps the major deterninant of whether or not the condition will or will not settle. So it is a tough decision.

You've just signed Dan's death warrant. The man goes through FIVE POUNDS of Kona coffee every month! And he lives to ride, run, swim, and now XC ski!



Fare thee well, Dan. We hardly knew ye...


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Re: Tim Noakes: we need you back for a moment [Fleck] [ In reply to ]
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Has there been a dramatic improvement in performance since triathletes began to ingest salt tablets?

Dr Noakes,

That would be a key question to ask.

It's funny, go back 10 years or so and this was not that big an issue in triathlon. Drink some Gatorade, eat a few bananas along the way and thousands of people every year were finishing 1/2 and full IM triathlons. Now the entire triathlon population has, for lack of better wording become salt obsessed. Of course the sports drink and sport nutritional companies have all jumped on board with this and now it's hard to find a sport drink, sport bar or gel that does not have salt in it, and almost every coach is admonishing triathletes to pop salt pills like candy! All of this happened in the last 5 years. What happened? How could we go from one extreme to the other in such a short period of time?

To answer your question, my feeling at a high level is that, "no" their has not been a dramatic improvement in performance with the massive across the board ingestion of salt by the triathlon masses.
In fact, when you look at average finish times and most big triathlons, of all distances, the average finish times are getting slower!


Fleck,

First off, if you were drinking Gatorade and eating bananas, you were getting plenty of electrolyte supplementation.
I hate bananas and Gatorade, hence I use electrolyte pills (and lots of 'em) instead.

Second, you've made the "average finishing times in X endurance activity are getting SLOWER" comment, oh, about a hundred zillion times.
And I have stated, that it is simply a matter of statistics: as more folks participate in a given activity, the *average *general skill and fitness level DECREASES, as you are simply adding a larger # of less capable people to the participant pool. Those folks who have a predisposition to a given activity well, are/were likely already doing it, as they are good at it.

Increasing an IM field from 1,000 to 2,500, mostly adds another 1500 MOP and BOP participants, and not so many FOPers, since he FOP'ers were already doing it.

Fun with math.


float , hammer , and jog

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Re: Tim Noakes: we need you back for a moment [Slowman] [ In reply to ]
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hether it's on this thread or elsewhere, i would eventually like to drill down to:

1. what relieves or delays cramping?
2. what bad thing can happen if i take salt pills during a race, during a workout, after a workout, assuming i'm not hypertensive?
3. what do we do with the very high incidence of salt pills taken by top triathletes? are they all indulging in mass cation hysteria?
4. and finally, anecdotal cases of hyponatremia in my experience pale in contrast to anecdotal cases of heart arrhythmias in otherwise very healthy athletes; can prolongued exercise in the absence of a certain factor be the proximate cause?
_______________________

Dan, I think we need to try an answer for you to some complex physiology issues ... that god forbid may never be answered by a definitive study at a molecular level. I appreciate Dr Noakes explanations and sincere attempts to be helpful ... I also could care less how many citations AC has ;-)
The other issue is how these get treated medically at IM events by those of us who actually do that as MDs (no offense meant but neither of the good doctors actually do that ... at least hopefully not:-))
Most - 90%+ of those who actually see the MD in the medical tent are dehydrated/ heat exhausion and simply need fluids with salt/ some cooling and they are fine. We just see those who need IV fluids because most are actually treated with PO fluids with salt by the intake crew ... everyone begs for IVs but most don't get them because they don't need them.
The hyponatremics are a different issue and are nearly all identified by the fact they gained weight during the event yet appear just like those who are dehydrated or worse. All those in question get their electrolytes drawn. Most of the hyponatremics get better as their bodies adjust in their 1-2 hour stay and they go home . Some are quite ill and go to the hospital where they stay overnight and are typically just observed and kept on minimal oral intake until their bodies correct the hyponatremia. Some require much more critical interventions and I think we should all appreciate Dr Noakes contributions in making us all more cognizant of these individuals that used to be treated just like those with dehydration and that can make for fatal outcomes in bad circumstances.
Obviously athletes are seen with all sorts of other more complex issues ... but thats not for this discussion.
Many of us who treat these patients also have done many IM races and lived our own issues in addition.

1. What relieves/ prevents cramps .... clearly taking electrolyte supplements works ... or just salt which is why chicken soup is always on the course. There are clearly many issues in getting electrolyes from the gut to where they are needed (timing/absorption issues). Competitors with severe cramps get IV salt and they promptly quit cramping and those of us who have done many hot IM events know if we take moderate salt we stop cramps during competition unless we can't keep it down. If you can't keep it down you won't be finishing the race.
2. Probably nothing except your legs will swell up for a few days afterwards if you take in too much ... until your kidneys correct that. You will probably learn fast by swelling how much is too much. I take in a lot of salt during a hot race and swell the next few days ... I accept that because I know it helps from experience in hot IM events.
3. It likely doesn't prevent hyponatremia .. but I think within reason it probably works on hot days .. like all things it probably should be in moderation.
4. Whole other issue with arrhythmias ... talk to your cardiologist.

What would help athletes most at long hot events .... using the scales to monitor their weight ... and they are always there, but hardly used ... I always use them.

Dave

Again, thanks to Dr Noakes on behalf of those who really treat this stuff.

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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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In the case of lone A-fib, yes, you are correct. In the general population, this isn't the case. There are numerous other causes of A-fibs.

Of course, if you look at A-fib without underlying pathologies, then I'm pretty sure simple odds ratios will show that it's a lot more prevalent in the very fit population.
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Re: Tim Noakes: we need you back for a moment [Murphy'sLaw] [ In reply to ]
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Second, you've made the "average finishing times in X endurance activity are getting SLOWER" comment, oh, about a hundred zillion times.

ML,

Yes, I know that. I'll try and dial it back! Thanks for pointing it out.

However, I was trying to address Dr. Noakes's question about salt supplementaion and performance head on - he's relativly new here and we are lucky to have him, I might add.




Steve Fleck @stevefleck | Blog
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Re: Tim Noakes: we need you back for a moment [dcsxtri10] [ In reply to ]
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I just wanted to check and make sure that "salt" (= Sodium or Natrium) and the term "electrolytes" don't get confused. Even you as an MD seem to exchange them deliberately.
I am with Noakes on the fact that Sodium is probably not the problem.
Other electrolytes (especially Magnesium) may be a different story.
Especially when it comes to damage of the neuromuscular junction (especially in the heart) or to cellular regulatory mechanisms in response to energy production and heat generation (Mg and other trace metals like Iron are important factors in this process).

So I think it would be worthwile figuring out which one is actually the limiter and what causes cellular dysregulation that leads to cramping (short term) or long term damage (e.g. to the heart), instead of all the handwaving going on right now.
And simply just analyzing sweat content or weighting people won't be cutting it.
But I guess some people are fine with swollen legs and other not immediately visible, more long-term consequences (ranging from accelerated aging to aforementioned heart defects) from not supplementing correctly of just randomly taking in "salt".

Wish there would be more money funding this kind of work.

In that respect, I hope you are not serious about god forbidding the advancement of science in the molecular aspects of this field.
Although I have the feeling that this is the case in certain circles, which would explain the funding problem.

.... carry on

___________________________________________
Ego numquam pronuncio mendacium,
sed sum homo salvaticus
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Re: Tim Noakes: we need you back for a moment [de-tri-mental] [ In reply to ]
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There is some good data and explanations here but also some that, non-pun intended, don't hold water.

1) You most certainly can have an overall sodium depleted state with a normal sodium blood value if you're hypovolemic. Much as I can bleed half of your blood volume and acutely have a normal hgb until the volume is replaced.

But I agree sodium isn't the cause of the cramps.

I venture to say maybe electrolytes are the wrong tree to bark up, and it's the bodies response to prolonged microstress or muscle damage that causes opposing muscles cramp in order to prevent further damage.

What the role of ECV in performance remains unclear to me. I certainly beileve Intravascular volume and ICV are extremely important for vascular and cellular functions.

2) I also disagree with the notion that people with normal GFR and functioning kidney's can drink enough water to cause life threatening hyponatremia. Can't happen. You can excrete the volume and retain sodium unless you have SIADH etc.

3) Electrolytes are necessary for the absorption of water in the gut. Whether absorption is better if the fluid contains the electrolytes or they have to first diffuse into the gut to then transort water back is unclear.

4) H+ and classic physiology taught Acid/Base relationships of H+ and HCO3- and strong Ions are simplistic and leave many holes. To fully understand electrolyte balance I reccomend reading a great text (especially for you MDs) which is available free at http://www.acidbase.org/index.php?show=sb

That being said, I drink plenty of fluids, and absolutely agree with the if it tastes sweet drink water, if it's weak drink more salt/sugar.

Where I think all this talk falls flat about glycogen stores, etc etc is that I am not looking for one 2-3h performance in isolation. So although I can completely drain all my stores and not drink or eat a drop and have 1 decent workout, why do that when you have countless workouts planned on your training regimen?
Last edited by: feldme: Apr 22, 09 19:25
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Re: Tim Noakes: we need you back for a moment [de-tri-mental] [ In reply to ]
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DTM,

You, and Noakes, and I agree that Salt (NaCl) is not the problem in causing hyponatremia.

If you have severe leg cramps(different issue), they can highly likely be stopped wit IV Na Cl .... or PO NaCl if you can take it with a time delay that is variable.

Do I think this should all be studied ... sure ... but remember these issues didn't get started with the onset of triathlon/marathon ... they have been treated by physicians and studied for a LONG time and the stuff we are talking about is treated in non-athletes as a daily issue (hyponatremia I'm referring to). SO .... old issue in medicine ... new issue in its occurrence in endurance athletes and actively considering it in competitors with medical problems.
Dave
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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"Has there been a dramatic improvement in performance since triathletes began to ingest salt tablets?"

i am going to give this some thought. keep in mind that salt tablets were widely in use in ironmans 15, maybe 20 years ago, and there are a lot of reasons why athletes might have gotten fast in a span of that length. but among individual athletes, pre and post taking salt tablets, that might yield something. maybe i'll just go back and ask a lot of those athletes for anecodotes. i keep in touch with quite a lot of them. one of them is on this thread, scott molina, perhaps he might chime in.


Dan Empfield
aka Slowman
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Re: Tim Noakes: we need you back for a moment [Slowman] [ In reply to ]
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I feel that I finished and won in Kona in '88 largely due to my large salt intake.
After my initial miserable deathmarches there in '81, '82 and '85 I knew I had to do something different.
I've been a massive sweater ever since I was a kid and have had lifelong cramp issues in all hot races even when I was extremenly fit and paced myself well.
Part of that process involved spending 11 days doing Epic Training in Palm Springs experiementing with different sodium intake, increasing magnesium a lot, and also reducing Calcium in my diet a lot.
I also tried sodium loading while I was there and decided it wasnt' going to work as I was peeing like never before!!!
I decided to go with normal table salt added to my bottles so I could take it in at a rate of 1.5-2 grams/hour and that included the run where I carried my own bottles which was a novelty at the time.
It tasted like crap but it helped get me through.
My previous heat acclimation camps in prior years only left me completely drained and utterly useless as an athlete and I put that down to lack of sodium.
Figuring out how to prevent cramps in long hot races has been a 34-year search for me so far, so I'm finding this thread is very interesting!
Cheers, Scott Molina
Last edited by: skid: Apr 22, 09 22:05
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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Sorry but I don't know how you know that dehydration caused this condition. As I said the fact that two events occur at the same time does not mean that they are causally related. And why was this lady the only one who developed the condition in that race (ie what is the control group that allowed you to draw your conclusion).

I have considered this problem for 20 years and have written about it extensively. You might want to read our most recent article in MSSE - first author is Dr J Swart. If dehydration is the real cause of heat stroke why does the condition occur so infrequently and why can some athletes finish marathons and ultramarathons after losing 10-12% of body weight and not die of heat stroke? And why do most cases of heat stroke occur in athletes and military personnel involved in short duration exercise and so often in mild environmental conditions. The dehydration explanation simply does not explain most cases of heat stroke.

You really need to read the ENTIRE literature on this topic and not just that section which you are currently reading.

We are currently beginning to test the hypothesis that most cases of heat stroke have a genetic basis and are related to as yet unrecognised conditions of skeletal muscle.

With regard to the frequency of life threatening EAH, I have been able to collect more than 1000 cases of the condition, most reported in the scientific literature since 1985. There is nowhere near the same number of cases of heat stroke reported in athletes during the same time.

So if you read the literature it is clear that heat stroke does not causes anywhere near the same number of cases of ill health in athletes as does EAH. Fortunately it looks like the tide has turned and the number of new cases of EAH each year is now quite low.

I do not discount the potential effects of dehydration. I just am unable to find any evidence in the scientific literature to support your conclusions and much to discount them.
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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In Reply To:
In Reply To:
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Wow, I have never heard someone so manipulate the interpretation of data to support their theory.

Oh, the irony...

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Perhaps you could elucidate for those of us who have been so misguided to think that dehydration might possibly result in eventual hyperthermia as to what the literature shows the cause of these many instances to be? One of the elite females at Sea Otter came across the finish line and collapsed. Medical personnel were seen "packing" her in ice before putting her in the ambulance. I understand she took 3 liters of fluid in the tent and is fine now. To what would you attribute this incident to, if not dehydration?

I don't know Frank... That woman was exercising pretty hard for hours, could it be that her core temp was up and she was exausted? Going out on a limb here...
That is what I like about you Paulo, always willing to go out on a limb. So, just give me an mechanism to explain her elevated core temperature. Exercising hard for hours (I think she exercised for about 90 minutes) and being exhausted doesn't quite cut it for me as a mechanism.
While exercising for 90 minutes and collapsing from dehydration doesn't cut it for me, especially since it happened right at the finish line, timing that is hard to believe to be coincidental. Indeed, IIRC, in the "Lore of Running" Noakes suggests that most finish-line collapses on hot days are due to lack of blood pressure as heart rate rapidly decreases post-exercise, but with the blood vessels still very dilated from the exercise in hot conditions. This is not serious; the athlete just needs to lie down for a few minutes. As a personal example, when I finished my first ever 100 mile time trial (also on a warm day, at least what counts as such in England), I collapsed directly after getting off the bike. Fortunately in the UK, even at a National Championship TT event, there aren't any medical staff to interfere, and so my condition was not misconstrued as something serious. After lying there on the grass for a few minutes, I was completely fine.
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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In Reply To:

Thus whereas all other creatures on earth are able to regulate their body temperatures and body water and sodium balance by responding to internal cues, all humans must be told exactly when, how much and what to eat and drink before, during and after exercise.
I have a question about this "responding to internal cues". Why do we need to respond to it with regard to drinking and salt intake, but not respond to it with respect to eating calories? I know no athletes who develop a feeling of hunger during sport, before it is too late. I get a feeling of hunger when I go from running to walking. Never ever do I get hungry before I completly block in a need of cola or something like that. Marathon runners develop this feeling mostly around 30-35 km or so. Why should they drink to thirst, but eat calories against their "internal cues". Why would the body regulate the salt and water content by these well developed mechanism you described, but not the calorie intake?
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Re: Tim Noakes: we need you back for a moment [duncan] [ In reply to ]
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The danger is always to try to reduce a complex phenomenon (the development of heat stroke) to one simple mechanism ie dehydration. To conclude that dehydration is the cause you have at least to exclude a number of other possibilities. Also if the activity was less than a few hours and the subject had been drinking, then what level of dehydration would have been present? And would that level of dehydration not have been precisely the same as that measured in many other athletes completing the race on the same day in the same conditions without any evidence for "heat illness".

But more to the point, much of the early work on heat stroke was done in the South African gold mines in the 1920's and 1930's when an epidemic of heat stroke began to develop as the mines went ever deeper. (The temperature of the rock face at 3-4km below the earth surface is 50 degrees C). The main risk for heat stroke were the environmental conditions, the amount of work performed, the level of heat acclimatization and most importantly the presence of intercurrent illness. These were not healthy people who suddenly developed the condition. In laboratory testing on the mines it was soon observed that those who started exercise with an elevated temperature (because of an intercurrent illness of which they might or might not have been aware) were unable to regulate their body temperatures appropriately and had to be stopped from exercise when their temperatures reached abnormally high levels. So in an case of heat stroke you have to be certain that there was not an intercurrent illness at the same time. But most importantly in my view whether or not there is also some underlying muscle disorder that causes an explosive production of heat (thermogenesis) which is the real cause of the heat stroke (according to the theory that we are currently evaluating).

Thank you for mentioning postural hypotension as the cause of your collapse. This is by far the most common cause of post-exercise collapse in all endurance athletes. Unfortunately it is labelled as "heat illness" and "dehydration" but both diagnoses are wrong. First the body temperature is not seriously elevated in these athletes and second they recover the instant their legs and pelvis are elevated above the level of the heart. This restores their blood pressures. Their symptoms as you correctly state are due to low blood pressure when standing (postural hypotension) which is corrected when the blood volume in the legs is redistributed to the centre of the body correcting a low filling pressure of the heart and again allowing a normal circulatory function.

Frank's interpretation is also dependant on the catastrophe model that he evokes for exercise in the heat. I mentioned this model in an earlier post - Basic Physiology 3 - the one to do with the sports drink industry's model of how the body works.

Thus according to his model humans will continue to exercise without drinking until they suddenly collapse from heat stroke. When this does happen it is the exception not the rule. The rule is that if you become too hot or if you don't drink enough during exercise the brain will eventually take over and change your behavior by slowing you down. When you slow down your rate of heat production is reduced and you start to cool down (since it is your rate of heat production and not your level of dehydration that is the primary determinant of your body temperature during exercise - presuming that you do not have an intercurrent illness). in this way dehydration (caused by the absence of drinking which causes thirst which causes you to slow down and to go and search for fluid to alleviate your symptoms of thirst) should actually protect from and not cause heat stroke.

Interestingly in the literature there are hundreds of individual cases of subjects who exercise in the heat without drinking. Often these subjects are acting as the controls in studies to show important it is to drink during exercise. But in none of these are there reports of ill health in the group who do not drink during exercise. The exception are a group of studies in which athletes exercise in such extreme heat that they are unable to regulate their body temperatures so that they will have to stop eventually because they are becoming too hot. But even in those experiments subjects usually stop because they develop postural hypotension with temperatures well below those measured in cases of heat stroke or even in winners of 10, 21 and 42 km races run in the heat.

These findings are best explained by a model in which the brain is clever enough not to want to kill itself every time its owner chooses to exercise in the heat. For the reality is that the brain also dies if the athlete dies from heat stroke. Furthermore it is only the brain that can determine how much heat your are producing (since the brain drives the muscles to exercise) and how much heat you are losing (by regulating the amount of sweat that is being secreted - this control is via the sympathetic nervous system).

Since it controls both heat production and heat loss the brain must determine whether or not to kill itself. Why would it choose suicide when it can simply choose to increase the rate of heat loss (by increased sweating) or if that fails simply reduce the rate of heat production by slowing the athlete down.

The rarity of heat stroke suggests (i) that these controls work very very weil in most individuals and (ii) when heat stroke does occur something has gone seriously wrong since the brain has chosen suicide over survival.

And evolution would not have allowed such a brain to survive.
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Re: Tim Noakes: we need you back for a moment [big slow mover] [ In reply to ]
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This is a great question. The only reasonable answer that I can offer is that the brain considers the regulation of the body's osmolality as a greater priority than its energy stores. Also the response to an energy deficit may simply be to cause the athlete to slow down.

My experience described in Lore of Running was that when I developed hypoglycemia (the Bonk) due to a falling rate of glucose production by the liver causing blood glucose concentrations to fall, my brain would tell me to stop running. And when I had stopped to seek food. This is the logical response. The organ at risk from hypoglycemia is the brain. If it allows you to continue running you simply compound the problem which can only be corrected by eating. So you eat, the blood glucose concentration rises and the brain releases the brake allowing you again to run.

This system works really well to protect the brain from hypoglycemia during exercise. But your point is excellent: Why does it not act "in anticipation" to force you to go and seek food BEFORE your blood glucose concentration falls since in all other systems the brain acts in anticipation to insure that failure does not occur?

I can only surmise that the need to eat during exercise was not a selective factor driving our biological evolution.

But others might have much better explanations.
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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I can only surmise that the need to eat during exercise was not a selective factor driving our biological evolution.

But this would mean that we have a "evolutionary limit" of about 2 hrs of running. I think it is better for this thread to not fall back into the previous evolutionary debate, but it would be a strange limit if we want to catch prey by running it down to exhaustion, because a lot of animals can outrun us in the 2 hr range. Humans are great long distance runners if they anticipate during the first 3 hrs (by eating against their hunger feeling) of running, but if we listen to our body we are more or less forced to slow down after 2 hrs. This slow down would also prevent us from the entire salt/hydration problem because in 2 hrs of running we could only transpire about 4-5 litres of water. This is not enough to completely dehydrate or inbalance our salt levels. Isn't it possible to say that the salt/hydration problem is only a problem if we start consuming energy during excersise against our feelings? The problem in the sports drink is in that case not the inbalance between water and salt, but the energy in it that enables us to proceed excersise until the salt or water concentration in our body drop to problematic values?

A different observation I made with this is that during long hikes, the body give a hunger/thirst feeling always in time. Wouldn't this be a clue that our bodies are made more for long and really easy excersise, compared to the long tempo endurance? And that during tempo efforts it is important to know for us we are doing something AGAINST our internal cues, and that we therefore have to anticipate before we get into trouble? I think this anticipating is important also for hydration. If I do an ironman in the heat my sweat rate will most likely be in the range of 1-2 litres/hr. If I would drink to thirst, I would start with real drinking after loosing 4-5 litres in the first 3 hours. If I afterwards drink with a maximum rate of 750 ml/hr (that would more or less be drinking to thirst for me after I lost 4 litres) I would still have 7* +-750 ml per hour loss of fluid. That is another 5 litres of fluid loss. I would finish with close to 10 litres of fluid loss. That must influence my performance. If I would start drinking from the start I would prevent this. A 10 hr race in the heat is simply further than we can do, if we rely on our feelings. We must anticipate. If we listen to our feelings, we would bonk before any of these things become a problem. Isn't anticipating what enables us to finish?


And thanks for the lenghty contribution to this great discussion. This must at least become the slowtwitch thread of the month. Great amount of good information to read here!

Last edited by: big slow mover: Apr 23, 09 3:33
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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Your thoughts about the cerebral mechanism for the salt intake is interesting, especially in light of the recent study with carbohydrate mouth rinse improving performance.

Also, If I recall, during WWII the military had soldiers exercising out in the desert to test the limits of water deprivation in the heat. What they found was that the soldiers simply stopped moving and could not be induced to keep moving, but they very quickly resumed with a water intake. They did not overheat.

_________________
Dick

Take everything I say with a grain of salt. I know nothing.
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Re: Tim Noakes: we need you back for a moment [duncan] [ In reply to ]
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Indeed, IIRC, in the "Lore of Running" Noakes suggests that most finish-line collapses on hot days are due to lack of blood pressure as heart rate rapidly decreases post-exercise

The majority of finish line collapses are a result of drama. "Look at me, I finished!! I worked so hard I can't even stand up!!!" Pleeze.

The post exercise hypotension will take at a minimum 30 sec, typically longer, so, for someone to collapse as they cross the finish line, it's something else, likely the need for attention.


Steve

http://www.PeaksCoachingGroup.com
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Re: Tim Noakes: we need you back for a moment [S McGregor] [ In reply to ]
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Reading further down the thread, I see Dr. Noakes mentions hypotension again as a cause of collapse in athletes. This is certainly the case in some instances (as I've been all too aware recently in our lab). My previous post was not to say this doesn't occur, it's just that it's not the case at the finish line; that is, unless one turns around and walks back.


Steve

http://www.PeaksCoachingGroup.com
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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In Reply To:
Fortunately there is not one case in the literature of heat stroke or kidney failure in an endurance athlete that can be linked directly to 'dehydration'.

The point as you know is that because two events occurs simultaneously, this does not mean that they are causally related.

In those studies that have been properly conducted there is no evidence that dehydration effects the body temperature response during exercise to an extent that would suggest that further dehydration would cause heat stroke. Again the key is that the brain is there to insure that the exercise intensity is reduced if the body temperature rises too high.

The most interesting recent work is by Dr Chris Byrne from the UK and reported in Medicine and Science in Sports and Exercise. His work shows that the body temperature response to exercise is determined by the exercise intensity (metabolic rate) not by the level of dehydration that develops during exercise.

My guess is that both conditions are related to abnormalities in skeletal muscle function and that is where we should seek the real causes of exercise-associated heat stroke and kidney failure.
I'm sorry but this is absurd. I can't believe that I am agreeing with Frank... Smile Putting aside clinical heastroke for a second, serious dehydration (variable by person) usually causes a significant drop in sweat rate in endurance athletes once you hit a certain "tipping point." Ask anyone who has become dehydrated and overheated and they'll all tell you "I just stopped sweating and got waaaay overheated." To suggest that dehydration is not the CAUSE of this drop in sweat rate and subsequent severe overheating is just totally bizarre. Here's some articles you might want to read:

http://jap.physiology.org/...t/abstract/73/4/1340
"The magnitude of dehydration accrued after 2 h of exercise in the four trials was linearly related with the increase in Tes (r = 0.98, P < 0.02), the increase in HR (r = 0.99, P < 0.01), and the decline in SV (r = 0.99, P < 0.01). LF attenuated hyperthermia, apparently because of higher skin blood flow, inasmuch as forearm blood flow was 20-22% higher than during SF and NF at 105 min (P < 0.05). There were no differences in sweat rate among the four trials."

The reason the sweat rate didn't change is no one went substantially above 4% body weight loss...which as the above IM study that de-tri-mental quoted indicates is "well tolerated" by trained athletes.

Here's another one...a goat study...lol
http://www.pubmedcentral.nih.gov/...r.fcgi?artid=1189275
"Dehydrated animals had lower sweat rates and higher Tr than hydrated animals, but f and Eresp were the same in hydrated and dehydrated animals. 3. When dehydrated goats were allowed to drink after 60 min of heat exposure, sweating began abruptly within 3 min of the start of drinking in every animal whether water or saline was drunk.....<snip>....The rapid recovery of sweating after voluntary drinking is not initiated by changes in Posm or in blood volume and does not appear to depend upon osmoreceptors in the mouth or gastrointestinal tract since it occurs after drinking either water or saline."

Regarding heat stroke itself, I'm quite aware that actual cases of heatstroke are rare. Usually the brain shuts down the body before actual clinical heatstroke occurs. It's a difference between the layman's terminology and the medical terminology. Those with true clinical heatstroke (above 105F) are either in extreme conditions where even ceasing excersize can't prevent the body from increasing in temperature (think Badwater at 2pm) or maybe some failure in the regulation mechanism.


Mad
Last edited by: triguy42: Apr 23, 09 7:38
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Re: Tim Noakes: we need you back for a moment [triguy42] [ In reply to ]
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Another comment based on one of your studies:

http://www.ncbi.nlm.nih.gov/...anel.Pubmed_RVDocSum
"Percent mass loss during the race (2.5 +/- 1.4%), post-race rectal temperatures (38.9 +/- 0.6 degrees C), and rates of sweat loss (1.0 +/- 0.3 1.h-1) were low. There was no statistical relationship between percent mass loss and post-race rectal temperature. Post-race rectal temperatures were significantly related to the metabolic rates for the full 42.2 km and for the last 21.1 and 6 km of the race, and to the average running velocity for the last 6 km (P less than 0.05 and P less than 0.01)."

As other studies have shown, dehydration rates of 3% or so are well tolerated by athletes. For myself, anything over about 3% (5lb on my 162lb self) are "okay" and anything over about 3% can be catastrophic, resulting in significant heat exhaustion. I know this because I started habitually weighing myself before and after workouts and noted a direct correlation between weight loss and the transition to the "death march" at the end of a long run or bike (typically 20+ miles running or 100+ biking). I'd suggest that you saw no correlation between temperature and percent mass loss because there were a ton of external factors that were not well controlled for outside of a laboratory space...and that none of your athletes went into the danger zone of substantially over 3%...making the above study inconclusive wrt significant dehydration and core temp.

To wit:
http://www.ncbi.nlm.nih.gov/...anel.Pubmed_RVDocSum
"Dehydration-mediated perturbations in blood volume and blood flow can compromise exercise heat loss and increase thermal strain. Although progressive dehydration reduces heat dissipation and increases Tre during exercise, the loss of plasma volume contributing to this effect is not always observed for prolonged running and may therefore complicate the predictive influence of dehydration on Tre for marathon running."


Mad
Last edited by: triguy42: Apr 23, 09 7:38
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Re: Tim Noakes: we need you back for a moment [skid] [ In reply to ]
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Scott, totally off topic, but are either of your two brothers still in the sport at all?





Where would you want to swim ?
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Re: Tim Noakes: we need you back for a moment [skid] [ In reply to ]
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I've been a massive sweater ever since I was a kid and have had lifelong cramp issues in all hot races even when I was extremenly fit and paced myself well.


Scott,

Thanks for sharing your experiences.

Could it be, like most things that there is a range - you need what would seem a lot of salt supplementation to keep going. Others less so.

My wife who is a Pro triathlete was recently tested at the University of Guelph in Ontario. I will disclose that the testing was part of a study that is being indirectly supported by Gatorade. What they found was that MissP was a heavy sweater - we knew that. Shes seems to sweat buckets. However, she actually looses, relative to her sweat rate, a low amount of sodium through her sweat. Now the knee-jerk reaction to this in the past, when people say they are heavy/massive sweaters is that they loose a lot of sodium and go crazy with the salt supplementation, but in MissP's case, that is
not the case.

As an interesting anecdotal aside, she raced twice last year in very hot conditions, at IM Lanzarote and Ironman Hawaii, and did reasonably well in both races. Yet we live in Ontario and only rarely do we get weather, that get's close to the types of conditions that she had to race in in Lanzarote and Kona. She did very little heat training in similar environments.






Steve Fleck @stevefleck | Blog
Last edited by: Fleck: Apr 23, 09 7:48
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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In Reply To:
Sorry but I don't know how you know that dehydration caused this condition. As I said the fact that two events occur at the same time does not mean that they are causally related. And why was this lady the only one who developed the condition in that race (ie what is the control group that allowed you to draw your conclusion).

I have considered this problem for 20 years and have written about it extensively. You might want to read our most recent article in MSSE - first author is Dr J Swart. If dehydration is the real cause of heat stroke why does the condition occur so infrequently and why can some athletes finish marathons and ultramarathons after losing 10-12% of body weight and not die of heat stroke? And why do most cases of heat stroke occur in athletes and military personnel involved in short duration exercise and so often in mild environmental conditions. The dehydration explanation simply does not explain most cases of heat stroke.

You really need to read the ENTIRE literature on this topic and not just that section which you are currently reading.

We are currently beginning to test the hypothesis that most cases of heat stroke have a genetic basis and are related to as yet unrecognised conditions of skeletal muscle.

With regard to the frequency of life threatening EAH, I have been able to collect more than 1000 cases of the condition, most reported in the scientific literature since 1985. There is nowhere near the same number of cases of heat stroke reported in athletes during the same time.

So if you read the literature it is clear that heat stroke does not causes anywhere near the same number of cases of ill health in athletes as does EAH. Fortunately it looks like the tide has turned and the number of new cases of EAH each year is now quite low.

I do not discount the potential effects of dehydration. I just am unable to find any evidence in the scientific literature to support your conclusions and much to discount them.
Dr. Noakes, you ask how I "know that dehydration caused this condition." Well, no one knows for sure as to which exact "straw" was the one that broke this camel's "hyperthermia back" But, I am a physician and my clinical jugement is that such conditions do not occur in the absence of dehydration except when the athlete has an underlying condition such as a predispposition to a condtion called malignant hyperthermia. While it is clear dehydration alone is not a sufficient condition to cause hyperthermia it seems it is a necessary condition, at least in some instances, to cause hperthermia in athletes. I find it simply amazing that you are so certain that dehydration is playing no role here. To me it is simply a clinical diagnosis. In your view, if dehydration is not one of them, what are the factors predisposing the athlete to severe hyperthemia?

I will admit that there is more than one potential cause of hyperthermia in athletes while there are not very many causes of hyponatremia, which makes your analysis of this issue rather simplistic, in my view. It seems to me that you should be looking at hydration strategies that could avoid all adverse consequences, not simply focusing on overhydration issues and railing against the sports drink industry.

So, let me get this straight. By your reading of the literature you don't see dehydration as causing much "ill health" where in this very thread someone who works the medical tent at races reports that 90% of those needing aid are suffering from "dehydrated/heat exhaustion". By my poor math skills that leaves only 10% who could be suffering from overhydration issues or other things. Of course, such reports don't mean much to you because it is not the "literature" but simply someone's clinical experience.

So, while I can't explain exactly why some people suffer from heat stroke when others don't (that is what, at least, some researchers are trying to figure out, even though some of them are being funded by sports drinks companies) under a wide variety of conditions and efforts, I would be very surprised that dehydration was not a necessary condition to be present in a portion of these cases.

And, then we have the seemingly related issue of cramps.

If you could point me to a study that demonstrates that dehydration cannot be associated with this condition in athletes I will change my mind. Until then, I will continue to recommend that endurance athletes take in reasonable amounts of fluid to prevent medical issues (including the admonition to not take in too much to avoid water intoxication), especially when conditions are hot and severe.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [triguy42] [ In reply to ]
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In Reply To:
Here's some articles you might want to read:

I am 100% confident that Dr. Noakes has read those articles - he simply chooses to ignore them.
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Re: Tim Noakes: we need you back for a moment [skid] [ In reply to ]
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Figuring out how to prevent cramps in long hot races has been a 34-year search for me so far, so I'm finding this thread is very interesting! \\

you and me both brother. Only problem is that no one is talking about cramping, like it does not exist, or some rare animal. Talking about the brain shutting down before it overheats, the bodies ability to regulate salt, ect. are all great topics. But what about when the bodies muscles shut down from cramps, long before fuel and water are gone? You and I cannot be the only ones that have suffered an entire career with this problem, and like you, salt and magnesium were my savoirs. I read this thread, and begin to doubt that they really worked, and hardly a mention. And of course you know as well as I do, there are a lot of pros out there eating salt pills like candy to get through their hot races. To try and come up with a solution that is generic is just crazy and illiogical in my mind. You are married to one of natures camels, seen her over a lot of years in a lot of races, how can one formula work for her, you and I? I wish it were so, but actual evidence for the past 40 years suggests otherwise...
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Re: Tim Noakes: we need you back for a moment [Fleck] [ In reply to ]
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Interestingly Fleck, I am probably similar to your wife in sweat rate/characteristics. I was always a heavy sweater but not a salty one. The problems came up when I started excersizing more than ~2 hours at a time because I could lose on the order of 4lb per hour in the Floriduh heat. Adding salt to my intake allowed me to digest the water quick enough to avoid serious problems. Without some salt or other electrolytes it would just end up sitting in my stomach on the bike and I'd hit catastrophic dehydration before my stomach would really absorb water well.

As another poster mentioned...back in the day you drank some gatorade (sugars and a bit of salt) and ate bananas. Do you have any idea how many electrolytes are in 1/4 of a banana? Something like 100-150mg Potassium, high levels of Vitamins A, C, B6, B12, Iron, and significant levels of magnesium, calcium and manganese. No significant sodium, but lots of other good stuff. For me the high level of fiber is a serious detractor...which is why I eat bananas on a regular daily basis but not during a race!


Mad
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Re: Tim Noakes: we need you back for a moment [Fleck] [ In reply to ]
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i'm going back and banging on the doors of the old guys. i think the era of skid, grip, and that whole group, tinley, the euros (pauli, rob barel, the germans), welchie, these were the guys who bridged the pre and post salt tab eras. today's top long distant triathletes pretty much all take salt tabs, i think. but i finding the guys who were in that late 80s, early 90s era, like skid, they have a nice long history of both pre and post salt tab racing.

Dan Empfield
aka Slowman
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Re: Tim Noakes: we need you back for a moment [monty] [ In reply to ]
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Cramp is not only a problem under hot conditions. Cramps are also common in very cold conditions, especially on the bike. I have seen lots of cramps in cold weather on longer duathlons in winter.
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Re: Tim Noakes: we need you back for a moment [big slow mover] [ In reply to ]
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 Cramps are also common in very cold conditions, \\

Not for me, but I do not doubt that it is for a lot of people. In cold conditions I hardly need to drink or eat at all. I fit Noakes profile to the T, except that it has to be under 50 degrees. I guess mmy evoloution was more in the north back in the day..(-;
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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What is the evidence that performance during prolonged exercise is related to the cardiac output and blood flow to the muscles? Surely if the exercise is submaximal and occurs at submaximal cardiac output and submaximal blood flow to the muscles, there is no reason to believe that it is limited by (submaximal) rates of oxygen delivery?

So although I would like to accept your explanation i am not certain it is likely to be correct.
Submaximal efforts are not limited by oxygen delivery. Only maximum and near maximum efforts are limited by oxygen delivery as far as I know. Submaximal efforts are limited, I suspect, by the "weakest link" in the complicated cascade that turns fuel into mechanical work. That could vary from person to person depending upon their training history and genetics. Oxygen delivery is not going to be the weak link in this cascade until oxygen delivery is maximized.

Of course, the cell can sense what the limiter is and, with repeated stress, can develop the enzyme systems to better perform when shown the stress again. This is called the training response. This requires no central mechanism to either identify or "correct" the weakness. Of course, we are able to learn what these efforts feel like so are able to voluntarily modify our efforts but this is a learned response and not an inherent central control, IMHO.

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Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [skid] [ In reply to ]
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The answer to why cramping occurs during races should be somewhere within, "Why doesn't cramping occur during training?"

Each of us has a control group - training efforts.

I know people who have gone to epic type training camps which demanded tremendous training load, on consecutive days, not being as anally attentive to salt and fluid intake as on race day, and involving similar workout intensity to racing. No cramps. Yet on race day 2-3 weeks later they cramp early in the run of a half ironman. Why??

For comparison, one must make a list of factors that differ between the 2 types of events, training and racing.

Differences during the event:
- generally higher level of intensity while racing
- no rest during racing
- adrenaline/other hormones are likely different
- probably more tuned in to salt/fluid/calorie replacement on race day

I think at least part of the answer may be in the days leading up to race day, however.

Diffferences before the event:
- decrease in work volume and overall load
- dysproportionate increased intake of fluid, calories, and electrolytes relative to demands

So how does the body's internal milieu change in response to the taper? And are those changes a set-up for race day failures?

It's the days leading up to the race that we have some control over; the race day factors are mostly inherent.


Coach at KonaCoach Multisport
Last edited by: Terra-Man: Apr 23, 09 9:03
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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Correct. The site from which the fluid is lost depends on the amount of sodium and potassium that are lost with the water. The more sodium that is lost, the more of the fluid loss will come from the ECF.

Sporting performance is strongly belief centred. If you believe that becoming "dehydrated" will effect your performance, then it will. Similarly if you believe that drinking ahead of thirst will improve your performance it probably will. But there is a point at which fluid retention will lead to an impaired performance perhaps as a result as much of brain swelling as of changes in the muscles caused by an increase in their water content.

The interesting point is that it seems to depend where you come from as to your view of how much you should be drinking during exercise. If you are an elite distance runner from Africa you will very likely drink to thirst during training and competition. If you come from Europe or North America, it seems to me that you would be more likely to believe that you must drink to "stay ahead of thirst". Is this because of differences in biology? Or of pre-programming?
Sporting performance may be strongly belief oriented but it is more strongly physiology oriented. Not believing severe dehydration can affect performance does not mean that severe dehydration does not affect performance or, even, health.

What is clear that peoples physiology varies somewhat in their ability to handle salt and water. Further, it seems peoples ability to handle salt and water can adapt based upon their experience. Unless we understand these differences and how to identify them it seems we cannot give good advice to people unless they have the physiology of either an African elite runner or Lance Armstrong, where the advice is: do what they do. Seems like a cope out to me.

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Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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There is no evidence that humans can run themselves into a catastrophic failure. Even the winners of the Ironman Triathlon do not die at the finish. They walk over to the medical tent etc showing that they finish with reserve. When death does occur it is almost always due to a pathological condition.
No evidence of catastrophic failure? Perhaps you might want to watch this video. "Walk" over to the medical tent, indeed.

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Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Terra-Man] [ In reply to ]
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"Why doesn't cramping occur during training?" \\

But they absolutly do happen in training. Once again not for everyone, but just look at you evening swim workout sometime, after the triathletes have put in a full day before, and you will see many on the deck stretching out cramps. All the cramps I have gotten in races, I have gotten in training. I think that it may happen more often in races, because it is just that, a race. During training you are not redllined, and thus can absorbe more fuel and electrolytes, and have the time to do it. I think we all know that when you are flat out, the body's ability to absorbe goes down, and the hotter it is, the worse it gets. It goes back to what I was comparing in the earlier studies of sedetary heat starved people, and all out racers. The race acclerates the losses, prevents the equal refueling of those losses, and the bodies indicators seem to lag behind the actual losses.

I was just talking to Dan on our dog walk, and I told him of people I know that have never had a cramp in their lives, don't even know what it is. Some people think a side stitch in a cramp. It is just that some people are predisposed to having great regletory systems, that conserve in a way that allows them to do just about whatever they want, without no negative affects. But then there are the others, and all you have to do is look at a cramping/salt/electrolyte/ thread to see how many of those folks are out there. I have had to live this nightmare throughout my career, and belive it was a large contributor to my heart damage. I have a lot of proofs that point to that too, not conclusive mind you, but then no one can be conclusive in these situations right now. The cardiologists are just as baffled as we are when it comes to direct causes of heart damage in athletes, but there are some strong signs...
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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The danger is always to try to reduce a complex phenomenon (the development of heat stroke) to one simple mechanism ie dehydration. To conclude that dehydration is the cause you have at least to exclude a number of other possibilities. Also if the activity was less than a few hours and the subject had been drinking, then what level of dehydration would have been present? And would that level of dehydration not have been precisely the same as that measured in many other athletes completing the race on the same day in the same conditions without any evidence for "heat illness".
Clearly, at least to me, heat stroke is multifactorial. In the absence of illness and genetic abnormalities (malignant hyperthermia susceptible) dehydration seems to be a necessary component of this multifactorial disease. If you have evidence to the contrary I would love to see it.
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But more to the point, much of the early work on heat stroke was done in the South African gold mines in the 1920's and 1930's when an epidemic of heat stroke began to develop as the mines went ever deeper. (The temperature of the rock face at 3-4km below the earth surface is 50 degrees C). The main risk for heat stroke were the environmental conditions, the amount of work performed, the level of heat acclimatization and most importantly the presence of intercurrent illness. These were not healthy people who suddenly developed the condition. In laboratory testing on the mines it was soon observed that those who started exercise with an elevated temperature (because of an intercurrent illness of which they might or might not have been aware) were unable to regulate their body temperatures appropriately and had to be stopped from exercise when their temperatures reached abnormally high levels. So in an case of heat stroke you have to be certain that there was not an intercurrent illness at the same time. But most importantly in my view whether or not there is also some underlying muscle disorder that causes an explosive production of heat (thermogenesis) which is the real cause of the heat stroke (according to the theory that we are currently evaluating).
Of course there is an underlying muscle disorder that could cause heat related illness. However, it is not likely that MH is the source of most of these problems as I am unaware of a single case where dantrolene was necessary to stop the reaction at an athletic event, once triggered. But, some of these people might have the trait. It would be easy to find out, simply do an MH diagnostic muscle biopsey on all those with heat related illness at the finish line (sometime after the event, not necessary to do the biopsey at the finish line).
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Thank you for mentioning postural hypotension as the cause of your collapse. This is by far the most common cause of post-exercise collapse in all endurance athletes. Unfortunately it is labelled as "heat illness" and "dehydration" but both diagnoses are wrong. First the body temperature is not seriously elevated in these athletes and second they recover the instant their legs and pelvis are elevated above the level of the heart. This restores their blood pressures. Their symptoms as you correctly state are due to low blood pressure when standing (postural hypotension) which is corrected when the blood volume in the legs is redistributed to the centre of the body correcting a low filling pressure of the heart and again allowing a normal circulatory function.
Ugh, seems to me that you think all the doctors at the finish line of these events are complete idiots, unable to tell transient postural hypotension from dehydration related hypotension. This difference is relatively easy to discern clinically. Perhaps you have never heard of the tilt test. It don't take much blood volume to keep the body alive when one is supine with the legs elevated. Perhaps you should spend a few days hanging around with some anesthesiologists (or ER physicians) and learn how they clinically assess blood volume/hydration status and the consequences of those conditions. It is a problem that comes up almost every day. We think we have gotten pretty good at it.
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Frank's interpretation is also dependant on the catastrophe model that he evokes for exercise in the heat. I mentioned this model in an earlier post - Basic Physiology 3 - the one to do with the sports drink industry's model of how the body works.
I don't believe I have ever heard this model referred to as the "catastrophe" model. I just thought it was basic physiology. Anyhow, how does the sport drink industry's model differ from the model taught in medical school as to how the body works?
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Thus according to his model humans will continue to exercise without drinking until they suddenly collapse from heat stroke. When this does happen it is the exception not the rule. The rule is that if you become too hot or if you don't drink enough during exercise the brain will eventually take over and change your behavior by slowing you down. When you slow down your rate of heat production is reduced and you start to cool down (since it is your rate of heat production and not your level of dehydration that is the primary determinant of your body temperature during exercise - presuming that you do not have an intercurrent illness). in this way dehydration (caused by the absence of drinking which causes thirst which causes you to slow down and to go and search for fluid to alleviate your symptoms of thirst) should actually protect from and not cause heat stroke.
Ugh, where did I ever say that continuing "to exercise without drinking" would sort of go unnoticed until the athlete "suddenly collapased"? I don't think that ever happens. As dehydration begins to get clinically significant performance will start to degrade as filling pressure will drop and cardiac output cannot be maintained at the previous high level. If the muscles are continued to be stressed at the same level though, one compensatory mechanism the body has to meet the demand is to divert blood from the skin to the muscles. This would be a good survival mechanism is being chased by a lion so we can see why evolution might have selected for this ability. It is an awful survival mechanism is in a hot marathon.

Slowing you down when dehydrated does not require a single neuron of brain activity. It is simply a matter of being able to maintain cardiac output and deliver oxygen to all the demands. If you don't slow down you will overheat. If you overheat, the proteins don't work so good anyhow and you will slow down. It is all a matter of rather simple physiology.
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Interestingly in the literature there are hundreds of individual cases of subjects who exercise in the heat without drinking. Often these subjects are acting as the controls in studies to show important it is to drink during exercise. But in none of these are there reports of ill health in the group who do not drink during exercise. The exception are a group of studies in which athletes exercise in such extreme heat that they are unable to regulate their body temperatures so that they will have to stop eventually because they are becoming too hot. But even in those experiments subjects usually stop because they develop postural hypotension with temperatures well below those measured in cases of heat stroke or even in winners of 10, 21 and 42 km races run in the heat.
Ugh, me thinks that is because the Human use committees would never approve a study that allowed the subjects to exercise long enough to risk any injury, let alone any substantial injury. Any body temperature more than a degree or so from the optimal 37ş will adversly affect performance. That is a different story than heat stroke which is life threatening. You don't seem to be able to put this "heat issue" into perspective. It is a continuum, just as water intoxication is.
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These findings are best explained by a model in which the brain is clever enough not to want to kill itself every time its owner chooses to exercise in the heat. For the reality is that the brain also dies if the athlete dies from heat stroke. Furthermore it is only the brain that can determine how much heat your are producing (since the brain drives the muscles to exercise) and how much heat you are losing (by regulating the amount of sweat that is being secreted - this control is via the sympathetic nervous system).
Phooey. It is not necessary to invoke any "brain cleverness" to explain any or all of these findings other than we learn from prior experience so are better able to gauge our efforts. Ugh, and most athletic activity, like running does not involve any "brain activity" as it is purely a spinal reflex activity, never getting any higher than the cerebellum except when the brain is used to initiate the activity or change the intensity. People do not have to think about moving those muscles.
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Since it controls both heat production and heat loss the brain must determine whether or not to kill itself. Why would it choose suicide when it can simply choose to increase the rate of heat loss (by increased sweating) or if that fails simply reduce the rate of heat production by slowing the athlete down.
The only way the brain "controls" the periphery is in its ability to put out hormones that will divert blood from other organs to itself in cases of extremis. During ordinary activity the brain has no control over heating (except, perhaps, for shivering and initiating muscle activity), cooling, or anything else. If the brain is involved in this peripheral physiology the entire body is in extremis.
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The rarity of heat stroke suggests (i) that these controls work very very weil in most individuals and (ii) when heat stroke does occur something has gone seriously wrong since the brain has chosen suicide over survival.
Well, I concur that heat stroke implies something has gone seriously wrong but I disagree that it was the primary fault of the brain unless we blame it for signing up for the race or whatever.
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And evolution would not have allowed such a brain to survive.
That is correct. That is why the physiology works the way it does. Luckily for us our brains are used mostly for thinking and not for making sure the muscles work right when exercising which allows us to study and figure some of this stuff out.

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Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Terra-Man] [ In reply to ]
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I agree with many of your points.
Why is electrolytes the answer for cramping in triathlon?? I think the answer to that question is culture. In long distance xc-skiing, nobody links cramping to lack of electrolytes. If you get cramps you are pushing too hard, your fitness level is not where it should be. Ultra runners in Scandinavia are not crazy users of salt tablets (I am talking about 6, 12 and 24 hours competitions). The top marathon runners in the world do not link electrolytes, salty sweaters and dehydration to cramping. But in triathlon, many need an electrolyte replacement plan for a sprint or Olympic. It must be culture.

This is how the best marathon runners are fueling. No focus on electrolytes.

During the long runs in Kenya (and in Ethiopia, too) normally the athletes drink only water. Sometime we meet runners going without any assistant (no car following them) in courses of 45 km, of course without any possibility to drink. Not only, but one of the most difficult problems to solve for training kenyan marathon runners is to teach them to drink. Many of them think that not drinking can strengthen their endurance in very bad conditions of weather. And, also when they drink, a lot of time they only put little water in their mouth, and after they spit out without swallowing.

Different is the situation during the race. Many athletes (not all, but many) use maltodestrines,if they have european or american coaches, knowing the system.
For example, in preparation of WCh of Osaka 2007, that we knew were very hot and humid, I went with Shami for any specific workout at lower altitude (Keiyo Valley), at 11:00 o'clock in the morning, in order to have full adaptation to the conditions of the race. Several times Luke Kibet came with our group. During that period, I always used Maltodestrines (in powder), melted in water, trying to create the best concentration for each athlete. In fact, the reaction in the stomach is individual, changing from every athlete. Somebody cannot use, because feels acidity after drinking, for some other everything is ok. In the case of Shami, we found a good solution using 2 normal spoons of powder in 250 ml of water. The same we use in Osaka, where he was able to win silver, in spite to have a sciatic problem that didn't allow him to run faster than 3:10 per km.
http://www.letsrun.com/forum/flat_read.php?thread=2959804&page=0


You will find some good readings here
http://www.sportsscientists.com/2008/01/featured-series-on-science-of-sport.html

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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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I take it you are not a fan of Noakes' central governor theory. What is that theory and why do you not agree with it?

________
It doesn't really matter what Phil is saying, the music of his voice is the appropriate soundtrack for a bicycle race. HTupolev
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Re: Tim Noakes: we need you back for a moment [HH] [ In reply to ]
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I take it you are not a fan of Noakes' central governor theory. What is that theory and why do you not agree with it?
Well, as I understand his theory, physical activity is limited by some brain "governor". I am sure he will correct me if I am wrong. While the brain is connected to all parts of the body and does have some control over aspects of our peripheral physiology, to say it is the primary limiter is just hair brained as far as I am concerned, especially as regulating peripheral muscle activity is concerned. I need a mechanism for both the sensing and control. Without that, the theory is just a bunch of conjecture. All these limits are better explained by local mechanisms that have been well studied for years. Of course, everything we "know" in medicine is subject to change. I was told in medical school that half of what they were teaching us was wrong, they just didn't know which half. Perhaps, Noakes is right. I just don't see the evidence that supports his theory. A theory must explain all that is observed to be true, otherwise it needs to be revised. So, until he comes through, I will hold his feet to the fire to give us a mechanism (beyond the brain is controlling things "mechanism") for this control and hold up examples where it seems to fail.

I have a similar issue with Dr. Coggan's "the heart is the limiter" theory. While some data could be interpreted to support both of these theories, for either of them to be correct the theory has to explain what initiates the "failure cascade". This initiation is better explained by peripheral limiters in my opinion. Dr. Coggan and I have gone back and forth on this many times here and if you do a search you can see what both of us have to say. Dr. Noakes is new to defending his theories here.

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Frank,
An original Ironman and the Inventor of PowerCranks
Last edited by: Frank Day: Apr 23, 09 10:33
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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I have a similar issue with Dr. Coggan's "the heart is the limiter" theory.

Not my theory, but the generally-accepted explanation (with the caveat that one should really say "cardiovascular system" instead of just "heart") for what primarily limits VO2max in humans.

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While some data could be interpreted to support both of these theories, for either of them to be correct the theory has to explain what initiates the "failure cascade". This initiation is better explained by peripheral limiters in my opinion.

1. VO2max is primarily limited by the cardiovascular system's ability to transport O2-carrying blood to exercising muscle.

2. Performance is primarily determined by metabolic events in exercising muscle.
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Re: Tim Noakes: we need you back for a moment [Andrew Coggan] [ In reply to ]
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I have a similar issue with Dr. Coggan's "the heart is the limiter" theory.

Not my theory, but the generally-accepted explanation (with the caveat that one should really say "cardiovascular system" instead of just "heart") for what primarily limits VO2max in humans.
Here is the big "problem" with this cardiovascular system limiter theory. VO2 max depends upon how it is measured. In the same person it can be different if measured on a bicycle, running, or rowing, or any other method. If the CV system were truly the limiter it should test the same regardless of the activity.

So, it may be generally accepted as right. But, if it cannot explain all the data it isn't right.
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While some data could be interpreted to support both of these theories, for either of them to be correct the theory has to explain what initiates the "failure cascade". This initiation is better explained by peripheral limiters in my opinion.

1. VO2max is primarily limited by the cardiovascular system's ability to transport O2-carrying blood to exercising muscle.

2. Performance is primarily determined by metabolic events in exercising muscle.
This actually is in agreement with what I have been saying all along. The cardiovascular system appears to be the limiting factor for VO2 max because of events that occur in the exercising muscle near maximum performance.

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Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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I have a similar issue with Dr. Coggan's "the heart is the limiter" theory.

Not my theory, but the generally-accepted explanation (with the caveat that one should really say "cardiovascular system" instead of just "heart") for what primarily limits VO2max in humans.
Here is the big "problem" with this cardiovascular system limiter theory. VO2 max depends upon how it is measured. In the same person it can be different if measured on a bicycle, running, or rowing, or any other method. If the CV system were truly the limiter it should test the same regardless of the activity.

Unless someone is specifically trained as a cyclist or rower, they are generally unable to achieve the same VO2 during such modes of exercise as during graded treadmill running. Hence, the highest VO2 achievable by non-cyclists or non-rowers (or cyclists during rowing or rowers while cycling) is considered to be a VO2peak, and not VO2max.

As for why this occurs, the answer again lies in the functioning of the cardiovascular system.

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So, it may be generally accepted as right. But, if it cannot explain all the data it isn't right.

The classical perspective on VO2max does indeed explain the available data.

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1. VO2max is primarily limited by the cardiovascular system's ability to transport O2-carrying blood to exercising muscle.

2. Performance is primarily determined by metabolic events in exercising muscle.

This actually is in agreement with what I have been saying all along. The cardiovascular system appears to be the limiting factor for VO2 max because of events that occur in the exercising muscle near maximum performance.

Do you mean "The cardiovascular system appears to be the limiting factor for VO2max..."? If so, that that is incorrect is clear from the fact that there is a VO2max in the first place.
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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Thank you. Which publication(s) by Noakes referencing the governor theory have you read?

________
It doesn't really matter what Phil is saying, the music of his voice is the appropriate soundtrack for a bicycle race. HTupolev
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Re: Tim Noakes: we need you back for a moment [dawhead] [ In reply to ]
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4) studies of both chimpanzee and orang-utan clans suggest that both males and females appreciate doing their nails to about the same extent.

you know, this is really making me rethink my annual 'do i really want to shave my legs this year' debate.
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Re: Tim Noakes: we need you back for a moment [dcsxtri10] [ In reply to ]
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"If you have severe leg cramps(different issue), they can highly likely be stopped wit IV Na Cl .... or PO NaCl if you can take it with a time delay that is variable."


This and several athletes testimonies about the efficacy of plain NaCl as a remedy against cramps bring up the interesting posssibility (propability) that NaCl intake may not directly be required for "topping off the tank", but may trigger (alleviate) other physiological processes that help maintain electrolyte balance under stress.

One could imagine that the physiological "window" for NaCl concentration differences is quite narrow, and adjustments of those levels and the timeframe required for it may in fact be limited during heavy exercise.

So measuring steady state electrolyte levels may not be the best way to study electrolyte concentration "gradients" and "windows" of optimal concentration DURING exercise.

___________________________________________
Ego numquam pronuncio mendacium,
sed sum homo salvaticus
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Re: Tim Noakes: we need you back for a moment [Bob Loblaw] [ In reply to ]
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4) studies of both chimpanzee and orang-utan clans suggest that both males and females appreciate doing their nails to about the same extent.

you know, this is really making me rethink my annual 'do i really want to shave my legs this year' debate.
It was a fair crack at the humor he was responding to.

JJ

Every night that I run, the thought crosses my mind that there's no way in hell I'll still be running a month from now.
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Re: Tim Noakes: we need you back for a moment [Halvard] [ In reply to ]
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Why is electrolytes the answer for cramping in triathlon?? I think the answer to that question is culture. In long distance xc-skiing, nobody links cramping to lack of electrolytes. If you get cramps you are pushing too hard, your fitness level is not where it should be. Ultra runners in Scandinavia are not crazy users of salt tablets (I am talking about 6, 12 and 24 hours competitions). The top marathon runners in the world do not link electrolytes, salty sweaters and dehydration to cramping. But in triathlon, many need an electrolyte replacement plan for a sprint or Olympic. It must be culture.

Why is it different in triathlon? That's a good question. Because it's triathlon . . it has to be different. Everything seems to be different in this sport! :-)



Steve Fleck @stevefleck | Blog
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Re: Tim Noakes: we need you back for a moment [Andrew Coggan] [ In reply to ]
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In Reply To:
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In Reply To:
I have a similar issue with Dr. Coggan's "the heart is the limiter" theory.

Not my theory, but the generally-accepted explanation (with the caveat that one should really say "cardiovascular system" instead of just "heart") for what primarily limits VO2max in humans.
Here is the big "problem" with this cardiovascular system limiter theory. VO2 max depends upon how it is measured. In the same person it can be different if measured on a bicycle, running, or rowing, or any other method. If the CV system were truly the limiter it should test the same regardless of the activity.

Unless someone is specifically trained as a cyclist or rower, they are generally unable to achieve the same VO2 during such modes of exercise as during graded treadmill running. Hence, the highest VO2 achievable by non-cyclists or non-rowers (or cyclists during rowing or rowers while cycling) is considered to be a VO2peak, and not VO2max.

As for why this occurs, the answer again lies in the functioning of the cardiovascular system.
Explain to me how it is the cardiovascular system knows what exercise the athlete is doing or is trained to do such that it knows to fail at different outputs for different exercises. That is a better argument for the central governor theory except neither one has a mechanism to explain how this "knowledge" is acquired by the cardiovascular system. You are right that the answer is integral to how the cardiovascular system operates except the cardiovascular system is reacting to systemic changes that are occurring from local failures peripherally. It is the only explanation that makes any sense to explain this variability.
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So, it may be generally accepted as right. But, if it cannot explain all the data it isn't right.

The classical perspective on VO2max does indeed explain the available data.
How, again, does it explain this variability? What is the mechanism to explain the drop off in cardiac output at different levels in the same person near VO2 peak, depending upon how one is tested?
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In Reply To:
1. VO2max is primarily limited by the cardiovascular system's ability to transport O2-carrying blood to exercising muscle.

2. Performance is primarily determined by metabolic events in exercising muscle.

This actually is in agreement with what I have been saying all along. The cardiovascular system appears to be the limiting factor for VO2 max because of events that occur in the exercising muscle near maximum performance.

Do you mean "The cardiovascular system appears to be the limiting factor for VO2max..."? If so, that that is incorrect is clear from the fact that there is a VO2max in the first place.
The question is not whether there is a VO2 max, clearly there is. The question is why is there a VO2 max (or peak if you prefer) and why is it what it is in any particular person being tested in any particular manner? What is the specific limiting factor that determines this number, be it VO2 max or VO2 peak?

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Fleck] [ In reply to ]
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Why is electrolytes the answer for cramping in triathlon??


Not true, everybody in any sport blames something else if things go not as planned.
Nobody will admit being not prepared sufficiently.
In ANY sport.
You may however be onto something with the cultural differences between continents ;-)

If you push to hard and go over your limits you go past the conditions your system is able to handle (ion balance or heat) your system will "shut down".
Cramping is just a sign of that. So, "electrolyte imbalances" are a good place to look, although taking electrolytes will in fact not substitute for proper training or taking PEDs.

Regarding top marathon runners: They barely sweat at all.
Much better adapted to heat stress (among other factors).

___________________________________________
Ego numquam pronuncio mendacium,
sed sum homo salvaticus
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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As a practicing ER physician - I'll say with 99 certainty that:

1) The doctors working the finish line are not idiots.
2) These same doctors can not judge blood volume or hydration reliably at all.
3) Most of these doctors don't know what a "tilt test" is and none ever do it.
4) If you studied a "tilt test" I assume it would be like "orthostatic vital signs" and in essence would be useless.
5) All the "patients" know that they are severly dehydrated and need an IV....99% of them are of course wrong. All of their family members agree with the patients. All of the non-M.D. people working the finish line agree with the pt. Some of the patients will pass out as you try to kick them out without an IV - they then will likely get at IV which will prove to all that the M.D. was wrong by initially refusing the IV and is actually an idiot.

Dave
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Re: Tim Noakes: we need you back for a moment [daveinmammoth] [ In reply to ]
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5) All the "patients" know that they are severly dehydrated and need an IV....99% of them are of course wrong. All of their family members agree with the patients. All of the non-M.D. people working the finish line agree with the pt. Some of the patients will pass out as you try to kick them out without an IV - they then will likely get at IV which will prove to all that the M.D. was wrong by initially refusing the IV and is actually an idiot.

That's classic!


Coach at KonaCoach Multisport
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Re: Tim Noakes: we need you back for a moment [daveinmammoth] [ In reply to ]
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"1) The doctors working the finish line are not idiots."
"they then will likely get at IV which will prove to all that the M.D. was wrong by initially refusing the IV and is actually an idiot."


Wow, I hope I never get to visit your ER.... you make no sense.

___________________________________________
Ego numquam pronuncio mendacium,
sed sum homo salvaticus
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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In Reply To:
Explain to me how it is the cardiovascular system knows what exercise the athlete is doing or is trained to do such that it knows to fail at different outputs for different exercises.

The cardiovascular system doesn't need to "know" since it is only truly limiting when VO2max is achieved (see more below). VO2peak, OTOH, is limited by other factors (e.g., muscle fatigue that prevents the subject from sustaining exercise at a high enough intensity for a long enough duration for the cardiovascular system to be limiting).

In Reply To:
What is the mechanism to explain the drop off in cardiac output at different levels in the same person near VO2 peak, depending upon how one is tested?

No such mechanism need exist, because such a leveling off or even drop in cardiac output only occurs when a true VO2max is achieved. At that point, VO2 either plateaus or even declines, depending on whether or not it is possible to further increase a-vO2 difference. (Cf. http://www.ncbi.nlm.nih.gov/pubmed/12591751).

(BTW, while I'm citing references, here's another of Jose's studies directly refuting some of Dr. Noakes' claims, which he also conveniently chooses to ignore:

http://www.ncbi.nlm.nih.gov/pubmed/9824726)

In Reply To:
The question is not whether there is a VO2 max, clearly there is. The question is why is there a VO2 max (or peak if you prefer) and why is it what it is in any particular person being tested in any particular manner? What is the specific limiting factor that determines this number, be it VO2 max or VO2 peak?

As I said, VO2max is primarily limited by the cardiovascular system's ability to transport O2-carrying blood to the muscles.
Quote Reply
Re: Tim Noakes: we need you back for a moment [Andrew Coggan] [ In reply to ]
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Good Lord, how can you not get tired of this? You should make him take a test to prove that he has read something other than his 40 yr old Anesthesiology text.


Steve

http://www.PeaksCoachingGroup.com
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Re: Tim Noakes: we need you back for a moment [S McGregor] [ In reply to ]
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In Reply To:
Good Lord, how can you not get tired of this?
In addition to having the memory of an elephant, I have the patience of a saint?
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Re: Tim Noakes: we need you back for a moment [Andrew Coggan] [ In reply to ]
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Quote:
In addition to having the memory of an elephant, I have the patience of a saint?

Evidently.


Steve

http://www.PeaksCoachingGroup.com
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Re: Tim Noakes: we need you back for a moment [daveinmammoth] [ In reply to ]
Quote | Reply
In Reply To:
As a practicing ER physician - I'll say with 99 certainty that:

1) The doctors working the finish line are not idiots.
2) These same doctors can not judge blood volume or hydration reliably at all.
3) Most of these doctors don't know what a "tilt test" is and none ever do it.
4) If you studied a "tilt test" I assume it would be like "orthostatic vital signs" and in essence would be useless.
5) All the "patients" know that they are severly dehydrated and need an IV....99% of them are of course wrong. All of their family members agree with the patients. All of the non-M.D. people working the finish line agree with the pt. Some of the patients will pass out as you try to kick them out without an IV - they then will likely get at IV which will prove to all that the M.D. was wrong by initially refusing the IV and is actually an idiot.

Dave
I wouldn't know the qualifications of the docs at the finish line at any particular race. However, if I were the medical director I would make sure that each of them were trained to distinguish these things (it is fairly simple) and that those with minimal experience were supervised by me. It is not the doc's job to treat what the patient thinks they need but to do a history and physical and, possibly, if necessary, some lab work, and treat according to what is best for the patient.

Where do you get the idea that orthostatic vital signs are "worthless" in this setting. I presume you would think pitting edema or temperature worthless also? All this stuff is part of the overall picture that the doctor needs to diagnose what is going on. If the patient walks into the medical tent it is unlikely that orthostatic vital signs need be done. If the patient was carried in, they probably should be.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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As a (miraculous) survivor of heat stroke (I was not dehydrated, it was related to a medication I was taking), I have obviously done some reading on heat stroke and its causes! From what I have read, the original theory was that there was a continuum of heat illnesses -- from heat illness, to heat exhaustion, to heat stroke. An updated version is that, while heat illness and heat exhaustion are on a continuum, heat stroke is a completely different animal. Heat stroke seems to be much more a neurological thing, where the brain loses its ability to correctly regulate body temperature. So, while heat illness and heat exhaustion may indeed have a dehydration component to them, heat stroke in fact may not. Dr. Noakes, is this why you don't correlate dehydration with heat stroke in particular? I think that a clear delineation needs to be made between the two related diagnoses -- heat illness/heat exhaustion, and the separate diagnosis of heat stroke. It may be that on this thread people are interchanging these terms, and that may be causing some of the resulting confusion.

Just my $0.02.
Sharon

Festina Lente
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Re: Tim Noakes: we need you back for a moment [Andrew Coggan] [ In reply to ]
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In Reply To:
In Reply To:
Explain to me how it is the cardiovascular system knows what exercise the athlete is doing or is trained to do such that it knows to fail at different outputs for different exercises.

The cardiovascular system doesn't need to "know" since it is only truly limiting when VO2max is achieved (see more below). VO2peak, OTOH, is limited by other factors (e.g., muscle fatigue that prevents the subject from sustaining exercise at a high enough intensity for a long enough duration for the cardiovascular system to be limiting).

In Reply To:
What is the mechanism to explain the drop off in cardiac output at different levels in the same person near VO2 peak, depending upon how one is tested?

No such mechanism need exist, because such a leveling off or even drop in cardiac output only occurs when a true VO2max is achieved. At that point, VO2 either plateaus or even declines, depending on whether or not it is possible to further increase a-vO2 difference. (Cf. http://www.ncbi.nlm.nih.gov/pubmed/12591751).

(BTW, while I'm citing references, here's another of Jose's studies directly refuting some of Dr. Noakes' claims, which he also conveniently chooses to ignore:

http://www.ncbi.nlm.nih.gov/pubmed/9824726)

In Reply To:
The question is not whether there is a VO2 max, clearly there is. The question is why is there a VO2 max (or peak if you prefer) and why is it what it is in any particular person being tested in any particular manner? What is the specific limiting factor that determines this number, be it VO2 max or VO2 peak?

As I said, VO2max is primarily limited by the cardiovascular system's ability to transport O2-carrying blood to the muscles.
LOL. As I said, give me a mechanism for the leveling, and then, dropping off in cardiac output during VO2 max testing. Is it the filling volume is so large that the actin-myosin molocules loose coupling bonds? Is it the brain just can't take any more and turns on the vagus nerve and reduces contractility? Is it we have run out of capillaries and simply no more blood can be pushed through at that pressure? (wait, that doesn't explain the drop off).

Sez Dr. Coggan, trust me, I am a doctor, I don't need no friggin mechanism and, in fact, "no such mechanism need exist". LOL Ignorance is bliss.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
Quote Reply
Re: Tim Noakes: we need you back for a moment [S McGregor] [ In reply to ]
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In Reply To:
Good Lord, how can you not get tired of this? You should make him take a test to prove that he has read something other than his 40 yr old Anesthesiology text.
I take it you don't need no friggin' mechanism either. Good for you. I will reiterate, ignorance is bliss.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
Quote Reply
Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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Frank, you haven't READ anything about the CGM other than what Noakes has presented to you here. I'm sure you probably aren't aware of his debate with "the man" regarding the VO2max, since you haven't heard of the "catastrophic" model of exercise failure/exhaustion. You haven't READ anything about the limitations of exercise in the literature... at all. I've told you this before, you've been around a long time and if you don't have the gumption to go out and learn about these issue in the literature, I'm not going to take the time to spoon feed it to you. Andy's been doing it for years, and it still hasn't taken hold. He clearly has more patience than I do.


Steve

http://www.PeaksCoachingGroup.com
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Re: Tim Noakes: we need you back for a moment [S McGregor] [ In reply to ]
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In Reply To:
Frank, you haven't READ anything about the CGM other than what Noakes has presented to you here. I'm sure you probably aren't aware of his debate with "the man" regarding the VO2max, since you haven't heard of the "catastrophic" model of exercise failure/exhaustion. You haven't READ anything about the limitations of exercise in the literature... at all. I've told you this before, you've been around a long time and if you don't have the gumption to go out and learn about these issue in the literature, I'm not going to take the time to spoon feed it to you. Andy's been doing it for years, and it still hasn't taken hold. He clearly has more patience than I do.
Just give me a friggin' mechanism to support what he says about what is going on with the CV system at VO2 max.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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In Reply To:
As I said, give me a mechanism for the leveling, and then, dropping off in cardiac output during VO2 max testing.


No, you did not. What you said was:

"The question is not whether there is a VO2 max, clearly there is. The question is why is there a VO2 max (or peak if you prefer) and why is it what it is in any particular person being tested in any particular manner? What is the specific limiting factor that determines this number, be it VO2 max or VO2 peak?"

To which I replied:

"VO2max is primarily limited by the cardiovascular system's ability to transport O2-carrying blood to the muscles."

Now if you want to change the question to "what limits the cardiovascular system's ability to transport O2-carrying blood to the muscles?", that is all well and good, but it doesn't in any way undermine my earlier answer (as Aristotle pointed out in Posterior Analytics).

Anyway, to address your new question: the answer is still unclear, but it has been postulated that hyperthermia and tachycardia combine to reduce stroke volume.
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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As you have already in your sig line:

Exercise physiologists don't DO "mechanisms".

___________________________________________
Ego numquam pronuncio mendacium,
sed sum homo salvaticus
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Re: Tim Noakes: we need you back for a moment [S McGregor] [ In reply to ]
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In Reply To:
Frank, you haven't READ anything about the CGM other than what Noakes has presented to you here. I'm sure you probably aren't aware of his debate with "the man" regarding the VO2max, since you haven't heard of the "catastrophic" model of exercise failure/exhaustion.
What I find ironic about Noakes' mention of the catastrophe theory of fatigue is that in introducing the term into the literature, Edwards emphasized that fatigue is a process, not an end-point.
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Re: Tim Noakes: we need you back for a moment [de-tri-mental] [ In reply to ]
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In Reply To:
Exercise physiologists don't DO "mechanisms".

No?

http://www.ncbi.nlm.nih.gov/pubmed/9277388
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Re: Tim Noakes: we need you back for a moment [Slowman] [ In reply to ]
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I just spent 45 minutes reading through this entire thread. Anecdotal or not, I think I'm still going to drink Gatorade, and I'm still going to utilize salt tabs when it's really hot out. From experience, I have found these to be beneficial (i.e., I delayed or avoided cramping). There may or may not be an element of placebo effect involved, but I'm ok with that if it's working for me.

Maybe, as Dr. Tim suggested, I'll stretch on occasion as well.

Thanks for the well thought out discussion.

mm
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Re: Tim Noakes: we need you back for a moment [Andrew Coggan] [ In reply to ]
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In Reply To:
In Reply To:
As I said, give me a mechanism for the leveling, and then, dropping off in cardiac output during VO2 max testing.


No, you did not. What you said was:

"The question is not whether there is a VO2 max, clearly there is. The question is why is there a VO2 max (or peak if you prefer) and why is it what it is in any particular person being tested in any particular manner? What is the specific limiting factor that determines this number, be it VO2 max or VO2 peak?"

To which I replied:

"VO2max is primarily limited by the cardiovascular system's ability to transport O2-carrying blood to the muscles."

Now if you want to change the question to "what limits the cardiovascular system's ability to transport O2-carrying blood to the muscles?", that is all well and good, but it doesn't in any way undermine my earlier answer (as Aristotle pointed out in Posterior Analytics).

Anyway, to address your new question: the answer is still unclear, but it has been postulated that hyperthermia and tachycardia combine to reduce stroke volume.
It seems to me that "specific limiting factor" goes beyond "cardiovascular system fails". You must be hell to work for always in your professorial one-upmanship mode. You are indeed the master of obfuscation. Anyhow, I am glad to see you don't really have a mechanism to explain this finding.

Anyhow, I have two questions for you.

1. hyperthermia occurs at VO2 max? How much? How fast?

2. Wouldn't a more reasonable hypothesis, other than "hyperthermia and tachycardia" be pH changes occur in the heart interfering with optimum metabolism and reducing contractility, causing the CO to level, then fall. We know that as we approach VO2 max that more and more lactate is produced which must be buffered, primarily by the bicarbonate system? This will drop the pH systemically and optimum performance of most enzyme systems occurs only in a very narrow pH range. Makes sense to me. But, what do I know?

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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I might add, that my hypothesis regarding the mechanism of the VO2 max limit doesn't require invoking any crazy central mechanism or place the heart at any specific risk by making it the limiting organ. The limitations come from simple, well understood, physiological principles.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
Quote Reply
Re: Tim Noakes: we need you back for a moment [S McGregor] [ In reply to ]
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In Reply To:
Frank, you haven't READ anything about the CGM other than what Noakes has presented to you here. I'm sure you probably aren't aware of his debate with "the man" regarding the VO2max, since you haven't heard of the "catastrophic" model of exercise failure/exhaustion. You haven't READ anything about the limitations of exercise in the literature... at all. I've told you this before, you've been around a long time and if you don't have the gumption to go out and learn about these issue in the literature, I'm not going to take the time to spoon feed it to you. Andy's been doing it for years, and it still hasn't taken hold. He clearly has more patience than I do.
Hey, at your urging I did a little search. Here is one thing I found. http://jap.physiology.org/...df_extract/106/1/343

If there were anything to this theory it would be able to be described in a couple of paragraphs here as to what the proposed mechanism is (I asked and got no answer) and one would suspect there would be substantial support for it in other laboratories by now. I guess not.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Andrew Coggan] [ In reply to ]
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That could (almost) be considered .


Let me try:
I would call what you guys do "longitudinal research". Or some sort of two-dimensional line of analysis.
Whenever you get to a crossroad that sticks out of your plane of thought, you always cite "other unidentified factors", although it is well known that there are in fact very plausible and well researched mechanisms that would continue those dead ends and really support exphys data and make the "story" complete.

Reading Ex. Phys. work for me is always like:

yes! yeS!! yES!!!.....
Oh No! Almost made it!

But I really can't complain and actually appreciate the cartographic work, it since it gives us molecular "miners" some good incentive to dig deeper, and get a more three-dimensional picture of the land.
I also have no problem admitting that there are probably a couple more dimensions out there that researchers still miss with their work.

Personally I enjoy working with you guys, since it also gives the molecular studies a real life connection and very often, neatly explains certain physiological processes resulting from what we observe in our dimension.

___________________________________________
Ego numquam pronuncio mendacium,
sed sum homo salvaticus
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Re: Tim Noakes: we need you back for a moment [Terra-Man] [ In reply to ]
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Terra-man, good points about cramping in racing vs training. The 2 points that your bring up that I think are the most relevant are change of routine up to race day and "uniterrupted intensity on race day".

For the former I mentioned this on one of the Boston marathon threads to one of the guys that banged out a 1:15 half marathon in the midst of huge training block and then "relatively" tanked at Boston with a 3:12. He thinks his problems occur when the race goes north of 2 hours. I think the problem is not in the race being longer, but the fact that for all races over 2 hours (typically his A races), he goes into a full taper, changing his daily fitness routine, and throwing off his hormones. There is a reason Tour de France cyclists still train 2-4 hours on "rest days".

Dev
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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Quote:
Hey, at your urging I did a little search. Here is one thing I found. http://jap.physiology.org/...df_extract/106/1/343

Good for you!! That wasn't so hard, now was it? Maybe, more than one page of the literature might be the next step?

Quote:

If there were anything to this theory it would be able to be described in a couple of paragraphs here as to what the proposed mechanism is (I asked and got no answer) and one would suspect there would be substantial support for it in other laboratories by now. I guess not.

I have no idea what you are saying, or what your point is.


Steve

http://www.PeaksCoachingGroup.com
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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Please explain how you would distinguish between the 2 on physical exam (no pre and post weights). I do believe in a good core temp reading - I had a pt with 107 recently - an adult no less. I also did not pack him in ice as that would be bad medicine (well depends on how you define pack.....). I also think pitting edema is useful. I'd love to learn some truly useful physical exam findings that show dehydration as I think the exam is rather useless for that (as unfortunately it is for most things - now you still need to do a good one but study after study after study has shown physical exam tests to be rather useless.......).

Also please let me know the sensitivity and specificity of orthostatic vital signs and how it changes the pretest probability of dehydration in a given pt. If you do that, you will quickly come to realize that orthostatic vitas signs are not particluarly useful as a test.

David
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Re: Tim Noakes: we need you back for a moment [S McGregor] [ In reply to ]
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In Reply To:
Frank, you haven't READ anything about the CGM other than what Noakes has presented to you here. I'm sure you probably aren't aware of his debate with "the man" regarding the VO2max, since you haven't heard of the "catastrophic" model of exercise failure/exhaustion. You haven't READ anything about the limitations of exercise in the literature... at all. I've told you this before, you've been around a long time and if you don't have the gumption to go out and learn about these issue in the literature, I'm not going to take the time to spoon feed it to you. Andy's been doing it for years, and it still hasn't taken hold. He clearly has more patience than I do.

You have to look at this belief of Frank's in context.

His belief that VO2max is limited by peripheral factors and not the cardio/pulmonary system is the foundation upon which he explains how PCs "work". By forcing more muscle mass to contribute to the pedal stroke (i.e. the hip flexor groups) you can magically raise your power at VO2max as the cardiovascular system simply steps up its capacity to meet the increased demand. Quite simply, he has no other way to explain how his invention could possibly do what he claims.
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Re: Tim Noakes: we need you back for a moment [JustCurious] [ In reply to ]
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that is not the case. if his invention reduced the amount of counter productive effort in the pedal stroke (1 foot resisting the other) it would do exactly what he claims.



In Reply To:
steps up its capacity to meet the increased demand. Quite simply, he has no other way to explain how his invention could possibly do what he claims.



Kat Hunter reports on the San Dimas Stage Race from inside the GC winning team
Aeroweenie.com -Compendium of Aero Data and Knowledge
Freelance sports & outdoors writer Kathryn Hunter
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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Actually, there is a bit of evidence for the 'brain is the limiter' thing--at least for some racing/training phenomena.
1. Some studies suggest that bonking actually occurs when the brain detects (for lack of a better word) that the glycogen stores are getting low (not yet gone) and this is, to some extent trainable.
2. The recent carbohydrate mouth rinse study, cited earlier, shows some of the same. The participants who used the tasteless carbohydrate mouth rinse performed quite a bit better than those receiving the placebo mouth rinse.

_________________
Dick

Take everything I say with a grain of salt. I know nothing.
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Re: Tim Noakes: we need you back for a moment [Slowman] [ In reply to ]
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Here we go, it's the Frank and Andy show, again.

_________________
Dick

Take everything I say with a grain of salt. I know nothing.
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Re: Tim Noakes: we need you back for a moment [jackmott] [ In reply to ]
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I'm a total idiot for getting into a pc debate, but I can't resist:

"counter productive effort in the pedal stroke (1 foot resisting the other)"

Please explain the foregoing statement. I'm confused because my legs and feet have pretty much the same mass. Thus, on conventional cranks my legs are balanced, as if on a see-saw. The mass of pushing leg serves to lift the rising leg. No (or negligible) effort is required to lift my rising leg. Except for chain-line losses (for which PCs do nothing) my pushing force goes to propulsion. What's the counter productive effort?

________
It doesn't really matter what Phil is saying, the music of his voice is the appropriate soundtrack for a bicycle race. HTupolev
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Re: Tim Noakes: we need you back for a moment [daveinmammoth] [ In reply to ]
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In Reply To:
Please explain how you would distinguish between the 2 on physical exam (no pre and post weights). I do believe in a good core temp reading - I had a pt with 107 recently - an adult no less. I also did not pack him in ice as that would be bad medicine (well depends on how you define pack.....). I also think pitting edema is useful. I'd love to learn some truly useful physical exam findings that show dehydration as I think the exam is rather useless for that (as unfortunately it is for most things - now you still need to do a good one but study after study after study has shown physical exam tests to be rather useless.......).

Also please let me know the sensitivity and specificity of orthostatic vital signs and how it changes the pretest probability of dehydration in a given pt. If you do that, you will quickly come to realize that orthostatic vitas signs are not particluarly useful as a test.

David
Well, it has been awhile since I have done some of this stuff at the pointy end of the stick but if you don't have left filling pressures sometimes you have to rely on less than perfect information. So, one can start with a history. If the patient is lucid the need for urgency is not so great. Part of the history should include asking weight. Most people doing a race have an idea what their weight was at the start of the race. and when was the last time they pee'd. Is the patient thirsty? If the patient is not lucid, then you have another story regarding urgency.

Then, physical exam would include

skin turgor
capillary refill
sunken eyes?
dry mucous membranes
sitting (legs dangling) or standing and supine blood pressure
is the patient moist or covered in dry salt
"measure" right filling pressure by looking at where jugular distention stops above heart level (the poor man's CVP)
look at respiratory variation in HR
temperature
weight

simple lab test could include a UA specific gravity and blood HCT.

There are rules of thumb regarding what the various physical exam findings mean regarding dehydration but I can't remember them. You asked about the orthostatic BP test specifically. As I remember a change of up to 10 mm HG is normal. If the change is as much as 20-30 mmhg you can be pretty certain dehydration is present. If more than 30 mm hg you can feel confident the patient is substantially volume depleted. I would suggest you ask an anesthesiologist in your hospital and I am sure they could help you out with better and more current rules of thumb in this regard.

Most of the "rules of thumb" are directed towards assessment in the surgery patient and not the athlete, but the principles should be similar. While no one sign is 100% certain, the more "positive" signs you have the more likely there is significant dehydration.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [docfuel] [ In reply to ]
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In Reply To:
Actually, there is a bit of evidence for the 'brain is the limiter' thing--at least for some racing/training phenomena.
1. Some studies suggest that bonking actually occurs when the brain detects (for lack of a better word) that the glycogen stores are getting low (not yet gone) and this is, to some extent trainable.
2. The recent carbohydrate mouth rinse study, cited earlier, shows some of the same. The participants who used the tasteless carbohydrate mouth rinse performed quite a bit better than those receiving the placebo mouth rinse.
Let us get back to discussing whether there is a central limiter to VO2max, isn't that what the CGM states (it isn't called the central performance model CPM but the central governor model CGM)? Neither of those studies go the that "governor"point.

If he can produce a study that shows the carbohydrate rinse changes VO2 max, then I will believe Noakes might be on to something. And, I would still like to hear a mechanism to explain that study and it would be nice to see the study repeated and confirmed. Let us presume the results noted above to be true and real. Despite my asking no one has ventured forth a proposed mechanism as to how this mouth rinse study would cause this performance benefit effect. This study sounds like homeopathy. I guess it is possible it works the way Noakes claims, but the evidence for it is almost non-existant and there is no proposed mechanism to guide researchers.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
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Terra-man, good points about cramping in racing vs training. The 2 points that your bring up that I think are the most relevant are change of routine up to race day and "uniterrupted intensity on race day".

For the former I mentioned this on one of the Boston marathon threads to one of the guys that banged out a 1:15 half marathon in the midst of huge training block and then "relatively" tanked at Boston with a 3:12. He thinks his problems occur when the race goes north of 2 hours. I think the problem is not in the race being longer, but the fact that for all races over 2 hours (typically his A races), he goes into a full taper, changing his daily fitness routine, and throwing off his hormones. There is a reason Tour de France cyclists still train 2-4 hours on "rest days".

Dev
Interesting theory and has some merit looking back over my training log this year. My idea of a taper is to take off the day before a race, and cut back mileage and intensity about a third the week before (usually). But the consistency of my training is such that a "taper week" is almost indistinguishable from the background of average weeks. Looking at what I considered my really good races this year, (and I race a lot but mostly short distances) I simply didn't go hard the last 3 days before the race and took off the day before. 4 days before my best 2-10-2 in ten years, about 5 weeks ago, I did a 10 miler on the trainer at what I consider to be my ftp. 6 days before last weekend's du where I placed 3rd overall, I did a 24 miler on the trainer at about 8 watts under my ftp. I didn't start out to ride that hard but it was a good night and I just kept upping the power. This brings me to another phenomenon, the post race training performances. That particular ride came the day after a balls out 10K where I didn't do great but didn't expect to because it was 6 days after the NO 70.3 where I slugged through a bare sub 2 hour 1/2 fighting cramps the whole way and was a walking wounded for the first 4-5 days after. That 10 miler at ftp came 3 days after another short du, a 2-12-2 and again, I wasn't trying to burn it up at the start but just felt good and kept upping the power. Back when I was young & foolish, (as opposed to being old and foolish now) I would occasionally do 2 races on a weekend and a lot of the time the second race was much better than the first. I know there's a theory that high intensity exercise triggers a short term rise in blood volume which could explain the second day performances but I'd be curious to know how long that effect would last.

JJ

Every night that I run, the thought crosses my mind that there's no way in hell I'll still be running a month from now.
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Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
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If you are not used to rest days, then never take one. Last year I tried to train without rest days, but if life gots in the way and I had one or two days off, I felt completely empty and slow. This year I take at least a day a week off. Now I can stand one or two days off without problems, so I don't "freak out" anymore if I can't train for one or two days. You can say you have to train doing nothing as well...
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Re: Tim Noakes: we need you back for a moment [jsquared] [ In reply to ]
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JJ,

After years of experimentation, this is what I arrived at:
  • C race taper is train normally all week, just be discplined about sleeping properly and trying to get 56 hours of sleep that week
  • B race taper is take Mon off/light, train normally (vol and intensity) Tue-Thu which typically includes "short course style intervals in all sports", take Friday light and Sat light with some intervals. Do a massive week of training from 14-8 days out
  • A race taper is go super light from 14-11 days out, then train really really hard (intensity with moderate volume) from 10-8 days out, and then back on the B race taper

I don't change my diet or over hydrate, over salt in the lead up...the simple fact of reduced volume on Fri and Sat before the race tops things up. I think there is too much "changing of routine" going on for most people and then they are flat and cramping on race day....that's why better to do the "Changing of routine" from 14-11 days out and then get back into it.

Furthermore wrt cramping, I really think that the culprit is "reduced rest interval" on race day. Race efforts are continuous at higher than normal intensities. In an Ironman or half Ironman I take every possible opportunity on the bike to tuck and coast to drop my effort to zero watts and let my heart rate recover. I can also do this in XC ski races. I have found that this has taking cramping to "almost zero". You can coast parts of the swim by drafting, and even on the run, one can vary the effort at redline (depeding on race distance) or just below. Even at 10K pace, I might do some sections at 3:40 pace and then drop it to 3:45-3:50 pace for just 50 meters, which really can help some recovery take place. For the same reason, I also find a mildly rolling course faster than a completely flat course. There is no place to rest on the flat course unless one takes coasting breaks.

Personally, I think that our brains cannot concentrate continuously at high intensity (I could not even do it for 3 hours in engineering school during exams doing Fourier Transforms which involves no physcial component) and cramping is just the body trying to preserve itself after the brain starts getting tired sending signals to do the same difficult thing. Yeah, salt, heat and hydration all play into it, but I think "continously concentrating at red line" and not coasting is something new that happens exclusively on race day.

As such, I feel that racing frequently, or in the void of racing, doing weekly Time Trials are important to help one figure out how to throttle being above and below the redline in whatever sport and avoid cramping.

One a side note, I have never heard of anyone complain of cramping in swimming aside from in the calves. I have managed to eliminate that completely by doing a warmup run to get the calves going, so that i am not sprinting off the beach, diving in the water after doing some dolphin kicks and then cramping in the calves 2 min later, when all my blood is sucked up to my upper body.
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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"This study sounds like homeopathy."
Perhaps, but interestingly, in infants, sucrose given by mouth gives pain relief. This occurs almost instantly and the effect is blocked by Naloxone.
This would suggest that there is an endorphin response. Before the use of local anestesia for circumcision became more routine, we used to give sucrose with water in a bottle during the procedure and the crying was reduced by well over 90%. We started doing this when a study in the 80s showed such an effect and it worked as advertised.

Many endurance athletes report almost instant relief of bonking with Coca Cola, at least the old fashioned sucrose variety. This happens awfully fast to be explained by the rise in blood sugar, which takes a number of minutes. Is this the same type of thing.

Lastly, if I recall, one of the effects of caffeine is decreased 'perceived' effort. While this might be part of the systemic effect, caffeine certainly has lots of CNS effects.


_________________
Dick

Take everything I say with a grain of salt. I know nothing.
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Re: Tim Noakes: we need you back for a moment [big slow mover] [ In reply to ]
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so I don't "freak out" anymore if I can't train for one or two days. You can say you have to train doing nothing as well.

You know what they say when the really good coaches look at most people's training - the hard days were not hard enough and the easy days were not easy enough! :)


Steve Fleck @stevefleck | Blog
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Re: Tim Noakes: we need you back for a moment [docfuel] [ In reply to ]
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In Reply To:
"This study sounds like homeopathy."
Perhaps, but interestingly, in infants, sucrose given by mouth gives pain relief. This occurs almost instantly and the effect is blocked by Naloxone.
This would suggest that there is an endorphin response. Before the use of local anestesia for circumcision became more routine, we used to give sucrose with water in a bottle during the procedure and the crying was reduced by well over 90%. We started doing this when a study in the 80s showed such an effect and it worked as advertised.

Many endurance athletes report almost instant relief of bonking with Coca Cola, at least the old fashioned sucrose variety. This happens awfully fast to be explained by the rise in blood sugar, which takes a number of minutes. Is this the same type of thing.

Lastly, if I recall, one of the effects of caffeine is decreased 'perceived' effort. While this might be part of the systemic effect, caffeine certainly has lots of CNS effects.
I don't doubt that there are a whole host of effects that are poorly understood and might have real effect especially on psychological perceptions. There is no doubt the brain and our mental state can affect performance and perceptions (I once "cured" a severe and long-lasting spinal headache using hypnosis - the headache was gone when the patient came out of the trance). But, to claim that the nervous system somehow can affect physiological maximums really requires some sort of reasonable theoretical mechanism or incontrovertible evidence that it exists (where the mechanism would remain a mystery) before I can accept it. Neither of those are currently available

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
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Furthermore wrt cramping, I really think that the culprit is "reduced rest interval" on race day.

30 years of endurance sports and I never cramped up except once( read on) in training or racing. Maybe I have been lucky. Maybe my metabolism/physiology has been well suited to this. For almost all of those years, I never gave a thought to salt supplementation. The only nod to it was that in Ironman races I would try and get a bottle of Gatorade in me every hour or so on the bike - that was about it.

The cramping incident happened in a bike road race, on a cool day I might add, two years ago. It was a 70 K race and I was a bit over matched in this race, but as you need to do when road racing, do EVERYTHING you can to stay with the front group. This meant repeated surges at max effort. There was also 10 minute stretch where I was away in a mini-break with two other guys and we were going full gas for much of this. We were unfortunatly caught and it came down to a bunch sprint for the win. I knew that I had little hope, but was prepared to have a go at it. Just as I was about to make my final jump with about 300m to go, I got out of my saddle and started to hammer - both my calves simultaneously cramped up. I had to back off at that point and just do what I could do to make it across the line. Race lasted about 2 hours and I was well hydrated throughout. I can only surmise that the cramping was the result of not really being ready for that type of riding and repeated on/off effort that you see in a bike road race.


Steve Fleck @stevefleck | Blog
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Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
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JJ,


I don't change my diet or over hydrate, over salt in the lead up...the simple fact of reduced volume on Fri and Sat before the race tops things up. I think there is too much "changing of routine" going on for most people and then they are flat and cramping on race day....that's why better to do the "Changing of routine" from 14-11 days out and then get back into it.

Good point. I never change my standard diet substantially, and at best will try to keep away from the megga feeds the last couple days. But that doesn't always work and I've had many great races the morning after the unavoidable party that I would face a divorce by missing, just by laying off the alcohol, but in many cases eating far more than I normally would pre race night.

Furthermore wrt cramping, I really think that the culprit is "reduced rest interval" on race day. Race efforts are continuous at higher than normal intensities. In an Ironman or half Ironman I take every possible opportunity on the bike to tuck and coast to drop my effort to zero watts and let my heart rate recover. I can also do this in XC ski races. I have found that this has taking cramping to "almost zero". You can coast parts of the swim by drafting, and even on the run, one can vary the effort at redline (depeding on race distance) or just below. Even at 10K pace, I might do some sections at 3:40 pace and then drop it to 3:45-3:50 pace for just 50 meters, which really can help some recovery take place. For the same reason, I also find a mildly rolling course faster than a completely flat course. There is no place to rest on the flat course unless one takes coasting breaks.

Cramping is still a bit of a mystery to me. Both sides of the argument are right. I know with absolute certainty that dehydration will cause it either during or post race. I do all my mid week training at 10:00 at night and learned years ago that I must weigh myself before and after any workout exceeding 45 minutes, and without fail if I do not replace the fluids and get back within a pound or two of pre workout weight, I WILL get an attack of cramps out of a dead sleep at 2-3:00 in the morning. Yet the last 2 nights doing 25 & 10 mile rides on the trainer at moderate at best intensity, I was getting twinges of calf cramps by the first few miles where neither hydration nor intensity was a problem. I never get cramps running unless I'm coming off the bike, or running long enough to get dehydrated, or running beyond my trained distance. My best guess on the recent early "twinges" of early cramp onset on the bike could be explained because I shipped my TT bike to Richmond and trained this week with the old Cdale on the trainer but prior to 1 1/2 weeks ago the Cdale lived on the trainer and I only used the Softride on weekends and just put it on the trainer to get a bit more time on it for about a week or so.



Personally, I think that our brains cannot concentrate continuously at high intensity (I could not even do it for 3 hours in engineering school during exams doing Fourier Transforms which involves no physcial component) and cramping is just the body trying to preserve itself after the brain starts getting tired sending signals to do the same difficult thing. Yeah, salt, heat and hydration all play into it, but I think "continously concentrating at red line" and not coasting is something new that happens exclusively on race day.

I've come to look at cramping as a formulation of events & bio conditions where different levels of the contributing conditions can all cause it. It's possible this could be one of the contributors but it would be a hard one to differentiate.

As such, I feel that racing frequently, or in the void of racing, doing weekly Time Trials are important to help one figure out how to throttle being above and below the redline in whatever sport and avoid cramping.

I'm a firm believer in racing your way into shape even if it's a 5K or short running race I'll do it most weekends if there's one available. I find it better than just trying to do TTs or hard running workouts and as long as the races are under an hour I've no problem doing them weekly. My best 1/2M in 7-8 years in early Feb came off a 9-10 week period with 4 1/2M's, a 25K, a 30K, and a 5M race. I only did my standard long run of 12-16 miles on the off weeks where there was no 1/2M or long race that week. The rest of the time was normal training with an eye to backing it down a couple days before and after the longer races.

One a side note, I have never heard of anyone complain of cramping in swimming aside from in the calves. I have managed to eliminate that completely by doing a warmup run to get the calves going, so that i am not sprinting off the beach, diving in the water after doing some dolphin kicks and then cramping in the calves 2 min later, when all my blood is sucked up to my upper body.

When I was attempting to learn to swim last year, calf cramps were always the limiter that told me it was time to call it a day. (at every workout)


JJ

Every night that I run, the thought crosses my mind that there's no way in hell I'll still be running a month from now.
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Re: Tim Noakes: we need you back for a moment [daveinmammoth] [ In reply to ]
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Dave,
I appreciated your post and got a good chuckle .... probably one of those doc chuckles that you can only appreciate when you do this stuff all day long!

1) Docs working the finish line are idiots ... we do it for free and even provide our own malpractice coverage because we do it so the competitors don't all have to be sent to an ER and get a $2000 bill for services. I'm still fine with that and glad to do it when I can. All of those who are really ill are much appreciative.
2) I think we can do a fair job at judging fluid status ... for many of us its what we do all the time anyway.
3) I think I can recall what a tilt test is ... but I've never used it ;-) ... most of the people I see at IM can't stand up anyway so the orthostatic thingy becomes sort of moot. Most are hypotensive flat on their backs.
5) LOL with you .... its always amazing how incredibly smart we suddenly become when somebody really ill crashes and needs some real skill applied.

Frank ... I don't think you'd ever be the medical director at one of these events ... I just doubt it :-)

Duncan .... glad you got up from your crash at the finish. You did have medical care .... it was called UK socialized medicine ... and what you recieved is what everyone gets under those circumstances. Lucky there wasn't much wrong with you ... and what you had is fairly common.

Dave
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Re: Tim Noakes: we need you back for a moment [Fleck] [ In reply to ]
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Are you suggesting that cramping could be due to overdoing it on race day? Racing beyond your fitness level? Or doing things in races that we don't do in training???

BLASPHEMY!!!! Its gotta be some mysterious (or common) electrolyte/mineral that some of us need on some days in some races.....ask any lay person off the street and they'll tell you to eat more bananas or in this thread - drink more milk....

I read the ST rule book and it clearly states that all racing problems can be attributed to:

1) Nutrition and/or
2) Electrolytes

Please fix your post so you don't confuse everybody.

David
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Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
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"I have never heard of anyone complain of cramping in swimming aside from in the calves."

I commonly cramp in the feet while swimming.. and have had quad cramps as well. However this is typically associated with going too hard trying to keep up with real swimmers in the Master's sessions; or in cold water; when undertrained. This fits perfectly with the new cramp theory of muscle fatigue and spinal reflex, outlined by Dr Noakes' graduates at
http://www.sportsscientists.com/...-cramp-part-iii.html
But that theory is not convincing when it comes to Monty and skid's experience..
Last edited by: doug in co: Apr 24, 09 8:09
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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While not available, it is certainly plausible that the brain monitors various parameters to keep us from killing ourselves.
(Are there other species that will willingly subject themselves to extremes of physical performance just for the hell of it.)

_________________
Dick

Take everything I say with a grain of salt. I know nothing.
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Re: Tim Noakes: we need you back for a moment [daveinmammoth] [ In reply to ]
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Are you suggesting that cramping could be due to overdoing it on race day? Racing beyond your fitness level? Or doing things in races that we don't do in training???

BLASPHEMY!!!! Its gotta be some mysterious (or common) electrolyte/mineral that some of us need on some days in some races.....ask any lay person off the street and they'll tell you to eat more bananas or in this thread - drink more milk....

I read the ST rule book and it clearly states that all racing problems can be attributed to:

1) Nutrition and/or
2) Electrolytes

Please fix your post so you don't confuse everybody.


Dave,

Brilliant. LOL :)

I was under no illusions on what had happened - I knew that the cuprit was - that I was not ready for that type of race. I needed to train more and I needed to do more specific kind of training so that I would be ready for those demands.


Steve Fleck @stevefleck | Blog
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Re: Tim Noakes: we need you back for a moment [Fleck] [ In reply to ]
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"...I was under no illusions on what had happened - I knew that the cuprit was - that I was not ready for that type of race. I needed to train more and I needed to do more specific kind of training so that I would be ready for those demands..."

Come on Fleck...you're really shitting us now. Clearly without a powermeter to provide quantitative feedback, you have no clue whether you were at or exceeding your fitness on that day. The cramps could have been due to the alignment of the moon and the sun. Without a powertap, you have no proof. Now go raise your FTP by 20W :-) :-) :-)
Dev
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Re: Tim Noakes: we need you back for a moment [doug in co] [ In reply to ]
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In Reply To:
"I have never heard of anyone complain of cramping in swimming aside from in the calves."

I commonly cramp in the feet while swimming.. and have had quad cramps as well. However this is typically associated with going too hard trying to keep up with real swimmers in the Master's sessions; or in cold water; when undertrained. This fits perfectly with the new cramp theory of muscle fatigue and spinal reflex, outlined by Dr Noakes' graduates at
http://www.sportsscientists.com/...-cramp-part-iii.html
But that theory is not convincing when it comes to Monty and skid's experience..
A theory doesn't have to explain every instance of a phenomenon if a phenomenon can have more than one cause. It only need explain those that fall under its pervue.

Cramps seem to me to be some sort of discoordinated contraction. When I get cramps in bed in my calves or feet I am continually surprised as to how the muscle that is so painful seems to be hardly contracted at all. It certainly isn't a rock hard muscle. A "few" fibers gone haywire sure can get your attention. There is something about a cramp that is completely outside the normal muscle contraction regime. This explanation makes as much sense, if not more, than anything else I have heard.

I wouldn't be surprised if electrolyte abnormalities might make one more susceptible to cramps, but it doesn't seem they could be the only problem.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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Sorry Frank - all those physical exam tests are relatively useless IMHO. You were likely taught physical exam skills/tests in an era/at a school that was very dogmatic. "This % blood loss causes this....". "You do orthostatics if you think the pt is dehydrated and they mean this...". These rules were passed down from generation of clinicians to generation of clinicians. Well, if you actually do studies - and test these "rules" or the dogma of medicine that has been passed from doc to doc - you find that they are wrong in many cases/lack sensitivity and specificity. Here are some examples - Homan's test for DVT = useless, Meniscal tests = useless, orthostatics = useless. You need to look carefully at the sensitivity and specificity of the tests (or positive predictive/negative predictive value) and the setting of the diagnosis you are looking for. Are you screening 100 IM finishers for 10 that are dehydrated? Are you screening thousands for the few with cancer?

Weight is great - but you rarely know a good pre-weight - and I specifically excluded it as its the only useful way to know how dehydrated someone is at the finish line (and even then it has problems). Skin turgor? Almost everyone over 60 has poor skin turgor and almost nobody under 40 does (unless they have cholera and are near death). Cap refill is full of false (+)'s and (-)'s as is orthostatics. I know of no connection with temp. Respiratory changes with HR???? Show me someone who can do that on physical exam - all finish line athletes will have high heart rates with little resp. variation I'd guess. JVP - VERY hard to get a group to agree on any measurement for that one. Dry mucus membranes - isn't everybody's mouth dry at the end of an IM? Moist or dried sweat - depends on the temp/how they finished the race/how long after the race they come to the tent/.....don't see much help there.

UA - I'd assume everyone's would be >1.030 - or at least most people who want an IV. Plus we are talking physical exam not lab. I doubt its available at the finish line....plus if they can give you a urine sample - they aren't that dehydrated probably.....

Hct - some people run 40 - some run 52 - can be useful if you know the pre-race value. Plus its a lab test and not applicable to our discussion.

History - can be useful in some cases but if they haven't pee'd in 6-10 hours does than mean they are 5% down or 10%+???? They'll also lie to get an IV.

Lucid? If the guy/gal is altered - different ball game and unlikely to be solely due to dehydration in this setting. I'd boot that one ASAP to the ER.

Back to my original point: I think its VERY difficult to tell on physical exam who is signifcantly dehydrated and who is mildy dehydrated.


David
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Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
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Clearly without a powermeter to provide quantitative feedback, you have no clue whether you were at or exceeding your fitness on that day. The cramps could have been due to the alignment of the moon and the sun. Without a powertap, you have no proof.

LOL

In bike road racing when the big break goes or the big acceleration comes, it does not matter what the Powermeter says or the heart rate monitor reads. You have one simple and clear goal - do EVERYTHING you can to stay in the group. I like road racing for it's clarity in this regard. If you don't make the break, your day is done!!

I actually looked at the cramps as a reward for hanging on till the end of that race. I knew I would never win a field sprint, but I had a reat time!


Steve Fleck @stevefleck | Blog
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Re: Tim Noakes: we need you back for a moment [docfuel] [ In reply to ]
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In Reply To:
While not available, it is certainly plausible that the brain monitors various parameters to keep us from killing ourselves.
(Are there other species that will willingly subject themselves to extremes of physical performance just for the hell of it.)
Maybe God watches over each of us and keeps us from exercising too much. Look at all the athletes who thank God as they cross the line (presumably for keeping them from killing themselves during their extraordinary effort). Seems like pretty good evidence right there. Just as plausible don't you think. Just don't ask me to tell you how he intervenes (or why) or to prove it.

There are much simpler explanations that don't involve the brain and involve known physiological principles.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [daveinmammoth] [ In reply to ]
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In Reply To:
Sorry Frank - all those physical exam tests are relatively useless IMHO. You were likely taught physical exam skills/tests in an era/at a school that was very dogmatic. "This % blood loss causes this....". "You do orthostatics if you think the pt is dehydrated and they mean this...". These rules were passed down from generation of clinicians to generation of clinicians. Well, if you actually do studies - and test these "rules" or the dogma of medicine that has been passed from doc to doc - you find that they are wrong in many cases/lack sensitivity and specificity. Here are some examples - Homan's test for DVT = useless, Meniscal tests = useless, orthostatics = useless. You need to look carefully at the sensitivity and specificity of the tests (or positive predictive/negative predictive value) and the setting of the diagnosis you are looking for. Are you screening 100 IM finishers for 10 that are dehydrated? Are you screening thousands for the few with cancer?

Weight is great - but you rarely know a good pre-weight - and I specifically excluded it as its the only useful way to know how dehydrated someone is at the finish line (and even then it has problems). Skin turgor? Almost everyone over 60 has poor skin turgor and almost nobody under 40 does (unless they have cholera and are near death). Cap refill is full of false (+)'s and (-)'s as is orthostatics. I know of no connection with temp. Respiratory changes with HR???? Show me someone who can do that on physical exam - all finish line athletes will have high heart rates with little resp. variation I'd guess. JVP - VERY hard to get a group to agree on any measurement for that one. Dry mucus membranes - isn't everybody's mouth dry at the end of an IM? Moist or dried sweat - depends on the temp/how they finished the race/how long after the race they come to the tent/.....don't see much help there.

UA - I'd assume everyone's would be >1.030 - or at least most people who want an IV. Plus we are talking physical exam not lab. I doubt its available at the finish line....plus if they can give you a urine sample - they aren't that dehydrated probably.....

Hct - some people run 40 - some run 52 - can be useful if you know the pre-race value. Plus its a lab test and not applicable to our discussion.

History - can be useful in some cases but if they haven't pee'd in 6-10 hours does than mean they are 5% down or 10%+???? They'll also lie to get an IV.

Lucid? If the guy/gal is altered - different ball game and unlikely to be solely due to dehydration in this setting. I'd boot that one ASAP to the ER.

Back to my original point: I think its VERY difficult to tell on physical exam who is signifcantly dehydrated and who is mildy dehydrated.


David
Actually, I wasn't taught those in school at all. If I was, I forgot them. I learned them during anesthesiology training. I learned them because we used them almost every day. These "tricks" are a way of quickly assessing the fluid status of a patient to determine how to best safely proceed. Is the patient safe for the procedure and chosen anesthetic technique or does one need to delay things to rehydrate or place additional monitors, central lines, etc. Most anesthesiologists are pretty good at it and, while not perfect, I would say we "guess" pretty close to correct about 98% of the time.

Everything must be put into perspective. Is there pain? Is the problem acute or chronic? Is the patient old or young? What is the condition that brings the patient to you? It is not some dogmatic rule passed down by old fogey's but useful clinical evaluation tools to help the clinician do his job well. But, they require skill and experience to be applied well. Without them, the choice for the clinician is to either "guess" or to monitor everyone to the max, increasing risk and delay.

Every test, be it a physical exam "test" or a laboratory test or an xray has the ability to have false positives and false negatives. That is part of the job of the clinician, to learn how to interpret those tests. Some clinicians do it extremely well, some don't. Most are pretty good (edit: at least with the stuff they use regularly).

Earlier I was told there was no reason to ever do an orthostatic blood pressure test because most of the people were hypotensive flat on their back. I am not sure what he means but I know many people whose normal BP is 85-90/55-60. Where others have normal BP's in the 140/90 range. I simply don't know how to interpret on the basis of a single reading whether a bp of 90/60 is completely normal in person A or is substantially hypotensive in person B. I guess if there are enough other signs to suggest one thing or another then maybe I wouldn't sit them up and repeat the BP (It doesn't take much time, all I look at in this situation is when the needle starts bouncing, no need to take the entire pressure, although I can get diastolic without using a stethascope in most instances also) but one reading in isolation doesn't mean much to me.

Temperature per se has no direct correlation with fluid status but I would be extra observant of someone in whome their initial temperature was 103-104. I would want to make sure it was going down, not up. And, it might determine how aggressive I was in treatment.

Your criticism of my comments suggest to me you simply do not have much experience in using these tests. You say, I would expect this or that. Well, so would I. Anything different from what I expected would give me pause. That is the whole idea of doing an exam, to confirm or refute your initial clinical assessment.

I personally think it is pretty easy to tell on physical exam who is significantly dehydrated and who is not. That was part of my job in the operating room and I tried to teach medical students and residents how to do it also. Nobody is ever 100%. That doesn't mean we can't be very good. I don't see how it is much different just because the venue moves to a finish line.

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Frank,
An original Ironman and the Inventor of PowerCranks
Last edited by: Frank Day: Apr 24, 09 9:29
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Re: Tim Noakes: we need you back for a moment [Fleck] [ In reply to ]
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Furthermore wrt cramping, I really think that the culprit is "reduced rest interval" on race day.

30 years of endurance sports and I never cramped up

Maybe that's why you didn't break 9:00...

:-)

----------------------------------
"Go yell at an M&M"
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Re: Tim Noakes: we need you back for a moment [docfuel] [ In reply to ]
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You are correct. These authors (and others studying US soldiers performing similar studies during World War 2) noted that the psychological effects of not drinking were much greater than the physiological effects but that recovery was very rapid when "dehydrated" subjects were given fluids to drink by mouth (note - not intravenously). The results are reported in the monograph by Adolph published in 1947.
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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Maybe it's God and maybe it's just our brainstem overriding our cortex. ("cortex you may be smarter, but we primitives down here in the brainstem and midbrain have final control.")

_________________
Dick

Take everything I say with a grain of salt. I know nothing.
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Re: Tim Noakes: we need you back for a moment [docfuel] [ In reply to ]
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Maybe it's God and maybe it's just our brainstem overriding our cortex. ("cortex you may be smarter, but we primitives down here in the brainstem and midbrain have final control.")
Perhaps. All I asked for was a mechanism to explain how it would work.

It is clear that a lot of the evidence that is being used to support this governor theory is simply showing that the mind can have effects of submaximal efforts. I actually believe that without needing to see any studies in support. If someone claimed otherwise I would ask to see their study data. However, the theory here is the brain is regulating the maximum effort. I see no evidence to support that theory and no one can give me a mechanism as to how it might work. That is all.

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Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [big slow mover] [ In reply to ]
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Study of modern hunts by the !Kung San hunters in the Kalahari Desert in the last decade especially by my South African college Dr Louis Liebenberg show that the factor which determines the duration of the hunt is the time for which it it really hot. Thus a modern hunter will only run down a large antelope (Eland or Kudu) if he has 4-6 hours of extreme heat (40-46 degrees C/104-114 degrees F) in which to do it. So the hunt will begin at midday (when it is starting to get really hot). Once it cools down in the late afternoon (4-6pm), the antelope will be able to cool down and will not be caught (since it is the high body temperature of the antelope which causes it to become essentially paralyzed and then possible to be speared at close range with no risk to the hunter).

Most of these hunts cover less than 30km. So perhaps it is the length of the midday heat that has something to do with the exercise duration for which we might be particularly well adapted.
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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@dr. noakes -- could you comment on fleck's point about cramping during races, which seem to be a result of effort and not dehydration? i've had similar experiences in road races where dehydraton doesn't seem to be the culprit.
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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Study of modern hunts by the !Kung San hunters in the Kalahari Desert in the last decade especially by my South African college Dr Louis Liebenberg show that the factor which determines the duration of the hunt is the time for which it it really hot. Thus a modern hunter will only run down a large antelope (Eland or Kudu) if he has 4-6 hours of extreme heat (40-46 degrees C/104-114 degrees F) in which to do it. So the hunt will begin at midday (when it is starting to get really hot). Once it cools down in the late afternoon (4-6pm), the antelope will be able to cool down and will not be caught (since it is the high body temperature of the antelope which causes it to become essentially paralyzed and then possible to be speared at close range with no risk to the hunter).

Most of these hunts cover less than 30km. So perhaps it is the length of the midday heat that has something to do with the exercise duration for which we might be particularly well adapted.
An interesting observation. It would seem that is really doesn't make much difference how one is specifically adapted as long as one is better adapted to their prey for certain conditions. I would assume it was a trial and error effort that allowed these tribesman to figure out what their prey should be and how to hunt to take advantage of their advantage. If we had slightly different water/salt conserving mechanisms I presume those tribesmen would be hunting different prey or hunting this prey in a different manner.

Interesting. Thanks for that.

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Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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Thanks for confirming that. All these things would suggest that the brain's anticipation of replenishment or sensation in the mouth of same, is enough for it to allow us to proceed (to try to kill ourselves.)

_________________
Dick

Take everything I say with a grain of salt. I know nothing.
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Re: Tim Noakes: we need you back for a moment [Carl Spackler] [ In reply to ]
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To take it a step further, I can have cramping on a very short high intensity set of step ups, lunges, calf raises, hamstring curls, or squats...and all of these have nothing to do with hydration or electrolytes.

For me, the higher the intenisty, the higher likelihood of cramps.

If the duration is really short, I need really high intensity to bring about cramps. If the duration is long (ex Ironman), then the intensity can be reasonably low.....seems like cramps are proportional to the intensity-duration product if you want to map it on a 2 d grid. Then I suppose you can make it a 3-D model by adding in hydration and then making 4-D by going with blood sodium level.

Now someone go and do the 2nd derivative of each 3-D surface on the 4-D space to show us where cramping is about to happen :-). While we're at it, program that into the powertap to warn us 2 minutes before aforementioned cramps that they are about to happen.

Seriously though, I think the entire discussion has been great, but cramping has to be related to a combination of intensity, duration, electrolytes and hydration, cause we all know from real life that they occur when a combination of these factors are present.

Dev
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Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
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Seriously though, I think the entire discussion has been great, but cramping has to be related to a combination of intensity, duration, electrolytes and hydration, cause we all know from real life that they occur when a combination of these factors are present.

Dev
They probably are also associated with your genetic make-up and predispositions. Finding a "one-size-fits-all" solution to this problem, I suspect, isn't going to happen.

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Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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As I think about this an interesting area to research might be to do a genetic comparison between athletes who have a lot of cramping problems and those who don't. Perhaps one could find some markers that show who is susceptible and then determine how those differences are reflected in the body which might give those who are susceptible better strategies for avoiding same.

I don't know who would pay for such a study but it would be interesting if it could be done.

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Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Just Old] [ In reply to ]
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Maybe that's why you didn't break 9:00...

Ken,

That's it!! :)




Steve Fleck @stevefleck | Blog
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Re: Tim Noakes: we need you back for a moment [triguy42] [ In reply to ]
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This industry-funded study was conducted in a laboratory that did not have proper convective cooling (wind speed). When we repeated the study in our laboratory which has a properly designed wind tunnel to insure that cyclists working hard in the heat did at least get the benefit of a decent facing wind speed as occurs in real world exercise, there was no difference in the rectal temperature of those who drank either the equivalent of "ad libitum" or "as much as possible" (A.Sanders et al. Acta Physiol Scand 2005). Thus the higher temperature in the "dehydrated" state was simply an adaptation that the body made to try to increase its heat heat loss without the need to sweat more when the environmental conditions in which the study was undertaken were sub-optimal.

This is a well-known phenomenon in free-living desert animals. The best way to regulate your body temperature at rest or during exercise is to allow your body temperature to rise. This is a water-conserving mechanism. The best example is the desert dwelling Oryx which allows its body temperature to rise to 46 degrees C when it has no access to water. When water is available, it will maintain a lower body temperature by sweating (until such time as it no longer has access to fluid). Similarly during exercise the African hunting dog maintains a higher body temperature than domesticated dogs. This allows the wild dog to run further with less water loss even though they are hotter. The African hunting dog has the highest hunting success rate of any African predator. Seems like running with a higher body temperature might be quite a good choice and not a sign that the animal is about to die from heat stroke.

Of course what the industry never wanted anyone to know about this study was that despite exercising at high intensity for 2 hours in quite extreme heat (33 degrees Centrigrade) with high humidity, none of the subjects became ill because they did not drink at all during the 2 hour exercise bout. Nor did they want you to know that the body temperatures of those who did not drink were not particularly high at the end of exercise (approximately 39 degrees C) compared to values of at least 41 degrees C routinely measured in winners of 10,21 and 42km races who are without symptoms (other than the emotional high of winning a race). Nor did they want you to know that there NO difference in the body temperature responses in the first hour of exercise between those who drank "to replace all their sweat losses" or who drank nothing. Nor did they want you to know that the difference in rectal temperature response between those who drank "ad libitum" and those who drank "to replace all their sweat losses" was about 0.5 degrees C, a biologically insignificance difference.

Nor did they want you to know that this study was designed to develop the highest possible sweat rates during exercise so that these could then be applied to everyone who exercises whether at high or low intensity or in the heat or the cold. This study formed the basis for the 1996 ACSM guidelines which for the first time proposed that athletes needed to drink "as much as tolerable" during exercise or between 600-1200ml per hour. Of course when these guidelines were applied to athletes like Cynthia Lucero running the 2002 Boston Marathon in 5-6 hours in a temperature of 10-12 degrees C, they were totally inappropriate since her sweat rate under those conditions were probably closer to 200-300ml per hour.

So please don't quote this study to me as evidence that dehydration causes heat stroke. This study and the way it was interpreted was the principal cause for the global pandemic of EAH that began shortly after the adoption of the 1996 ACSM guidelines.

Also sweat rate is regulated by the sympathetic nervous system not by cardiovascular system. Thus for the sweat rate to fall during exercise requires a change in the sympathetic supply to the sweat glands. Again why would the brain choose to reduce sweating if this would cause heat stroke to occur knowing that this effect must also kill the brain? Logically the brain would only choose to lower the sweat rate if there was some logic to this choice (as occurs in the Oryx in the desert).
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Re: Tim Noakes: we need you back for a moment [triguy42] [ In reply to ]
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There are new data (in review in the scientific press) showing that weight losses in excess of 3% in marathon runners in real competition are not associated with body temperature elevations in excess of those that would be predicted from their running speed (exercising metabolic rate). Some of these runners reached levels of dehydration of up to 10%.

Events that occur at the same time may not be causally related. To develop a level of dehydration in excess of 3% you have to exercise for longer. The longer you exercise, the more tired you become and the closer to a (non)catastrophic failure. The fact that you enter a "danger zone" when you develop a weight loss of 3% may be simply because that is the duration of exercise at which your brain begins to find another reason why it should slow you down (ie muscle and liver glycogen depletion amongst many other possibilities).

Of course it is much easier to explain the complex phenomenon of fatigue on something that is easy to understand (ie dehydration) especially if that is all you ever read about in threads like this and in the adverts of those industries that benefit most from your believing this simple explanation (and for the cure of which surprisingly they provide the sole cure).
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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Also sweat rate is regulated by the sympathetic nervous system not by cardiovascular system. Thus for the sweat rate to fall during exercise requires a change in the sympathetic supply to the sweat glands. Again why would the brain choose to reduce sweating if this would cause heat stroke to occur knowing that this effect must also kill the brain? Logically the brain would only choose to lower the sweat rate if there was some logic to this choice (as occurs in the Oryx in the desert).
Sweating can be caused by the nervous system but I am unaware that it can be turned off by either the sympathetic or parasympathetic nervous system. Beta blockers, which can stop "nervous sweating", will not stop sweating during exercise.

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Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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The fact that you enter a "danger zone" when you develop a weight loss of 3% may be simply because that is the duration of exercise at which your brain begins to find another reason why it should slow you down (ie muscle and liver glycogen depletion amongst many other possibilities).
Or not.

I suspect this is not a one issue phenomenon.

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Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Fleck] [ In reply to ]
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These data would predict that your wife has adapted to a low habitual salt intake like the Kenyan runners that we studied. What appears in the sweat is the dietary excess that has not been excreted in the urine and has nothing to being a "salty sweater". Salty sweaters are simply salty eaters (and this includes those with the gene for cystic fibrosis. If patients with that condition - which causes higher than normal sweat sodium concentrations - were not eating a high salt diet they would very rapidly die from salt deficiency). The reason why the scientists supported by the sports drink industry have yet to discover this surprising truth is because they seem not to understand that if you wish to study sodium balance in humans you cannot do so simply by measuring the salt content of sweat. You need to analyze urinary losses and habitual dietary intakes as well.

So when you see reports of "salty sweaters" (apparently the sweat of Tiger Woods and Maria Sharapova amongst many other stellar athletes has also been tested to determine whether or not they are "salty sweaters") just ask what was their urinary sodium losses and their dietary sodium intakes before concluding that they are "salty sweaters".
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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Dr Noakes, thank you very much for your contributions.

Can you offer any insight into 'night cramps'? Those brutally painful calf cramps that wake you up from a dead sleep. Or the dreaded 'just woke up - yawning - stretching - calf cramp' that has been severe enough to cause me to limp for hours.

Thanks

______________________________________
"Competetive sport begins where healthy sport ends"
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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Of course not because beta-blockers do not block the specific sympathetic nervous system messenger (acetylcholine) that causes sweating.

I found this at http://www.diagnose-me.com/cond/C511064.html

"Two different sets of nerves supply these many glands: the sympathetic nerves, which tend to increase sweating when one is excited, nervous, or afraid (the "fight or flight response"), and the parasympathetic nerves, which tend to decrease sweating of the skin. At the ends of these nerves, the body releases special chemicals called neurotransmitters, which carry the electrical signal from the nerves onto the cells near the nerve endings. For the sweat glands, the chemical at the tips of the sympathetic nerves is acetylcholine; too much of this chemical present next to the sweat glands stimulates them to produce large amounts of fluid".
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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Of course not because beta-blockers do not block the specific sympathetic nervous system messenger (acetylcholine) that causes sweating.

I found this at http://www.diagnose-me.com/cond/C511064.html

"Two different sets of nerves supply these many glands: the sympathetic nerves, which tend to increase sweating when one is excited, nervous, or afraid (the "fight or flight response"), and the parasympathetic nerves, which tend to decrease sweating of the skin. At the ends of these nerves, the body releases special chemicals called neurotransmitters, which carry the electrical signal from the nerves onto the cells near the nerve endings. For the sweat glands, the chemical at the tips of the sympathetic nerves is acetylcholine; too much of this chemical present next to the sweat glands stimulates them to produce large amounts of fluid".
Well, I am unaware that sweating is fully dependent upon an intact sympathetic nervous system. Sweating is induced to collect seat for sampling to diagnose systic fibrosis not by stimulating the sympathetic nerves but by simply heating a small area of the skin to induce blood flow to that small area, which causes sweat that can be collected.

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Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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This industry-funded study was conducted in a laboratory that did not have proper convective cooling (wind speed). When we repeated the study in our laboratory which has a properly designed wind tunnel to insure that cyclists working hard in the heat did at least get the benefit of a decent facing wind speed as occurs in real world exercise, there was no difference in the rectal temperature of those who drank either the equivalent of "ad libitum" or "as much as possible" (A.Sanders et al. Acta Physiol Scand 2005). Thus the higher temperature in the "dehydrated" state was simply an adaptation that the body made to try to increase its heat heat loss without the need to sweat more when the environmental conditions in which the study was undertaken were sub-optimal.

<snip>

Of course what the industry never wanted anyone to know about this study was that despite exercising at high intensity for 2 hours in quite extreme heat (33 degrees Centrigrade) with high humidity, none of the subjects became ill because they did not drink at all during the 2 hour exercise bout. Nor did they want you to know that the body temperatures of those who did not drink were not particularly high at the end of exercise (approximately 39 degrees C) compared to values of at least 41 degrees C routinely measured in winners of 10,21 and 42km races who are without symptoms (other than the emotional high of winning a race). Nor did they want you to know that there NO difference in the body temperature responses in the first hour of exercise between those who drank "to replace all their sweat losses" or who drank nothing. Nor did they want you to know that the difference in rectal temperature response between those who drank "ad libitum" and those who drank "to replace all their sweat losses" was about 0.5 degrees C, a biologically insignificance difference.

<snip>

Also sweat rate is regulated by the sympathetic nervous system not by cardiovascular system. Thus for the sweat rate to fall during exercise requires a change in the sympathetic supply to the sweat glands. Again why would the brain choose to reduce sweating if this would cause heat stroke to occur knowing that this effect must also kill the brain? Logically the brain would only choose to lower the sweat rate if there was some logic to this choice (as occurs in the Oryx in the desert).

First off I can't find the Sanders article in Acta Physiologica Scandinavica anywhere printed in 2005...but found it under "Saunders" finally:
http://www3.interscience.wiley.com/...l/118680040/abstract
"On five occasions nine subjects cycled for 2 h at 33.0 ± 0.4 °C with a relative humidity of 59 ± 3%. Air velocity was maintained at 0.2 km h&#8722;1 (0 WS), 9.9 ± 0.3 km h&#8722;1 (10 WS), 33.3 ±2.2 km h&#8722;1 (100 WS) and 50.1 ± 3.2 km h&#8722;1 (150 WS) while subjects replaced 58.8 ± 6.8% of sweat losses. In the fifth condition, air velocity was maintained at 33.7 ± 2.2 km h&#8722;1 and subjects replaced 80.0 ± 6.8% of sweat losses (100.80 WS)."

Okay, so you replicated the test using a windtunnel that provides substantial convective cooling...and concluded that except at low velocities (0, 10km/h) body temperature was consistently regulated. At 20 and 30mph I would expect this to be the case when the ambient temperature was 33C (91.4F) and less than core temperature...i.e. providing a substantial cooling effect through convection as mentioned in the results. At running speeds (10km/hr) shockingly body temp and PE was higher...big surprise. Maybe you can enlighten us as to the total percent of dehydration of the subjects in the 58.8% replacement...since it isn't specified in the abstract. For instance, at 1.9L/hr sweat rate if I replaced 1.1L/hr after 2 hours I would not be significantly dehydrated, having lost only about 3.4lb bodyweight (2.1%) and would not have any noticeable symptoms of dehydration. At the moment I would have to say your study is interesting and useful but ultimately does not contradict the earlier study. What this study shows is that subjects with mild dehydration and high windspeed fared the same as subjects with very little dehydration and high windspeed...and those with mild dehydration and low windspeed (running) were significantly higher in temperature. I could have guessed those results without the test, but having actual numbers on the effects is always good.

BTW-extreme heat 33C/91F? I run in that temperature every day in the summer! Smile

Actually I did think of one other possible reason that I have issues with high temperatures and excersizing...my normal resting body temperature is marginally higher than normal at 99.4F/37.4C...I wonder if this could have something to do with it. Maybe I am 1F closer to overheating than the normal person...?

My take on the change in sweat rate is that the mind is simulataneously shutting down the body's ability to excersize at high intensity while slowing down (or nearly stopping) the sweat rate in order to conserve water. This sounds exactly like what happens with the Oryx and seems entirely logical. Not great if you are being chased by a lion, but as a self-protection mechanism in extreme conditions it seems reasonable.

http://www3.interscience.wiley.com/...RETRY=1&SRETRY=0
"Consequently, average mean power output during the five sprints was lower in hyperthermia (558.0 ± 146.9 W) compared with control (617.5 ± 122.6 W; P < 0.05)."
As evidence of the above...power output drops when overheated. As you (or someone else) mentioned earlier, it may be possible to train this response, but looking at my training logs over the past years I have consistently gone 30-40s slower per mile in the summer heat (Floriduh sauna-like humidity) compared to winter (60F and 30-40% humidity). When I first started seriously running down here the summers were just brutal and I had to run in the early mornings and be done well before noon or I was toast. After a couple years of acclimatizing I can run noon-3pm in the mid 90s and 85% humidity without problems...as long as I am drinking enough water.


Mad
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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Also sweat rate is regulated by the sympathetic nervous system not by cardiovascular system. Thus for the sweat rate to fall during exercise requires a change in the sympathetic supply to the sweat glands. Again why would the brain choose to reduce sweating if this would cause heat stroke to occur knowing that this effect must also kill the brain? Logically the brain would only choose to lower the sweat rate if there was some logic to this choice (as occurs in the Oryx in the desert).
Well, let me hypothesize a reason "why" the brain would choose to stop sweating despite that might mean hyperthermia. It is a matter of choosing the lesser of two bad alternatives. Stopping sweating will raise peripheral vascular resistance in an instance where BP is falling too low to maintain vital functions in the vital organs, the brain and the heart. It would do this to avoid immediate damage and take on the risk of possible later damage. Unfortunately, the conscious control the brain sometimes exerts doesn't always make the body stop doing the activity that caused all the problems in the first place. If the person would stop exercising when the sweating stopped there would probably be little risk of causing heat related damage.

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Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [triguy42] [ In reply to ]
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Maybe you can enlighten us as to the total percent of dehydration of the subjects in the 58.8% replacement...since it isn't specified in the abstract. For instance, at 1.9L/hr sweat rate if I replaced 1.1L/hr after 2 hours I would not be significantly dehydrated, having lost only about 3.4lb bodyweight (2.1%) and would not have any noticeable symptoms of dehydration.
Actually, you will be more down than that because you are forgetting insensible losses, those that occur from the huidification of the inspired air with each breath. This can be substantial depending upon the conditions. No electrolytes are lost this way, this is pure water so it has a smaller impact on the vascular volume than the sweat loss where sodium is lost also. But, it all adds up.

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Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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1. Fast running speed (high metabolic rate) which increases the rate of heat production.

2. High humidity and air temperature.

3. Genetic muscle disorder that may cause an even higher than expected rate of heat production (thermogenesis) and which maintains a high rate of heat production when the athletes has stopped running and for the correction of which the athlete must be placed in ice. If exercise alone was the cause for the excessive heat production then it would not be necessary to cool these athletes in ice AFTER exercise since the moment they stop running, their body temperatures would fall very rapidly (because they have stopped producing the excess heat and because of of a larger than usual gradient between their core temperatures and the air temperature).

4. Presence of some other factor that can activate excessive thermogenesis in the (genetically-predisposed) skeletal muscles. Drug use needs to be considered.

5. Failure of the brain to detect that a body temperature in excess of 41.5 degrees C will be reached before the expected end of the exercise bout. Normally the brain will cause the athlete to slow down and so maintain only that pace that will allow a temperature of 41.5 degrees C to be reached at the finish line.

6. Use of medication especially amphetamines that prevent the normal action of the Central Governor to slow the athlete so that heat stroke cannot occur.

7. Intercurrent illness causing exercise to begin with an elevated body temperature (greater than 38 degrees Centigrade) and to rise excessively during exercise.

8. Some factor interfering with sympathetically-mediated sweating causing impaired sweating and hence impaired heat loss.

To develop heat stroke you need a number of these factors to be acting at the same time.

Our study (Holtzhausen L et al. MSSE 1994) showed that most (~85%) athletes collapse AFTER they finish exercise so that dehydration cannot be a factor (since if dehydration causes collapse as a result of cardiovascular failure then it must happen when the athlete is exercising not when he or she has stopped exercising and the stress on the circulation is falling. Also we know that athletes with heat stroke collapse with high not low cardiac outputs showing that cardiac "failure" does not explain their heat stroke). Rather it is the act of STOPPING EXERCISE that causes these collapses, not the act of continuing exercise. We also showed that these athletes did not have higher body temperatures than the control group of runners who did not collapse after exercise. Thus the athletes were not suffering from "dehydration induced heat illness'. Next we showed that a majority of ultramarathon athletes develop postural hypotension (Holtzhausen L and Noakes T. MSSE 1995) suggesting that the more rapid onset of postural hypotension probably explained why some athletes collapse immediately they terminate exercise. Then we found empirically that treating these athletes by elevating their legs and pelvises above the level of the heart reversed all their symptoms. At the 2000 and 2001 South African Ironman Triathlons at which I was the Medical Director we did not use a single intravenous infusion to treat our collapsed athletes; instead we simply treated all collapsed athletes according to what we diagnosed to be the problem. It they had postural hypotension we simply treated them by elevating their legs and pelvises. In those races we also had the lowest proportion of medical complications in any Ironman yet reported (Sharwood K et al. CJSM 2002; BJSM 2004) and only one case of EAH encephalopathy in an athlete who ignored our advice to drink only to thirst (Noakes et al. BJSM 2004). There was no evidence that this model of treatment delayed the recovery of any of these athletes or that the advice that all athletes should drink to thirst during the competition was harmful to anyone's health.

This model of treatment has since been adopted by the International Medical Marathon Directors Association at all marathons directed by their members. Included in this group is the Berlin Marathon in which aid stations are placed only every 5km on the course (as also in the Rotterdam and Rio de Janiero Marathons). The Rio de Janiero and Berlin Marathon have amongst the lowest rates of medical treatments of any of the large city marathons. Which seems surprising if it is the prevention of "dehydration" that prevents marathon collapses. Rather it seems as if the opposite applies - the more fluid that is provided in marathon races (and perhaps also in triathlons) the greater the percentage of starters that will seek medical care at the finish.

I will discuss in a subsequent post the evidence that the level of hydration during exercise cannot be the explanation for the very high temperatures measured in athletes with heat stroke.
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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Not sure that either of these ladies died. Also their gait is very primitive suggesting that there has been a major change in brain function. My diagnosis is that they have an encephalopathy of unknown cause. What were their rectal temperatures? If elevated above 41.5 degrees C it seems reasonable to suggest that hyperthermia was the cause and the reasons why they might have developed heat stroke are listed in a separate response to you. And what were their blood sodium concentrations? This could also be compatible with the encephalopathy due to EAH. Also how many athletes have completed the Ironman Triathlon without this happening? Which is the more common occurrence - this condition or its absence? If there was no regulator trying to insure that this condition does not occur surely every Ironman triathlete would develop the condition. Thus the presence of such cases suggests the presence of a regulator, not its absence.
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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There are new data (in review in the scientific press) showing that weight losses in excess of 3% in marathon runners in real competition are not associated with body temperature elevations in excess of those that would be predicted from their running speed (exercising metabolic rate). Some of these runners reached levels of dehydration of up to 10%.

Events that occur at the same time may not be causally related. To develop a level of dehydration in excess of 3% you have to exercise for longer. The longer you exercise, the more tired you become and the closer to a (non)catastrophic failure. The fact that you enter a "danger zone" when you develop a weight loss of 3% may be simply because that is the duration of exercise at which your brain begins to find another reason why it should slow you down (ie muscle and liver glycogen depletion amongst many other possibilities).

Of course it is much easier to explain the complex phenomenon of fatigue on something that is easy to understand (ie dehydration) especially if that is all you ever read about in threads like this and in the adverts of those industries that benefit most from your believing this simple explanation (and for the cure of which surprisingly they provide the sole cure).
When it happens consistently regardless of the duration or intensity of training, then I have to conclude that the issue is dehydration. For instance, 2 hours riding in the sauna-like Florida summer heat with little water intake can easily cause me to lose 3% of bodyweight. Likewise running for 1-1.5 hours at 98F/85% humidity can do the same. Neither of these are even remotely close to my endurance limits, having ridden races of 200 miles and run several ultramarathons (and frequently run 6+ hours every weekend during ultra training). I don't disagree that it's a complex phenomenon, but on days of intense heat water loss seems to be the only consistent factor.

For instance, 3 weekends ago it was about 88F and moderate 50% humidity and I ran from about 10am to 4pm. I ran 7.5 mile loops in the forest (swamp) on sandy trails. At about mile 5 into the 3rd loop (~mile 20) I was really hurting and went from running a ~8:30 pace down to having to run/walk at an aggregate 10-11min pace. My running bottle was empty so I couldn't drink any more, and my sweat rate had dropped dramatically. I finally got back to the car and drank about 0.5L of water/Heed mix. Within a few minutes I was sweating again, my "perceived" temp dropped and I could go back to running again. After another 5 miles I started feeling even worse, and shuffle-walked the last 2 miles back to the car (miles 28-30). Based on a couple of studies mentioned in this thread, I would guess the following:

1) The combination of high temp and high humidity caused me to significantly dehydrate. Pre-run I was 162.2lb (about normal), post-run I was 156.8lb, a 3.3% drop. Without the extra 1lb of water I was about 4% down (danger zone for me).
2) The studies showed increased blood glucose and increased sweating immediately after a sugarwater mouth rinse and from drinking water. This is consistent with feeling better immediately after drinking about 1lb of water.
3) As I shed the extra lb of water over the next 30-40 minutes of running I went right back to the non-sweating, overheated, extremely low energy, can't run at all level.
4) The water was pretty hot from being in the car, so no conductive cooling was possible.
5) The weekend before I had run the same course with slightly lower temps (83-85F) and proactively drank 0.25-0.5L of water/Heed mix at the end of each 7.5 mile lap. I finished the last lap at 158.5lb and was overall nearly 30 minutes faster.

So what do I conclude from this? Drink enough water to maintain a maximum body weight loss of about 3lb. I can give plenty of other examples, with power meter files on the bike, etc. There's a definite point where I go from "fine" to "bonk" (200-220W versus struggling to push 175W) and it consistently happens at about 4-5lb weight loss. Not only that, it's a fairly rapid thing, usually within 5-10 minutes I'm fine and then bonking. If I stay within that "safe" range I can ride literally all day at 200W, so it's not a glycogen thing.


Mad
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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Maybe you can enlighten us as to the total percent of dehydration of the subjects in the 58.8% replacement...since it isn't specified in the abstract. For instance, at 1.9L/hr sweat rate if I replaced 1.1L/hr after 2 hours I would not be significantly dehydrated, having lost only about 3.4lb bodyweight (2.1%) and would not have any noticeable symptoms of dehydration.
Actually, you will be more down than that because you are forgetting insensible losses, those that occur from the huidification of the inspired air with each breath. This can be substantial depending upon the conditions. No electrolytes are lost this way, this is pure water so it has a smaller impact on the vascular volume than the sweat loss where sodium is lost also. But, it all adds up.
Well, the sweat rate measurement was before/after excersize while drinking a known volume of water, so you would expect to see the exhaled water be a part of this. No doubt it does matter, even on cold days when you aren't sweating a lot in comparison...


Mad
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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The CGM is best described in a series of 5 articles we wrote in the British Journal of Sports Medicine in 2004/5. There are a number of recent updates many of them published in the BJSM in the last few months. The model predicts that the brain regulates the exercise performance by determining the number of muscle fibers that are recruited in the exercising limbs. It does this to insure that exercise is always regulated to insure that the exercise bout terminates before there has been a catastrophic loss of homeostasis in any bodily system.

To my knowledge it is the only model that can explain why athletes begin exercise at different paces dependent on the duration that they expect to be exercising, and their ability to speed up in the last 10-15 % of most events (the end spurt) including interestingly the 42km marathon. If exercise were regulated by a progressive fatigue that develops in the exercising muscles (and is not influenced by the brain) then all exercise bouts would start at the same intensity and continue at that pace until fatigue began to appear causing a slowing of performance. The body would also not be able to increase the pace at the end of the exercise bout since it is not possible to reverse the (irreversible) muscle fatigue (failure) that had caused the slowing of pace up to that point.

You are welcome to read all our articles which present the other evidence that supports this model. Of course if the brain has no influence on performance, why do athletes ever worry about things like "mental preparation" and "mental coaching"?

If irreversible failure of the muscles is the main cause of fatigue then you cannot flog a dead horse, so to speak, by preparing your mind.
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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Our study currently in press showed that it is not possible for physicians at the end of the race accurately to assess the level of dehydration in athletes.

Sensitivity and specificity of clinical signs for assessment of dehydration in endurance athletes.
McGarvey J, Thompson J, Hanna C, Noakes TD, Stewart J, Speedy D.
Br J Sports Med. 2008 Nov 3. [Epub ahead of print]

If you don't measure the body weight before and after exercise you have no hope of determining how "dehydrated" is the athlete at the finish of the race using the usual clinical measures of "dehydration".
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Re: Tim Noakes: we need you back for a moment [docpeachey] [ In reply to ]
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We no longer promote the use of the term heat illness. If the body temperature is not above 41.5 degrees C or the athlete clearly shows abnormal brain function (not due to EAH) then on what ground is a heat illness being diagnozed?

The condition normally called "heat illness" in athletes who collapse after exercise is usually exercise-associated postural hypotension which as I indicated in another post cannot be due to dehydration. Since the body temperature is not elevated in heat illness, then dehydration cannot be the cause of the appropriately elevated body temperatures in patients with "heat illness".

See: A modern classification of the exercise-related heat illnesses. Noakes TD.
J Sci Med Sport. 2008 Jan;11(1):33-9. Epub 2007 May 23.

Heat stress in sport--fact and fiction. Noakes TD.
J Sci Med Sport. 2008 Jan;11(1):3-5.

Thank you for confirming that medications need to be considered in all cases of heat stroke (see my previous post).
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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1. Fast running speed (high metabolic rate) which increases the rate of heat production.

2. High humidity and air temperature.

3. Genetic muscle disorder that may cause an even higher than expected rate of heat production (thermogenesis) and which maintains a high rate of heat production when the athletes has stopped running and for the correction of which the athlete must be placed in ice. If exercise alone was the cause for the excessive heat production then it would not be necessary to cool these athletes in ice AFTER exercise since the moment they stop running, their body temperatures would fall very rapidly (because they have stopped producing the excess heat and because of of a larger than usual gradient between their core temperatures and the air temperature).

4. Presence of some other factor that can activate excessive thermogenesis in the (genetically-predisposed) skeletal muscles. Drug use needs to be considered.

5. Failure of the brain to detect that a body temperature in excess of 41.5 degrees C will be reached before the expected end of the exercise bout. Normally the brain will cause the athlete to slow down and so maintain only that pace that will allow a temperature of 41.5 degrees C to be reached at the finish line.

6. Use of medication especially amphetamines that prevent the normal action of the Central Governor to slow the athlete so that heat stroke cannot occur.

7. Intercurrent illness causing exercise to begin with an elevated body temperature (greater than 38 degrees Centigrade) and to rise excessively during exercise.

8. Some factor interfering with sympathetically-mediated sweating causing impaired sweating and hence impaired heat loss.

To develop heat stroke you need a number of these factors to be acting at the same time.
I would agree that the development of heat stroke is multifactorial. It is clear that not all these factors need be present and no one factor is on that list is always present. I would add that the "Some factor interfering with sympathetically-mediated sweating causing impaired sweating and hence impaired heat loss" could be severe dehydration.
In Reply To:

Our study (Holtzhausen L et al. MSSE 1994) showed that most (~85%) athletes collapse AFTER they finish exercise so that dehydration cannot be a factor (since if dehydration causes collapse as a result of cardiovascular failure then it must happen when the athlete is exercising not when he or she has stopped exercising and the stress on the circulation is falling. Also we know that athletes with heat stroke collapse with high not low cardiac outputs showing that cardiac "failure" does not explain their heat stroke). Rather it is the act of STOPPING EXERCISE that causes these collapses, not the act of continuing exercise. We also showed that these athletes did not have higher body temperatures than the control group of runners who did not collapse after exercise. Thus the athletes were not suffering from "dehydration induced heat illness'. Next we showed that a majority of ultramarathon athletes develop postural hypotension (Holtzhausen L and Noakes T. MSSE 1995) suggesting that the more rapid onset of postural hypotension probably explained why some athletes collapse immediately they terminate exercise. Then we found empirically that treating these athletes by elevating their legs and pelvises above the level of the heart reversed all their symptoms. At the 2000 and 2001 South African Ironman Triathlons at which I was the Medical Director we did not use a single intravenous infusion to treat our collapsed athletes; instead we simply treated all collapsed athletes according to what we diagnosed to be the problem. It they had postural hypotension we simply treated them by elevating their legs and pelvises. In those races we also had the lowest proportion of medical complications in any Ironman yet reported (Sharwood K et al. CJSM 2002; BJSM 2004) and only one case of EAH encephalopathy in an athlete who ignored our advice to drink only to thirst (Noakes et al. BJSM 2004). There was no evidence that this model of treatment delayed the recovery of any of these athletes or that the advice that all athletes should drink to thirst during the competition was harmful to anyone's health.
I am not sure why you think that collapse after the finish line is evidence against dehydration. Clearly, athletes or others can increase sympathetic tone to maintain adequate cardiac output under stressful conditions and then when the stress is removed and "normal" feedback is returned the person collapses. This happens in war and in athletics.

I don't know that athletes with heat stroke collapse with "high" cardiac outputs. Cardiac failure could mean the inability to provide the demand, whatever the output. There is such a thing as "high output cardiac failure" you know. I mean I would expect them to be high as I would expect the body would be trying to cool itself but if the filling pressures are not high, it seems that the CO would not be as high as the body would like it to be. If the person is not sweating I think one can say the CO, whatever it is, needs to be higher. People with MH would have very high CO's (they are not dehydrated) but I am not so sure of other etiologies and what is meant by "high". Can you point me to a reference?

I am a little confused. You state athletes with heat stroke collapse with high cardiac outputs then you say that athletes who collapse do not have higher temperatures than those who don't. What kind of temperatures are you talking about?

Anyhow, I am glad to see that you have a low incidence of problems in your medical tent. But, we are trying to discuss what the issue is with those who do develop these disorders. Why do they occur and how can they be prevented? Your recommendations seem to work well for EAH. Not so sure for heat related illness.
In Reply To:

This model of treatment has since been adopted by the International Medical Marathon Directors Association at all marathons directed by their members. Included in this group is the Berlin Marathon in which aid stations are placed only every 5km on the course (as also in the Rotterdam and Rio de Janiero Marathons). The Rio de Janiero and Berlin Marathon have amongst the lowest rates of medical treatments of any of the large city marathons. Which seems surprising if it is the prevention of "dehydration" that prevents marathon collapses. Rather it seems as if the opposite applies - the more fluid that is provided in marathon races (and perhaps also in triathlons) the greater the percentage of starters that will seek medical care at the finish.
Can you point me to a reference? Lots of things can result in "marathon collapse". I suspect dehydration is just one of them. It seems as if you are saying that the incidence of problems would go to zero if only the RD would not provide any fluids on the course. Aren't we trying to strike a balance here?
In Reply To:

I will discuss in a subsequent post the evidence that the level of hydration during exercise cannot be the explanation for the very high temperatures measured in athletes with heat stroke.
I will look forward to seeing that. I will state beforehand that not all cases of heat illness are related to hydration state. I look forward to seeing how you show that no cases could be related to hydration state.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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The VO2max test is a brainless test since the experimenter not the athlete sets the work rate. Thus it can never be an appropriate test of the CGM. Please see the following:

Testing for maximum oxygen consumption has produced a brainless model of human exercise performance.
Noakes TD. Br J Sports Med. 2008 Jul;42(7):551-5. Epub 2008 Apr 18.

If you wish to prove or disprove the CGM you must study self-paced exercise. Which does not mean that there is not plenty of evidence that the brain limits the VO2max test. But if you don't study the function of the brain during the VO2max test, how would you ever be able to determine whether or not it is the regulator?
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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The VO2max test is a brainless test since the experimenter not the athlete sets the work rate. Thus it can never be an appropriate test of the CGM. Please see the following:

Testing for maximum oxygen consumption has produced a brainless model of human exercise performance.
Noakes TD. Br J Sports Med. 2008 Jul;42(7):551-5. Epub 2008 Apr 18.

If you wish to prove or disprove the CGM you must study self-paced exercise. Which does not mean that there is not plenty of evidence that the brain limits the VO2max test. But if you don't study the function of the brain during the VO2max test, how would you ever be able to determine whether or not it is the regulator?
Let me get this straight. Are you saying that the brain modulates how hard we exercise (duh?) or that there is an inherent central mechanism that prevents one from exercising too hard, to the point of say, causing a heart attack or something? A governor prevents an engine from going above a certain speed. It does not prevent the engine from doing anything it wants below that certain speed. By self paced exercise are you referring to a 100 m pace or a 100 mile pace?

If one wants to test that there is a maximum limit to the engine then one needs to test that limit. As far as I know the best test of that is the VO2 max test, mindless as it is (if it required thinking it wouldn't be very reproducible). BTW, although the tester sets the work loads, the subject determines when the test is over.

So, could you state in a paragraph or two exactly what your CGM states?

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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Here is what I am getting from reading some of what you have written. Correct me if I am wrong.

You are stating that VO2 max is a brainless test because the effort is set by the tester and when people race the effort is set by the racer. Of course, if we define what the maximum effort the athlete can do is what the athlete actually does then I think we can all agree that there is a central governor. But, where we disagree is whether what the athlete actually does is all the athlete is capable of doing.

The only way to test what the maximum any athlete can do is to test them to exhaustion. The standard for doing that has been the VO2 max test. No one expects the athlete to actually compete at their VO2 max but people do use that value to compute how athletes should compete, especially in this day and age of power meters, when the athlete can actually measure what they are doing.

I don't understand your complaint with this test.

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Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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Not sure that either of these ladies died. Also their gait is very primitive suggesting that there has been a major change in brain function. My diagnosis is that they have an encephalopathy of unknown cause. What were their rectal temperatures? If elevated above 41.5 degrees C it seems reasonable to suggest that hyperthermia was the cause and the reasons why they might have developed heat stroke are listed in a separate response to you. And what were their blood sodium concentrations? This could also be compatible with the encephalopathy due to EAH. Also how many athletes have completed the Ironman Triathlon without this happening? Which is the more common occurrence - this condition or its absence? If there was no regulator trying to insure that this condition does not occur surely every Ironman triathlete would develop the condition. Thus the presence of such cases suggests the presence of a regulator, not its absence.
The reason I posted that link is you wrote: "There is no evidence that humans can run themselves into a catastrophic failure."

I submit that both those ladies ran themselves into catastrophic failure and that video is evidence of same. And, while you may think this is evidence to support your central regulator theory, it proves to me this central regulator, if it exists, is not very reliable, since it certainly failed in these two instances. That doesn't make it much of a regulator or governor does it. There are others. You might want to check out the name Julie Moss who had a similar failure in 1982 (see the video), well before the advent of EAH issues. Or multiple world champion Paula Newby-Frasier who had a similar failure about 1/2 mile from the finish in 1995.

I am not sure why you are choosing to ignore these obvious "catastrophic failures" that are, seemingly, the result of "simple" running. But, unless they are investigated and can be shown to not conflict with your theory I am afraid your theory has some serious holes. Some "governor"

While I don't know the medical findings associated with any of these incidents, I am sure you could find out if you were really interested as I suspect Ironman keeps those records. Maybe not. Or, perhaps you could contact the people involved. They might have access to the records of those incidents. Let us know what you find out.


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Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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This is a great question. The only reasonable answer that I can offer is that the brain considers the regulation of the body's osmolality as a greater priority than its energy stores. Also the response to an energy deficit may simply be to cause the athlete to slow down.

My experience described in Lore of Running was that when I developed hypoglycemia (the Bonk) due to a falling rate of glucose production by the liver causing blood glucose concentrations to fall, my brain would tell me to stop running. And when I had stopped to seek food. This is the logical response. The organ at risk from hypoglycemia is the brain. If it allows you to continue running you simply compound the problem which can only be corrected by eating. So you eat, the blood glucose concentration rises and the brain releases the brake allowing you again to run.

This system works really well to protect the brain from hypoglycemia during exercise. But your point is excellent: Why does it not act "in anticipation" to force you to go and seek food BEFORE your blood glucose concentration falls since in all other systems the brain acts in anticipation to insure that failure does not occur?

I can only surmise that the need to eat during exercise was not a selective factor driving our biological evolution.

But others might have much better explanations.

I'm certainly not qualified to comment as my reading of the science is limited to one book about running, but a rather lengthy one (Ibid. your reference.)

While riding today, this thought occurred to me: why presume eating during exercise was not a selective evolutionary factor? Maybe a gene was evolved to create a hunger during running which would prompt hunters/runners/athletes to eat during exercise. While beneficial in the short term (e.g. during the hunt, during the race), perhaps longer term effects disfavored this trait. Thus, could it be that the reason we run or exercise only for two hours before bonking is that longer term exercise without rest is bad for us?

________
It doesn't really matter what Phil is saying, the music of his voice is the appropriate soundtrack for a bicycle race. HTupolev
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Re: Tim Noakes: we need you back for a moment [HH] [ In reply to ]
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I don't think any other animals eat at a moderately high percentage of their aerobic capacity. Most are sitting around when eating. Perhaps because packaged nutrition is not available in the wild (aside from berries and bananas) :-) This alone is a good reason to stick to 10 k's, half marathons and olympic tri or less. I don't think doing longer events on a one off basis are bad for you, but I do think that day in day out long training (in excess of 2 hours per day) does take its toll over time.

Dev
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Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
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I don't think any other animals eat at a moderately high percentage of their aerobic capacity. Most are sitting around when eating. Perhaps because packaged nutrition is not available in the wild (aside from berries and bananas) :-) This alone is a good reason to stick to 10 k's, half marathons and olympic tri or less. I don't think doing longer events on a one off basis are bad for you, but I do think that day in day out long training (in excess of 2 hours per day) does take its toll over time.

Dev
I think it is pretty easy to explain why animals don't eat when hunting (exercising). It takes time and energy to digest and absorb food. During this time the energy requirement diverts from the energy available to the muscles. To account for this all animals store energy to be used during this period. As long as we stay under the limits that we can convert energy stores into high energy molecules used in metabolism we should be able to exercise continuously "forever", as long as we replace the lost water and electrolytes (for which there is no large storage repository).

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Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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Dr. Noakes,

Thanks very much fo taking the time to post here and answer so many questions.

I purchased Lore of Running 7 months ago and would rate it as probably one of the top 3 books I own. It is so informative and comprehensive. I have even brought it into my gastro-endocrinologists' office, for him to peruse in my diagnosis of Colitis last year.

I live and train in South East Asia and have done my very best to educate myself, regarding :dehydration / hyponaetremia / electrolytes.

Just recently, I completed a small duathlon 10km R / 40km B / 10km R. Although the temperature at commencement 07:30 was 29C with highish humidity, 2 hours later it was 35C and exceptionally humid ( apologies for the lack of humidity data ). The run course had absolutely no shade , there were no clouds at all and was run on black asphalt.

I considered myself to be as prehydrated as possible ,at commencement and had pre-loaded for 4 days prior , with 4000mg sodium phosphate / 2000mg glutamine in addition to +_ 3 Litres of diluted (Realemon Juice ) daily ,excluding training drinks.

My sweat rate is at least 2L per hour during this type of weather at this intensity and has been as high as 2.5L. Slightly lower during evening training ,at lower intensities +_1.5L per hour.

Throughout the event I hydrated , ( after the first 45 min segment ) , I drank 2.75 Litres comprising of :
- 1450 mg's sodium
- 4000 mg's sodium phosphate
- 400 mg's potassium ( and a banana on top of that )
- 50 mg's calcium
- 100 mg's magnesium sulphate
- 1150 mg's Vit C
- 2000 mcg Vit B2
- 2000 mg's glutamine.

In addition to this I consumed a 600 ml custom designed carbohydrate sports drink on the bike.

Considering that I feel that I raced the first 2 events of the race well within my personal capabilities , I found myself running out of breath running at a sedentary 5.30-6.00 min/km's!
I will add here that I run 3.35 marathon's , I have completed numerous 70.3's and 4 Ironman events.

I was 72kg's when I left home and 69.5 when I returned. 5'9".

Which brings me to the long drawn out question ( apologies )..... to what extreme does heat / humidity play in a "supposedly" hydrated athlete , racing within their respective ability and the corresponding increase in HR ?

I think I understand why the HR elevates , to facillitate cooling , but I am really unsure how to avoid this without slowing down.

Apologies for the drawn out nature of ths question , but I wanted to include as much detail as possible to facillitate your opinion.

Thank you in advance and again for posting here on ST.

Terry

"You are never too old to set another goal or to dream a new dream" - Les Brown
"Discipline is the bridge between goals and accomplishment" - Jim Rohn
Last edited by: canuck8: Apr 27, 09 11:25
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Re: Tim Noakes: we need you back for a moment [canuck8] [ In reply to ]
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I think I understand why the HR elevates , to facillitate cooling , but I am relly unsure how to avoid this without slowing down. \\\[/url]

When someone figures out how to keep your HR down in extreme heat while still running at normal race pace for normal weather, then I can come out of retirement and take my rightful place among the Ironman greats..(-; You answered your own question just about as well as anyone else can. The hotter it gets, and the longer the race, the more you just have to slow down. To what degree depends on a lot of factors, the biggest is your own bodies paticular tolerance to heat, and how well you managed it during the race...There are lots of potential winners in Hawaii, but when filtered through this formula, there are very few...
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Re: Tim Noakes: we need you back for a moment [monty] [ In reply to ]
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Monty,

That was not the answer I was looking for :)

Funny that . I was discussing this with my wife ,whilst cooling in the pool that afternoon . I was telling her , that perhaps , I am just not genetically designed to perform well in heat. After all ,I am Canadian and it is very hot and humid.

I just figure that at some point my body would say to itself that "hey this idiot keeps exposing us to this extreme environment and intensity , perhaps we should adapt ?".
Well after 16 years here of which 8 has involved endurance training , perhaps it was too late of a start in this climate. Or I am just not genetically designed to perfor i this environment.

Coincidentally , I raced Kona some years back and did not find it hot at all. Additionally , I should add that I found the temperature and humidity VERY comfortable.

Thanks for your post:)

Terry

"You are never too old to set another goal or to dream a new dream" - Les Brown
"Discipline is the bridge between goals and accomplishment" - Jim Rohn
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Re: Tim Noakes: we need you back for a moment [canuck8] [ In reply to ]
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I was telling her , that perhaps , I am just not genetically designed to perform well in heat. After all ,I am Canadian and it is very hot and humid\\

This may or may not be true in your case, but being Canadian has nothing to do with it. I have known folks that have never been exposed to heat, lived in cold climates all their life, and do great in the heat. And conversely, there are folks that are from hot enviorments, famalies have lived there for generations, and they suck in the heat. That is why I believe there are some factors that have not really been isolated yet that we have no control over. Other things we can tweek to some degree, but you can go only so far until you bump against those walls you were born with. Each person will find those walls once they do enough racing in hot enviorments, and like me, they will deny it for awhile, fight it tooth and nail, try every approach that someone can come up with, and in the end realise that fightning your nature is a losing battle..

On the other hand, I can kick serious butt in 40f degree weather, with wind, rain, or snow. I guess I was meant to be a real biathlete, not the bike/ run kind, oh well..
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Re: Tim Noakes: we need you back for a moment [monty] [ In reply to ]
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I do well at both ends of the spectrum.....35C and humid and minus 15C.

Where I fail miserably is 5-12C in the rain. I cannot keep my body working in wet cold. Dry cold is fine and heat and humidity is fine. I believe both these extemities requires the delivery of core heat to the extremities and skin surface, but low sweat rate (when you sweat profusely in really cold, you get wet and immediately freeze). In the case of minus 15 and cold, there is a layer of clothing that the heat then stays trapped under. But when it is 5-12C and raining, the heat delivered to the extremities is constantly sucked out of my body making me colder and colder and colder. I don't have a large enough layer of natural insulation (muscle mass and fat) to keep the heat trapped in my core which is somewhat required in wet.

I think to succeed in heat, you need to be lean, not hugely muscled, and have a very low sweat rate (In Kona 2006 for example, I only consumed 6 bottles of Gatorade during the entire bike and then whatever coke and gatorade during the run. Barely did 6L of liquid over a 10 hour race. This is somewhat the opposite of the well muscled, high sweat rate athlete that will succeed in wet cold (Monty is that you)?

Dev
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Re: Tim Noakes: we need you back for a moment [monty] [ In reply to ]
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Thans for that response , vry nformative.

I hav bumped into those walls quite a few times........I'm still trying to bust straight through them.

I will be racing IM Canada in August , which from what I recall , although hot , is substantially cooler than what I am used to. All things being equal , I usually do better in cooler climates ( Kona and IMWA).

I think I may join you in one of those cooler 40f races and see if I excel there too :)

Thanks again !

Terry

"You are never too old to set another goal or to dream a new dream" - Les Brown
"Discipline is the bridge between goals and accomplishment" - Jim Rohn
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Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
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This is somewhat the opposite of the well muscled, high sweat rate athlete that will succeed in wet cold (Monty is that you)? //

I dont know if I'm well muscled, but 5'10" 160lbs was my usual racing weight. I think size is a factor, but not a limiting one. Lot of guys that were well over 6ft, and 175lbs+ have done well in Hawaii. Dave Scott was quite well muscled, and not a little guy. When I watch the top 20 guys over the past few years, there are a lot of big guys mixed in there with the smaller ones. I have no excuse in size area, probably most of the ironman top 10 since its inception were guys my size and bigger. The Greg Welch body size was the exception, not the rule...It is mostly about heat tolerance, regardless of your size. I expect that Matt Reed and Lifetime champion(name escapes me right now) will do very well in Hawaii, and they are huge by triathlete standards....
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Re: Tim Noakes: we need you back for a moment [canuck8] [ In reply to ]
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I am not sure it is possible to know from the data you provided whether you were over hydrated or dehydrated. Both could have affected your ability. The one quesition I am sure Dr. Noakes would be asking is what was your weight at the end compared to the beginning?

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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That is a great point Frank , thanks for the reminder on that :)

I was 72kg's when I left home and 69.5 when I returned.5'9"for what it's worth !

I will insert in my original post.

Thanks again !

Terry

"You are never too old to set another goal or to dream a new dream" - Les Brown
"Discipline is the bridge between goals and accomplishment" - Jim Rohn
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Re: Tim Noakes: we need you back for a moment [canuck8] [ In reply to ]
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In Reply To:
That is a great point Frank , thanks for the reminder on that :)

I was 72kg's when I left home and 69.5 when I returned.5'9"for what it's worth !

I will insert in my original post.

Thanks again !

Terry
Well, from that I think it is unlikely that you were suffering from dringking too much and it is not likely that you were severely dehydrated. I guess it is possible your electrolytes were all screwed up if you were drinking water and you needed sodium or you were drinking sodium and you needed water. Hard to know from this data. Perhaps Dr. Noakes or others can give their personal experience from the medical tent as to what this presentation most commonly represents.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [Frank Day] [ In reply to ]
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In Reply To:
In Reply To:
That is a great point Frank , thanks for the reminder on that :)

I was 72kg's when I left home and 69.5 when I returned.5'9"for what it's worth !

I will insert in my original post.

Thanks again !

Terry
Well, from that I think it is unlikely that you were suffering from dringking too much and it is not likely that you were severely dehydrated. I guess it is possible your electrolytes were all screwed up if you were drinking water and you needed sodium or you were drinking sodium and you needed water. Hard to know from this data. Perhaps Dr. Noakes or others can give their personal experience from the medical tent as to what this presentation most commonly represents.

I was actually drinking from a 2.75Litre Camelbak which I premixed with:
- 4 Nuun's.
- One daily dose of RaceDay Boost ( Hammer Nurtition).

I threw it on for the bike ,as this particular event had few hydration points and I preferred to just stay aero ,for the short bike ( 40km ).

I drank roughly 1.75-2L of this on the bike ,with a separate biddon of INFINiTT (600ml).

I refrain from drinking plain water, so as to not dilute the electrolytes in my body. I will of course drink some "if" I do not have an electrolyte mixture available.

Thanks

Terry

"You are never too old to set another goal or to dream a new dream" - Les Brown
"Discipline is the bridge between goals and accomplishment" - Jim Rohn
Last edited by: canuck8: Apr 27, 09 19:09
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Re: Tim Noakes: we need you back for a moment [canuck8] [ In reply to ]
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Well, I suspect that if Dr. Noakes shows up again he will be quite critical of your plan since you were not letting thirst be your guide and you preloaded. I would love to hear his evaluation of why you performed so badly though since there is no evidence of EAH.

--------------
Frank,
An original Ironman and the Inventor of PowerCranks
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Re: Tim Noakes: we need you back for a moment [canuck8] [ In reply to ]
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budump !..........................:)

"You are never too old to set another goal or to dream a new dream" - Les Brown
"Discipline is the bridge between goals and accomplishment" - Jim Rohn
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Re: Tim Noakes: we need you back for a moment [canuck8] [ In reply to ]
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I think your problem is you live in a ridiculously humid country that famously under-reports its acutal temperatures, never mind the humidity-adjusted temperature. <looks around for black helicopters>

Long time no talk. It's been far too hot here of late.

_____________________________________________________
"Oh man, it's going to take days to kill all these people!" - Jens Voigt
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Re: Tim Noakes: we need you back for a moment [jsivvy] [ In reply to ]
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Hey John :)

Yes I have been undercover !

My car thermo reported 40C outside when I returned from 15 mins at H.Village at lunch the day after (y/day).

Hoping there is something I DON'T already know, that I can learn from this thread (regarding my personal high HR problem in this extreme environment and intensity )

Best regards

Terry

"You are never too old to set another goal or to dream a new dream" - Les Brown
"Discipline is the bridge between goals and accomplishment" - Jim Rohn
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Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
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Fascinating to the physiologist, and way over everyone else's head. I am an MD and I hard a hard time getting through it. For the athlete, they need to take in salt tablets, drink electrolyte drinks and not only water, and most of all, mark their weight on their bib or write it with marker on their forearm. When they make it to the med tent or ambulance, if their weight is up, then dont give them any normal saline. The only IV they should ever get would be a sodium concentrate at low volume. As far as having a hydration strategy, this can be easily formulated by weighing onself before and after a long work out. This stuff doesnt have to be rocket science, unless you want it to be. It isn't that hard.
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Re: Tim Noakes: we need you back for a moment [shacking] [ In reply to ]
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shacking wrote:
Fascinating to the physiologist, and way over everyone else's head. I am an MD and I hard a hard time getting through it. For the athlete, they need to take in salt tablets, drink electrolyte drinks and not only water, and most of all, mark their weight on their bib or write it with marker on their forearm. When they make it to the med tent or ambulance, if their weight is up, then dont give them any normal saline. The only IV they should ever get would be a sodium concentrate at low volume. As far as having a hydration strategy, this can be easily formulated by weighing onself before and after a long work out. This stuff doesnt have to be rocket science, unless you want it to be. It isn't that hard.


But Noakes is saying you don't need to take in salt tablets and you should drink to thirst.
Last edited by: Trev: Jul 13, 15 14:15
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Re: Tim Noakes: we need you back for a moment [Trev] [ In reply to ]
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I have come to believe the biggest problem with the debate over drinking to thirst or not it that the two sides of the argument are failing to recognize the affect which training can have on human physiology. I fully believe that we are inherently born with a thirst reflex which as Noakes argues allows us a great ability to self regulate. However I also believe that through training athletes can effectively learn to suppress this reflex to the point they effectively lose it. Lionel Sanders talked about a suppressed reflex in his recent interview (http://www.slowtwitch.com/...l_Sanders__5168.html) and I feel similarly to him. My body has acclimatized to years of distance running training without any mid-workout hydration/nutrient by shutting down thirst and hunger reflexes during intense activity. I will always hit the wall before I physically feel the need to drink and/or eat and that makes it impossible for me to follow Noakes advice.
As far as I am aware experienced athletes are far more likely to suffer from extreme dehydration while it tends to be novice athletes who get into serious trouble with overhydration. The failure to recognize these physiologic differences makes it impossible to declare one side is right and the other is wrong.
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Re: Tim Noakes: we need you back for a moment [shacking] [ In reply to ]
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shacking wrote:
Fascinating to the physiologist, and way over everyone else's head. I am an MD and I hard a hard time getting through it. For the athlete, they need to take in salt tablets, drink electrolyte drinks and not only water, and most of all, mark their weight on their bib or write it with marker on their forearm. When they make it to the med tent or ambulance, if their weight is up, then dont give them any normal saline. The only IV they should ever get would be a sodium concentrate at low volume. As far as having a hydration strategy, this can be easily formulated by weighing onself before and after a long work out. This stuff doesnt have to be rocket science, unless you want it to be. It isn't that hard.


Weighing athletes is a good idea on paper... but the devil is in the details and execution. The method I've seen in races is basically a poorly controlled 3rd grade science experiment.
  • What is the accuracy and precision of the scales being used?
  • Are the scales used at weigh in the same as used in the med tent
  • Are the scales rated to perform 1000-2000 measurments (and retain accuracy)
  • Should the scales be calibrated during the weighing process?
  • What type of resolution and accuracy is required to detect a "weight up" situation
  • What is the expected rate of false positives/negatives?
  • How risky is a false positive?
  • Do you pre-weigh people with their street clothes?
  • In the med tent do you towel dry people off before weighing them? any clothing taken off during weighing?



For example I was weighed this year at Challenge wanaka. The scale was placed on a rubber mat over grass and obviously not level. Scale was cheap bathroom dial type. Person reading the scale glanced over from their seated position to read the scale, parallax error. I had on jeans, long sleeve t-shirt, glasses, hat, street shoes... just after a lunch meal. I was recorded as 77kg. My home scale (high quality and trusted) recorded me as 67.5kg with my skin suit on 2 days prior to the race measurement. I think you can see what would go wrong with using weight as an indicator.
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Re: Tim Noakes: we need you back for a moment [shacking] [ In reply to ]
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This stuff doesnt have to be rocket science, unless you want it to be. It isn't that hard.

I agree.

I trained for years and years - long and hard, racing 9 IM races all 9:40 or under. I never ounce really thought long and hard about hydration and nutrition. I just took in what I needed on the fly as I needed it.


I will admit that this was fine tuned over hours and hours and years and years of training. I recall a few minor bonk episode when I first got into 3 hour plus bike rides, but after that, rarely issues in training or racing.


I never cramped. I never consciously took in salt, although Gatorade was a normal and regular drink on long rides, runs and in racing.


I think a BIG part of the problem with this is that too many, are trying too hard to go too long and too hard, too soon. It took me many years of gradually building up distance and pace, to the point of even considering doing an Ironman.


Steve Fleck @stevefleck | Blog
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Re: Tim Noakes: we need you back for a moment [Trev] [ In reply to ]
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 Clearly, there is sodium lost in sweat, and it is only pragmatic and logical to make some effort at partial replacement. You are right, it doesn't have to be a salt tablet, it can be an alternate form of electrolyte.
We don't need a PHD to know the value of a scale. Weigh yourself before and after. It is so easy. Try not to dip under 2%. Simple. I dont really care about the ECF, and intracellular sodium. I dont care about evolutionary theory. It makes no pragmatic difference. One simple test will not only measure % dehydration, it will also lead you to a possible diagnosis of hypervolemic hyponatremia. Not complicated science... is it??
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Re: Tim Noakes: we need you back for a moment [Pantelones] [ In reply to ]
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One simple way to win a debate is to exaggerate the opposing position, or your own. You are saying there was a 10kg difference in scales, that's 22 lbs. That is not commonplace or what one would typically expect. You make a good point, but you exaggerate the potential for differences. The scale at this point is the only real piece of evidence to guide emergency personell as to whether fluids should be given or not. Even sodium levels can be high or low in a dehydrated state, so even if you could check sodium in the field, it wouldnt help you alot. My guess is that by the time medical personell realize that the patient is actually fluid overloaded rather than dehydrated, it is already too late, and they have jacked them with 3-5 liters of fluid, making their brain swelling worse. I would say you do make an excellent point however, that having accuracy or precision in scales is important. I would say self reporting weight would be more accurate.
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Re: Tim Noakes: we need you back for a moment [shacking] [ In reply to ]
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I'm curious if the good Dr. changed his views at all during the 5 years that elapsed btwn post 231 and 232.
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Re: Tim Noakes: we need you back for a moment [shacking] [ In reply to ]
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shacking wrote:
One simple way to win a debate is to exaggerate the opposing position, or your own. You are saying there was a 10kg difference in scales, that's 22 lbs. That is not commonplace or what one would typically expect. You make a good point, but you exaggerate the potential for differences.

Call it an single data point or an anecdote but I have not exaggerated the numbers from my experience. It is one example of how inaccurate the weighing system can be if used to determine weight gain during a race. For my case there would be at least 5kg of weight gain during the race that weighing would not have detected.
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Re: Tim Noakes: we need you back for a moment [Bob Loblaw] [ In reply to ]
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Bob Loblaw wrote:
I'm curious if the good Dr. changed his views at all during the 5 years that elapsed btwn post 231 and 232.


Doesn't seem like he has.

Exercise-associated hyponatremic encephalopathy and exertional heatstroke in a soldier: High rates of fluid intake during exercise caused rather than prevented a fatal outcome.

http://www.ncbi.nlm.nih.gov/pubmed/25586818

Two wheels good. Four wheels bad.
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Re: Tim Noakes: we need you back for a moment [DrTriKat] [ In reply to ]
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DrTriKat wrote:
[

Exercise-associated hyponatremic encephalopathy and exertional heatstroke in a soldier: High rates of fluid intake during exercise caused rather than prevented a fatal outcome.

http://www.ncbi.nlm.nih.gov/pubmed/25586818


wow - brutal abstract:
Abstract Athletes are often advised to drink in order to "fully replace bodyweight losses" in order to prevent exertional heatstroke (EHS) during exercise in the heat. There is little evidence that "dehydration" in the range experienced by athletes adversely affects thermoregulation or is the exclusive cause of EHS. In contrast it is established that excess fluid intake can cause exercise-associated hyponatremia (EAH) sometimes associated with encephalopathy (EAHE). As part of a series of experiments to determine optimal fluid replacement during exercise in the heat, we studied a group of exceptionally well-conditioned and heat-adapted members of the South African National Defence Force. A 20 year old male started a time restricted 50 km route-march in a dry bulb temperature that reached 37.5°C (WBGT of 33.6°C, relative humidity of 85%). Pre-march plasma osmolality, serum [Na(+)] and total body water measures indicated euhydration. Fluid was available ad libitum and isotonic sports drinks at 5 km intervals. Fluid intake and core body temperature (Tc) were recorded throughout while he was tracked by a global positioning system measuring distance travelled, position and speed. Comparing the total fluid intake of the soldier (12930 mL) to the rest of the participants (mean intake of 9 038 mL) up to 40 km, it is evident that his intake was 3892 mL (approximately 300 mL h(-1)) more than the mean for group. At approximately 17h14 the soldier was found lying by himself at the side of the route, 2.24 km from the finish point. He passed away the next day in a medical care facility. This tragic event provides the valuable opportunity to present data on the pacing, temperature regulation and fluid consumption of an exceptional athlete during the development of a fatal case of combined EAHE and EHS. Pacing, fluid intake, Tc and environmental condition data are presented for 5km intervals throughout the march. We propose a novel hypothesis on the possible contribution of EAHE to the development of EHS.
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Re: Tim Noakes: we need you back for a moment [shacking] [ In reply to ]
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shacking wrote:
One simple way to win a debate is to exaggerate the opposing position, or your own. You are saying there was a 10kg difference in scales, that's 22 lbs. That is not commonplace or what one would typically expect. You make a good point, but you exaggerate the potential for differences. The scale at this point is the only real piece of evidence to guide emergency personell as to whether fluids should be given or not. Even sodium levels can be high or low in a dehydrated state, so even if you could check sodium in the field, it wouldnt help you alot. My guess is that by the time medical personell realize that the patient is actually fluid overloaded rather than dehydrated, it is already too late, and they have jacked them with 3-5 liters of fluid, making their brain swelling worse. I would say you do make an excellent point however, that having accuracy or precision in scales is important. I would say self reporting weight would be more accurate.


Self-reported weight wouldn't be more accurate. In the endurance community, just as in the general population, you will see a tendency to under-report weight.
As mentioned before, scale accuracy is critical, and with 2000 athletes at the start, often wearing more clothes before the race than after, after often times several days of 'carbo loading' etc. you're likely to not get good data. So indeed the weigh before and after is likely a very poor strategy, with the typical number of athletes seen at big races.
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Re: Tim Noakes: we need you back for a moment [Bob Loblaw] [ In reply to ]
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The soldier who died definitely had an "iron will"; pushed himself all the way to death. Don't mean to sound uncaring but he must have been very highly motivated to finish this 50 km march, to the point of pushing himself to literal physical collapse 2.2 km from the finish. Very impressive actually.


"Anyone can be who they want to be IF they have the HUNGER and the DRIVE."
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Re: Tim Noakes: we need you back for a moment [Francois] [ In reply to ]
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Monty has told stories here about the early days of Ironman and how they gamed the scale during a weigh in. You just can't trust the athlete to tell the truth.


Francois wrote:
Self-reported weight wouldn't be more accurate. In the endurance community, just as in the general population, you will see a tendency to under-report weight.
As mentioned before, scale accuracy is critical, and with 2000 athletes at the start, often wearing more clothes before the race than after, after often times several days of 'carbo loading' etc. you're likely to not get good data. So indeed the weigh before and after is likely a very poor strategy, with the typical number of athletes seen at big races.
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Re: Tim Noakes: we need you back for a moment [svennn] [ In reply to ]
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svennn wrote:
Monty has told stories here about the early days of Ironman and how they gamed the scale during a weigh in. You just can't trust the athlete to tell the truth.


Francois wrote:
Self-reported weight wouldn't be more accurate. In the endurance community, just as in the general population, you will see a tendency to under-report weight.
As mentioned before, scale accuracy is critical, and with 2000 athletes at the start, often wearing more clothes before the race than after, after often times several days of 'carbo loading' etc. you're likely to not get good data. So indeed the weigh before and after is likely a very poor strategy, with the typical number of athletes seen at big races.

Cast iron cavity inserts?
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Re: Tim Noakes: we need you back for a moment [Francois] [ In reply to ]
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Then what you are saying is that when we find an athlete passed out, we should pump him full of IV fluids for 6 hours until a CT scan shows brain swelling? Since we have identified no reliable way to recognize hypervolemic dilutional hyponatremia in the field, since weight is somehow unreliable. Like any data, it is just data, you take it for what it is worth. It is uncorrect to totally dismiss weight as useful data. I totally disagree with you.
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Re: Tim Noakes: we need you back for a moment [shacking] [ In reply to ]
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It's not what I'm saying, it's what you're wrongfully inferring I am saying. I haven't said either that we need to totally dismiss weight. I don't care if you totally disagree with me. You seem to infer things very fast. Maybe you need to think a bit more carefully.
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Re: Tim Noakes: we need you back for a moment [Pantelones] [ In reply to ]
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now you are back pedalling a little, which is appropriate. If you studied scales, their use, with and without clothes, and all these other holes you are poking in the "use the scale" argument, you won't generally find a 22lb difference. Maybe a 5-10 lb difference. No piece of data in any equation is 100% reliable all the time. I am a doctor, I know that. I treat the patient, not the data. The point I want to make is-- the scale is probably the only useful piece of data in the field... we need to use it, albeit with the knowledge of some normal variation and also margin of error. DONT THROW AWAY THE SCALES!! I want to know how many people died in the hospital, who could have been saved if they hadnt been over-aggressively hydrated? That is the real MEAT of this story. And one we may never find out about.
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Re: Tim Noakes: we need you back for a moment [shacking] [ In reply to ]
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From my recollection, it seems most people run into problems long before they ever reach a hospital. They hit a med tent, and get diagnosed with dehydration, in goes the IV.
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Re: Tim Noakes: we need you back for a moment [triguy42] [ In reply to ]
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I wonder if Dr. Noakes has ever raced an Ironman in hot, humid conditions?
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Re: Tim Noakes: we need you back for a moment [shacking] [ In reply to ]
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No but he has raced the Comrades Ultra multiple times if memory serves, that's a pretty hot one.

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Re: Tim Noakes: we need you back for a moment [shacking] [ In reply to ]
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shacking wrote:
now you are back pedalling a little, which is appropriate. If you studied scales, their use, with and without clothes, and all these other holes you are poking in the "use the scale" argument, you won't generally find a 22lb difference. Maybe a 5-10 lb difference. No piece of data in any equation is 100% reliable all the time. I am a doctor, I know that. I treat the patient, not the data. The point I want to make is-- the scale is probably the only useful piece of data in the field... we need to use it, albeit with the knowledge of some normal variation and also margin of error. DONT THROW AWAY THE SCALES!! I want to know how many people died in the hospital, who could have been saved if they hadnt been over-aggressively hydrated? That is the real MEAT of this story. And one we may never find out about.

There...instead of 'totally disagreeing' with everybody... ;-)
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Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
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I found this... it appears that an immediate effect of altitude change is for your body to try to increase its oxygen carrying capacity by concentrating hemoglobin by the means of what is termed "altitude diuresis" and this is a normal physiologic response.


http://ismm.org/index.php/normal-acclimatization.html

Dramatic changes take place in the body's chemistry and fluid balance during acclimatization. The osmotic center, which detects the "concentration" of the blood, gets reset so that the blood is more concentrated. This results in analtitude diuresis as the kidneys excrete more fluid. The reason for this reset is not understood, though it has the effect of increasing the hematocrit (concentration of red blood cells) and perhaps improving the blood's oxygen-carrying ability somewhat; it also counteracts the tendency for edema formation. It is normal at altitude to be urinating more than usual. If you are not, you may be dehydrated, or you may not be acclimatizing well.
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Re: Tim Noakes: we need you back for a moment [shacking] [ In reply to ]
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shacking wrote:
I found this... it appears that an immediate effect of altitude change is for your body to try to increase its oxygen carrying capacity by concentrating hemoglobin by the means of what is termed "altitude diuresis" and this is a normal physiologic response.


http://ismm.org/index.php/normal-acclimatization.html

Dramatic changes take place in the body's chemistry and fluid balance during acclimatization. The osmotic center, which detects the "concentration" of the blood, gets reset so that the blood is more concentrated. This results in analtitude diuresis as the kidneys excrete more fluid. The reason for this reset is not understood, though it has the effect of increasing the hematocrit (concentration of red blood cells) and perhaps improving the blood's oxygen-carrying ability somewhat; it also counteracts the tendency for edema formation. It is normal at altitude to be urinating more than usual. If you are not, you may be dehydrated, or you may not be acclimatizing well.

If I remember correctly, the diuresis is a transient adaptation. By reducing plasma volume, Blood is effectively slowed through the pulmonary tissue increasing the time for it to become oxygenated. As EPO is stimulated and RBC #s increased, the blood volume rises as well.

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Re: Tim Noakes: we need you back for a moment [Bob Loblaw] [ In reply to ]
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Soldier: 12930ml total
Others: 9038ml
At ~300ml / hr more than the others, that means they were out around 13 hours.

Therefore:
Soldier 994 ml / hr (almost a liter)
Others: 695 ml / hr

a 20 oz water bottle (standard) is ~ 591ml.
a 24 ox bottle is ~710ml

The other soldiers drank approximately 1.15 bottles per hour.
The deceased soldier drank ~ 1.68 bottles per hour for 10 hours.

It seems like people end up in a bad spot when they drink ~1L an hour for an extended period of time.

It would be interesting to note his core temp and other things. I'll have to look for the full text.
Their equipment / sweat rate/ evaporative losses would also be interesting to know.

I still think a standard recommendation of " 1 bottle an hour" is a solid safe place to be.
I think we all agree that 1L per hour is over-doing it.

Bob Loblaw wrote:
DrTriKat wrote:
[

Exercise-associated hyponatremic encephalopathy and exertional heatstroke in a soldier: High rates of fluid intake during exercise caused rather than prevented a fatal outcome.

http://www.ncbi.nlm.nih.gov/pubmed/25586818


wow - brutal abstract:
Abstract Athletes are often advised to drink in order to "fully replace bodyweight losses" in order to prevent exertional heatstroke (EHS) during exercise in the heat. There is little evidence that "dehydration" in the range experienced by athletes adversely affects thermoregulation or is the exclusive cause of EHS. In contrast it is established that excess fluid intake can cause exercise-associated hyponatremia (EAH) sometimes associated with encephalopathy (EAHE). As part of a series of experiments to determine optimal fluid replacement during exercise in the heat, we studied a group of exceptionally well-conditioned and heat-adapted members of the South African National Defence Force. A 20 year old male started a time restricted 50 km route-march in a dry bulb temperature that reached 37.5°C (WBGT of 33.6°C, relative humidity of 85%). Pre-march plasma osmolality, serum [Na(+)] and total body water measures indicated euhydration. Fluid was available ad libitum and isotonic sports drinks at 5 km intervals. Fluid intake and core body temperature (Tc) were recorded throughout while he was tracked by a global positioning system measuring distance travelled, position and speed. Comparing the total fluid intake of the soldier (12930 mL) to the rest of the participants (mean intake of 9 038 mL) up to 40 km, it is evident that his intake was 3892 mL (approximately 300 mL h(-1)) more than the mean for group. At approximately 17h14 the soldier was found lying by himself at the side of the route, 2.24 km from the finish point. He passed away the next day in a medical care facility. This tragic event provides the valuable opportunity to present data on the pacing, temperature regulation and fluid consumption of an exceptional athlete during the development of a fatal case of combined EAHE and EHS. Pacing, fluid intake, Tc and environmental condition data are presented for 5km intervals throughout the march. We propose a novel hypothesis on the possible contribution of EAHE to the development of EHS.

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Last edited by: xtrpickels: Jul 15, 15 8:47
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Re: Tim Noakes: we need you back for a moment [xtrpickels] [ In reply to ]
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xtrpickels wrote:
Soldier: 12930ml total
Others: 9038ml
At ~300ml / hr more than the others, that means they were out around 13 hours.

Therefore:
Soldier 994 ml / hr (almost a liter)
Others: 695 ml / hr

a 20 oz water bottle (standard) is ~ 591ml.
a 24 ox bottle is ~710ml

The other soldiers drank approximately 1.15 bottles per hour.
The deceased soldier drank ~ 1.68 bottles per hour for 10 hours.

It seems like people end up in a bad spot when they drink ~1L an hour for an extended period of time.

It would be interesting to note his core temp and other things. I'll have to look for the full text.
They're equipment / sweat rate/ evaporative losses would also be interesting to know.

I still think a standard recommendation of " 1 bottle an hour" is a solid safe place to be.
I think we all agree that 1L per hour is over-doing it.

Bob Loblaw wrote:
DrTriKat wrote:
[

Exercise-associated hyponatremic encephalopathy and exertional heatstroke in a soldier: High rates of fluid intake during exercise caused rather than prevented a fatal outcome.

http://www.ncbi.nlm.nih.gov/pubmed/25586818


wow - brutal abstract:
Abstract Athletes are often advised to drink in order to "fully replace bodyweight losses" in order to prevent exertional heatstroke (EHS) during exercise in the heat. There is little evidence that "dehydration" in the range experienced by athletes adversely affects thermoregulation or is the exclusive cause of EHS. In contrast it is established that excess fluid intake can cause exercise-associated hyponatremia (EAH) sometimes associated with encephalopathy (EAHE). As part of a series of experiments to determine optimal fluid replacement during exercise in the heat, we studied a group of exceptionally well-conditioned and heat-adapted members of the South African National Defence Force. A 20 year old male started a time restricted 50 km route-march in a dry bulb temperature that reached 37.5°C (WBGT of 33.6°C, relative humidity of 85%). Pre-march plasma osmolality, serum [Na(+)] and total body water measures indicated euhydration. Fluid was available ad libitum and isotonic sports drinks at 5 km intervals. Fluid intake and core body temperature (Tc) were recorded throughout while he was tracked by a global positioning system measuring distance travelled, position and speed. Comparing the total fluid intake of the soldier (12930 mL) to the rest of the participants (mean intake of 9 038 mL) up to 40 km, it is evident that his intake was 3892 mL (approximately 300 mL h(-1)) more than the mean for group. At approximately 17h14 the soldier was found lying by himself at the side of the route, 2.24 km from the finish point. He passed away the next day in a medical care facility. This tragic event provides the valuable opportunity to present data on the pacing, temperature regulation and fluid consumption of an exceptional athlete during the development of a fatal case of combined EAHE and EHS. Pacing, fluid intake, Tc and environmental condition data are presented for 5km intervals throughout the march. We propose a novel hypothesis on the possible contribution of EAHE to the development of EHS.

The soldier drank less than 1.5 times what the others did and he died.
It isn't as if he was drinking twice the amount or 3 times the amount.
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Re: Tim Noakes: we need you back for a moment [shacking] [ In reply to ]
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shacking wrote:
Then what you are saying is that when we find an athlete passed out, we should pump him full of IV fluids for 6 hours until a CT scan shows brain swelling? Since we have identified no reliable way to recognize hypervolemic dilutional hyponatremia in the field, since weight is somehow unreliable. Like any data, it is just data, you take it for what it is worth. It is uncorrect to totally dismiss weight as useful data. I totally disagree with you.

Actually this is what happened to me at IMLP 2003. I walked into the medical tent hypervolemic (likely around 10 lbs), but they had no scales back then. They mistook my symptoms for being dehydration and pumped me with 4 more IV bags making a bad situation near death. At least at North American IM's since then, it seems they generally have been using scales at check in and in the medical tent. While a bit imprecise, the post race weight with skinsuit and running shoes and wet body would still have to be quite a bit higher to surpass the pre race weight from a mid day check in with breakfast and lunch in the body, street clothes on and street shoes (might be the same running shoes, but the street clothes will be heavier. Also pre race race week weight will be higher due to the water being retained with all that glycogen stored on the body.

In general if post race weight is higher than pre race weight, even with discrepency of scales, that weight is going to have "worked really hard" to surpass pre race weight, meaning something is likely wrong enough that the medical staff should not pump you full of IV's.

As a point of reference, since 2003 when I do an IM (and I have done 20 since then some with scales some without), on race week I "tend" to be 2-3 lbs heavier than my weight early in the week. Then on race day I tend to be down 3-4 lbs, which basically ends up meaning I lose around a lb on my early week weight while racing. This is barely 1% of my body mass at 138 lbs race weight.

In Kona 2006, I weighed in at 140 lbs and ended the day at 137 lbs while my early week weight was 138 lbs. That day, I consumed only 4-5 large bottles of Gatorade EF on the bike, zero water and a cup of gatorade at every water station on the run (so something like 26 half cups because those cups are not even close to a quarter full). Estimate is 4L of liquid over 10:20, or around 9 lbs of liquid intake over 10+ hours on a 138 lbs body with no performance degradation. That year in Kona they had Gatorade Endurance Formula with more sodium per bottle and the on course gels were Powergel 3x Sodium, so that was plenty of sodium (even though Trev and Noakes say we don't need any).

If I recall correctly Macca who would routinely blow up in Kona until he nailed his electrolyte intake the previous year ended up running 2:42. 2005 or 2006 may have been the first years they have Gatorade EF + Powergel 3x sodium in unison on the course. Noakes etc will say "not neccessary", but with a decent amount of sodium from these two sources alone, it just took away the need for many to get sodium from additional sources. If I recall the 3x Sodum was around 1250 mg sodium per 100 g of gel so around every 2 gels you got 1000 mg of Sodium. Add to that around 400 mg of Sodium per bottle of Gatorade EF, and someone who takes in 5 bottles and 8 gels ends up taking in around 6000 mg over a long day.

If an average human has around 50 g of sodium in the entire body and an average western diet is 3 g intake, then 5-6 g intake over a humid hawaii raced does not seem that excessive that it should cause trouble provided that you don't over drink plain water coupled with it, because I can see how salt and water retention can go hand in hand. The over drinking athlete likely is better off with no sodium intake, because they will likely retain less of the over consumed water (from my understanding), but best plan is to not over drink. No your sweat rates and even if you can't drink to thirst because the thirst quench instinct is all screwed up during racing, you already know now much fluid you lose worst case under racing load and personal heat generation (one might need more liquid dissipating the heat of a 250W effort which generates 1000W of heat than a 150W effort that only generates 600W of heat).
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Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
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I'm not aware Noakes has ever said salt supplementation is harmful but he says it is not 'needed' and does not enhance performance.

As so many do supplement with extra salt and are successful in ironman events it clearly does not harm performance.

The issue is liquid intake. And it seems that now Noakes views on over drinking are now accepted and understood. Sadly many athletes do not understand and still make the same mistake and over drink.

I take issue that the thirst mechanism does not work during training or racing. People assume that because they consume less liquid if they drink to thirst than they do when they follow the usual guidelines that thirst is wrong or delayed or late. This is not the case. Thirst allows some mild dehydration, thirst allows you to end the event or session lighter than you started. This is normal and correct because you should lose weight because you will have burnt off calories and water is lost with every calorie burnt. If thirst is behind the guidelines it is more likely that thirst is correct and the guidelines are wrong.

So first, some loss of weight is normal, this is not dehydration, it is the correct weight because water should be lost with the calories burnt.

Second, some dehydration is acceptable and correct. We evolved to dehydrate and rehydrate. It is not a problem it is normal. As Noakes keeps pointing out, performance is not affected by dehydration, within limits. And it is thirst which keeps you within those limits.

Overhydration is detrimental to performance. If you have drunk 2 pints more than you need you weigh more. And we all know what happens if you continue to over drink.

I do not accept thirst goes wrong, I argue people consume more liquid than is optimal for performance because they drink ahead of thirst.

I also contend that many people live in a perpetual state of over hydration. Fear of dehydration, beleif that drinking lots of water improves skin, following advise to drink 2 cups of water for each coffee, addiction to soft drinks and the completely mental idiotic moronic habit of carrying a bottle of liquid everywhere in case they drop dead of dehydration causes people to consume vast amounts of liquid and waste the planets water because they urinate every 5 minutes.

So if you start a race a kilo overweight because you are retaining liquid which you don't need, then drink a kilo more than you need, you do much of the race weighing 2 kilos more than you need. Add to that time lost urinating. How many minutes does a kilo cost in an ironman?

Add to this extra water the body retains with extra salt.

I'm not saying anyone should dehydrate to weigh less, but I am saying you should not race over hydrated and you should not be afraid to trust in your thirst.

I'm not claiming everyone or most over hydrate. But some do. It might be worth thinking about it. It would be interesting to know if those that die or have problems with consuming too much liquid start the event over hydrated.
Last edited by: Trev: Jul 15, 15 0:27
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Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
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It is entirely possible that there is a point at which over supplementation of sodium becomes detrimental to performance.

Certainly salt intake is associated with water retention. Unnecessary weight in the form of water retention must be detrimental to performance.

There may well be other detrimental effects to performance with too much sodium intake.
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Re: Tim Noakes: we need you back for a moment [Trev] [ In reply to ]
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Trev wrote:
It is entirely possible that there is a point at which over supplementation of sodium becomes detrimental to performance.

Certainly salt intake is associated with water retention. Unnecessary weight in the form of water retention must be detrimental to performance.

There may well be other detrimental effects to performance with too much sodium intake.

I definitely agree that too much water is detrimental to performance and one should lose a few pounds automatically while generating mechanical work and burning through glycogen. Carrying around one or even two kilos less by end of a race is going to be positive to performance which is why I am baffled why cyclists carry around so many bottles often even in short TT's. There were guys in the Tour De France this year carrying round none aero bottles in the Utrecht 13k TT...what is that all about. or I remember in the Torino Olympics in a 44 min 15k XC ski race a coach giving Canadian Medal contender a bottle at the 10k mark...shortly thereafter she fell off the pace, cramped and slid into 4th and the entire time I was thinking, "you would never see a 10,000m track runner going anywhere near liquid at that intensity for those short durations". It seems most coaches are also relatively clued out on the topic as mild dehydration is not a performance limiter...as you said, hauling around less weight alone is not a bad tradeoff. We might diverge a bit on the sodium topic but not dramatically. I can't see mild sodium top up which is slightly more than a normal day when one may only train 1-2 hours and sit around for 8 being bad, given that on an IM day one is going much harder for 8-17 hrs. Maybe it is psychological that after 5 hours of racing by lunch time your body starts asking for a change free sweet foods to salty foods. We generally start lunch and dinner with salty and might end with a sweet desert. During the day of an IM it seems like food is sweet through lunch and dinner time. Perhaps we don't need the sodium physically, and we're just culturally tuned to get an over supply of sodium by lunch time...then you get to race day and you don't and you are mentally messed up and cravingg salt even though according to you and Noakes the person has not lost enough out of the 50 or so grams in the body for the losses to have a real impact. Are the on course salt cravings our bodies asking for more simply because we are in a chronic state of sodium oversupply? Or maybe our bodies are so used to the over supply that we have difficulty on race day not being in that range?
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Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
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I think the problem these days, is so many people are habituated to constantly over consume liquid, sugar and salt. It is as much emotional dependence as physical dependence. People seem to train themselves to think they need or even actually need a constant supply of liquid, sugar and salt.

It is very possible these people can't perform to their best without this constant supply and topping up. There is a reverse placebo affect.

If you spend your life taking in liquid sugar and salt every few minutes you are not going to feel normal going without for 30 minutes let alone an hour or two swimming cycling and running. Look at how the alcoholic can't function without alcohol or the smoker without nicotine. Look at the coffee addictct, he goes through real physical and emotional withdrawal if deprived. Their dependence is both emotional and physical. I'm not trying to compare salt and sugar to alcohol and nicotine but if our system is habituated to a constant supply of something it is going to make things go wappy if you suddenly make it cope without that supply.

Obviously in an ironman you must take on carbohydrate and liquid. But there is only so much you can take in and actually use.

Your comparison of runners to cyclists is a good point. Look how little elite marathon runners eat and drink compared to cyclists. Part of that is cycling does make it far easier to eat and drink on the move, but I'm convinced there is more to it than that. Cyclists seem to be far more worried about hydration and food intake than runners, their mind set seems to be different.

I'm not proposing we go back to the days of consuming too little liquid and using alcohol and amphetamines like Tom Simpson, but it seems to me the mindset has gone to the opposite extreme.
Last edited by: Trev: Jul 15, 15 3:44
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Re: Tim Noakes: we need you back for a moment [Trev] [ In reply to ]
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Trev wrote:


Your comparison of runners to cyclists is a good point. Look how little elite marathon runners eat and drink compared to cyclists. Part of that is cycling does make it far easier to eat and drink on the move, but I'm convinced there is more to it than that. Cyclists seem to be far more worried about hydration and food intake than runners, their mind set seems to be different.

I'm not proposing we go back to the days of consuming too little liquid and using alcohol and amphetamines like Tom Simpson, but it seems to me the mindset has gone to the opposite extreme.


Actually, the difference in intake from elite cyclists vs runners has a lot to do with race and training length. Most elite runners (not ultrarunners) race <26 miles, often <13 miles, so no need for significant nutrition on the run. Elite cyclists will often not only race longer (esp multiday races), but go right back to high-volume bike training the next day (you can't do that with running at the elite level - run that fast so often = injury!) so they need to keep things as topped off as reasonable as well as maintain their ability to intake significant calories while putting out hard efforts.

Ultrarunners who run 50+ miles start looking more like long-course triathletes in terms of closely monitoring weight, salt intake, and calories intake.

In general though, I completely agree with you - AG triathletes, esp at the non-IM distance, hugely overdo the nutrtition aspect of their training/racing. They see pro IM athletes obsessing over their caloriec intake per hour (for good reason!) and then assume they need to emulate that for sprint/oly and even HIM distances, when you dont even need calories for the shorter stuff. Even at the longer distances, training will trump nutrition for overall performance for AGers by far - many AGers just love using nutrition as an excuse to explain why they didn't go as fast as they dreamed they could. Even at IM distance, if you've been doing those long training rides with the 'train like you race' mentality, your nutrition shouldn't been throwing you under the bus on race day, as poor fueling strategies should have been pretty exposed on those training rides.
Last edited by: lightheir: Jul 15, 15 7:26
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Re: Tim Noakes: we need you back for a moment [lightheir] [ In reply to ]
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True, my comments are more aimed at chaps who train one or two hours a day at most. Obviously an elite cyclist out for a 5 or 6 hour training ride will need to take liquid & food.

But you see people out for an hour armed with 3 bottles and pockets full of gels, salt sticks and an app to remind him to eat and drink every 10 minutes. Then after their one hour ride they down a protein shake and a recovery bar and spend the next 2 hours going over their power data whilst they eat a pizza which contains enough salt to last a week.

These are the sort of people who only ride for longer than an hour when their GPS stops working and they can't find their way home.

Then they do some event, drink so much they need to urinate on the bike, get cramp and blame lack of salt even though they consumed a weeks supply of salt the day before in the bloody pizza.

Bloody Stages users, really wind me up.
Last edited by: Trev: Jul 15, 15 7:58
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Re: Tim Noakes: we need you back for a moment [Trev] [ In reply to ]
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Yeah, I got totally flamed on a cycling forum last year when I responded to a recreational (non-racing) cyclist suggesting that his alleged big underperformance on his 70 minute bike ride was a matter of training, not nutrition. (He said he bonked out on the 70 minute ride, and learned a lesson in that he was going to take at least 350 kcal/hr even for a 60 minute total ride.)

Seriously, like 20 people piled in on that one telling me how wrong I was, and how you had to replace the calories you burn, etc. I responded that marathon runners and other elite endurance athletes barely take in any calories for 2x the duration, and they just pointed at Tour De France riders and said cycling was 'different.' Yeah, right.
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Re: Tim Noakes: we need you back for a moment [shacking] [ In reply to ]
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shacking wrote:
I wonder if Dr. Noakes has ever raced an Ironman in hot, humid conditions?


He has has run more than 70 marathon and ultra-marathon races, including 7 Comrades Marathons (56 miles) and 15 Two Oceans Marathons. I assume he ran mostly in South Africa where it does get hot.
Last edited by: Trev: Jul 15, 15 8:47
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Re: Tim Noakes: we need you back for a moment [Trev] [ In reply to ]
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Trev wrote:
shacking wrote:
I wonder if Dr. Noakes has ever raced an Ironman in hot, humid conditions?


No but he has has run more than 70 marathon and ultra-marathon races, including 7 Comrades Marathons (56 miles) and 15 Two Oceans Marathons.

Was that using the "The Ideal Sports Drink" guidelines from "The Lore of Running"?
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Re: Tim Noakes: we need you back for a moment [Trev] [ In reply to ]
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Noted- thank you. One phrase still haunts me... "drink to thirst". This is a recipe for disaster. It does depend on the athlete, the context. For me, the classic scenario is to dry up like a raisin on the bike, then bonk the run. I am a heavy sweater though. If I "drink to thirst", I will fall apart.
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Re: Tim Noakes: we need you back for a moment [J_R] [ In reply to ]
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J_R wrote:
Trev wrote:
shacking wrote:
I wonder if Dr. Noakes has ever raced an Ironman in hot, humid conditions?


No but he has has run more than 70 marathon and ultra-marathon races, including 7 Comrades Marathons (56 miles) and 15 Two Oceans Marathons.

Was that using the "The Ideal Sports Drink" guidelines from "The Lore of Running"?

As far as I'm aware Noakes is very open about how and when he changed his advice. The fact he is open about when and why he changed his mind is something to applaud.

Typical of those who can't argue to attack the person rather than the argument.

Why don't you read his book Waterlogged?
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Re: Tim Noakes: we need you back for a moment [Trev] [ In reply to ]
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Trev wrote:
The soldier drank less than 1.5 times what the others did and he died.
It isn't as if he was drinking twice the amount or 3 times the amount.

1. We do not know the other soldiers were optimal
2. It may be a "fine line"
3. There could be other confounding factors (To think this is entirely based on fluid consumption is a bit simplistic)

I talk a lot - Give it a listen: http://www.fasttalklabs.com/category/fast-talk
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The above poster has eschewed traditional employment and is currently undertaking the ill-conceived task of launching his own hardgoods company. Statements are not made on behalf of nor reflective of anything in any manner... unless they're good, then they count.
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Re: Tim Noakes: we need you back for a moment [xtrpickels] [ In reply to ]
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xtrpickels wrote:
Trev wrote:

The soldier drank less than 1.5 times what the others did and he died.
It isn't as if he was drinking twice the amount or 3 times the amount.


1. We do not know the other soldiers were optimal
2. It may be a "fine line"
3. There could be other confounding factors (To think this is entirely based on fluid consumption is a bit simplistic)


That is my point, we don't know if the other soldiers also drank too much and got away with it, or if they drank optimally.

It probably is a fine line which is actually worrying.

Agreed there may well be other factors.

It is also possible the soldier started over hydrated. Perhaps he was low on sodium at the start, might have been ill recently?

As I said, it isn't as if he drank that much more than the others.

Anyway, I'm getting thirsty defending Noakes so I'm off to the pub.
Last edited by: Trev: Jul 15, 15 9:09
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Re: Tim Noakes: we need you back for a moment [Trev] [ In reply to ]
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I have read it.
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Re: Tim Noakes: we need you back for a moment [J_R] [ In reply to ]
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J_R wrote:
I have read it.


You will have read this then.


"Dehydration" is a physiological term indicating a reduction in the total-body water content. Once the reduction in body water causes the solute concentration, especially the sodium concentration (actually the osmolality), of the blood to rise, the brain detects the change and develops the symptom of thirst. This is a normal biological response that has evolved in all creatures to ensure that they maintain a constant body water content at least once each day, usually after the evening.
When fluid is lost from the body, either in sweat as a result of exercise or from the gastrointestinal tract in diseases like cholera or typhoid, the concentration of solutes, especially sodium in the blood, rises, causing the blood osmolality to increase. This rise stimulates receptors in a special part of the brain, the hypothalamus, which in turn interact with three other nuclei, which increase secretion of the hormone AVP/ADH (arginine vasopressin, also known as antidiuretic hormone), whose function is to increase water reabsorption by the kidney. In response to the action of AVP/ADH, the kidney reduces the amount of fluid secreted. As a result, urine flow into the bladder is reduced. Nucleus 5 also stimulates the cells in another part of the brain, the cingulate gyrus, which increases thirst. As a result, the desire to drink is increased and water (and sodium through the action of aldosterone) is reabsorbed by the kidneys. The result is that the blood osmolality returns to its homeostatically regulated value, switching off the desire to drink.

Thus the only symptom of dehydration is thirst. If, however, the thirst cannot be quenched because fluid is unavailable, as occurs in those stranded in the desert, then the body activates a series of emergency adaptations that prolong life for a period but ultimately cause death when all the major bodily organs fail, leading probably to cardiovascular collapse.

The remarkable achievement of the sports drink industry was that it convinced recent generations that these control mechanisms do not exist. Instead, we've been told, all athletes must drink to ensure that they do not lose any body weight during exercise. But there are no known receptors that regulate thirst by monitoring the extent of the body weight lost or gained. In addition, this myth also convinced exercisers that they could become dangerously dehydrated not just when lost in the desert for more than 48 hours but when running for a few minutes in, for example, a big-city marathon, during which they have unrestricted access to as much fluid as they might wish. I am unaware of any other human activity in which so much fluid is freely available as in a modern big-city marathon. How is it possible under these circumstances to become dehydrated except according to a definition that has no proper biological basis?

In response to the body's pure fluid loss, the usual human living in a Western society with easy access to fluid will develop the sensation of thirst and will usually drink fluid as a result. Receptors in the back of the mouth and the esophagus, but particularly in the stomach, then detect how much fluid has been ingested. Once the stomach is filled, the desire to drink is temporarily curtailed but resumes as the stomach empties, especially if food is eaten at the same time. Eventually enough fluid (and sodium) has been ingested to return the solute concentration of the extracellular fluid (ECF) back to the normal range. Since the ECF (and hence whole body) osmolality is then within the homeostatically regulated range, the symptom of thirst is switched off; as a result, most people will stop drinking.

SYMPTOMS OF INADEQUATE FLUID INGESTION
When athletes sweat during exercise, they lose both water and electrolytes, especially sodium, in varying amounts. Because sodium is the dominant solute lost in sweat, and since the sweat sodium concentration is always less than its concentration in the ECF, sweating will always cause a greater loss of water than solute from the ECF. As a result, in the absence of any fluid ingestion, sweating must cause the ECF solute concentration to rise. Ultimately this will change enough to stimulate thirst in everyone.

However, this response is highly individualized—some athletes will become thirsty at quite low levels of weight loss, whereas the thirst of others allows them to lose up to 12 percent of body weight during ultra-endurance exercise, as in the Ironman Triathlon, without developing any more severe symptoms of homeostatic failure. To understand the real symptoms that develop when people drink less than their thirst dictates, we need to look at those studies in which participants are forced to exercise for prolonged periods while they have access to less fluid than their thirst dictates. These people develop both an unquenched thirst and additional symptoms caused by a progressive biological failure due to a falling total-body water content. One of the original studies to define these symptoms was performed in the Nevada Desert during the early years of World War II.

The Nevada Desert study reported the sequence in which symptoms of unreplaced water losses, since conveniently termed "dehydration," developed. Of course, one can equally argue that some of these symptoms are due to an absence of drinking and the knowledge that drinking will be allowed only when the activity is completed. We now appreciate that the brain responds not just to biological stimuli but also to what it anticipates will happen in the future. Knowing that a demanding activity must be performed without fluid replacement will cause all symptoms to be experienced more intensively.

The head of the Nevada Desert study wrote, "The order of appearance of the signs and symptoms is particularly characteristic. Thirst is noticeable very early, but does not increase much in intensity as the water deficit continues to increase. Vague discomfort, not experienced by controls who drank water, gradually becomes defined in the flushing of the skin, heat oppression, weariness, sleepiness, impatience, anorexia and dizziness. At about the time that the walking pace can no longer be maintained, dyspnea, tingling and cyanosis, as well as a suggestion of tetany, appear. Still later, a man cannot stand alone, either because of impaired coordination or fainting." The Nevada researchers also recognized that the inability to stand was due to the development of a low blood pressure, postural hypotension: "The inability to continue muscular work (exhaustion) seems to be a consequence of circulatory inadequacy. Temporarily, the movements themselves help in some degree to improve the return of blood to the heart. When the movements stop, failure is suddenly imminent; some persons faint at this point. Lying down promptly relieves the circulation and the symptoms."

Another Nevada Desert researcher described his experiences: "Aside from thirst, the symptoms of dehydration were in large part indications of impending collapse. A vague, generalized discomfort and a feeling of restlessness followed closely the stage of 'mouth thirst.' There was a great desire to sit or lie down. Drowsiness was often noted. A feeling of heat oppression was a frequent complaint; it was often more serious than thirst. Muscular tiredness grew more acute progressively, although manual coordination was not measurably altered. Among the signs of approaching collapse, the most reliable were a rising pulse rate and a rising rectal temperature. Sometimes there was a noticeable dyspnea. Frequently, the subject was cyanotic and his face became flushed. In the exhausted state, tingling in hands, arms and feet occurred in some cases."

So described are the real symptoms that develop when people exercise in extremely hot conditions without any chance to replace their fluid losses appropriately. Of course this is not what happens in modern marathon races in which athletes exercise usually for relatively short periods of a few hours in much cooler conditions while they have access to unlimited amounts of fluid.

The extensive research of the Nevada Desert research group established a range of findings that subsequent research has not contradicted. Not all these findings have received equal exposure over the years. Those findings that dehydration may not be quite as dangerous as the dehydration myth proposes have not been as widely propagated as those supporting the value of fluid ingestion during exercise. The principal findings were as follows:

1. Even when given free access to adequate fluids, people drank less than they lost in sweat or urine. Hence they developed "voluntary dehydration," which was corrected only after exercise and when food was eaten, especially at the evening meal.

2. In the experiments in which groups of soldiers either drank freely or not at all during day-long marches in desert heat, a much greater percentage of those who did not drink during exercise were likely to terminate the exercise bout prematurely.

3. Subjects in the groups who did not drink during these marches usually stopped when they had lost 7 to 10 percent of their starting body weights. In this state they experienced postural hypotension (EAPH), but after they experienced the symptoms of fainting caused by EAPH, they recovered rapidly within minutes of lying down and ingesting fluid.

4. Dehydration reduced neither the sweat rate, nor the rate of urine production during exercise. However, the rectal temperature and heart rate rose as linear functions of the level of dehydration. The body temperature rose about 0.2 to 0.3 degrees C for each 1 percent level of dehydration.

5. There were no immediate health risks associated with the level of dehydration of 7 to 10 percent present at the termination of exercise in those who did not ingest any fluids during exercise. The authors considered that only at very high levels of dehydration (15 to 20 percent) was there a serious risk of organ failure.These studies, which clearly established the value of fluid ingestion during exercise, had little impact on the athletic community. Instead, for at least the first two decades after the publication in 1947 of the book describing these studies, athletes continued to be advised not to drink at all during exercise. Only after the development of Gatorade and the publication of relevant studies was proper attention finally paid to the use of fluid ingestion during exercise.

Another set of U.S. Army studies occurred soon after American troops began to fight in jungle heat in Burma during World War II. It soon became apparent that on first exposure to conditions of high temperatures and suffocating humidity (caused by the transpiration of water from the leaves of the jungle vegetation), soldiers were essentially incapacitated but began to adapt within a few days. To study the special physiological challenges posed by jungle heat, a special research group was established at Fort Knox, Ky., where a "hot room" was built in which the environmental conditions present in either the desert or the jungle could be reproduced.

These studies showed that the major cause for incapacitation on first exposure to both desert and jungle heat was the development of EAPH, beginning the moment the exercise bout terminated. This disappeared within a few days of repeated heat exposures. An important contribution of these studies was to establish the condition of EAPH as a cause of post-exercise collapse and to show that this condition was not simply due to dehydration, as would become the industry-driven mantra after the 1980s.

These researchers were also interested in the psychological effects of exercising in the heat without fluid replacement. Thus they wrote the following: "An important change which the chart does not show was the actual condition of the men, their low morale and lack of vigor, their glassy eyes, their apathetic, torpid appearance, their 'don't-give-a-damn-for-anything' attitude, their uncoordinated stumbling, shuffling gait. Some were incapable of sustained purposeful action and were not fit for work. All they wanted to do was rest and drink." This shows that the symptoms of dehydration are largely of a psychological nature, the goal of which is to stop the athletes from continuing to exercise. It's a built-in mechanism to prevent bodily damage.

Scientists at the United States Army Research Institute of Environmental Medicine have conducted a study to evaluate the influence of unreplaced fluid losses on the development of various symptoms. The study used fluid restriction and exercise to produce four levels of loss of body weight (0 percent, 3 percent, 5 percent, and 7 percent) and showed that the intensity of sensations of thirst, tiredness, weakness, lightheadedness, weariness and dizziness increased linearly with increasing levels of weight loss. But thirst was the symptom that was felt with the greatest intensity.

The study is important for two reasons. First, it shows that thirst is the symptom that best indicates the presence of a fluid deficit caused by exercise and fluid restriction. This conflicts with the myth developed in the 1990s that thirst is an inadequate guide to the fluid needs of the body. Rather, in this study, a weight loss of 7 percent produced near-maximal thirst sensations.

Second, during competition, some athletes develop levels of weight loss in excess of 7 percent without developing the same intensity of symptoms experienced by the participants in this study. This shows the individuality of the thirst response. Athletes who lose substantial amounts of weight during exercise without becoming as thirsty either prevent a large increase in the solute content of their ECF (as a result of internal relocation of body sodium stores) or because their brains are less sensitive to any large changes in ECF solute concentrations.

These individuals are, in fact, dehydrated because they have lost total-body water; however, this water loss is easily replaced by drinking normally, often with a meal, after the race. It does not lead to myriad ill effects, as the sports drink industry would like us to believe. In fact, the best endurance athletes in the world are typically those who lose the most weight during exercise, who have the least thirst and who run the fastest when they are quite markedly dehydrated, perhaps because the weight loss is beneficial to performance, just as the avoidance of thirst must have been an advantage to early hominid persistence hunters.

More recent studies further confirm that the sensations of thirst are always sufficient to ensure proper hydration both before and during exercise. Participants who began exercise in a dehydrated state (-3.4 percent BW) drank 5.3 times as much fluid during 90 minutes of exercise than when they started exercise normally hydrated such that, provided they were able to drink during exercise, it made no difference whether subjects began exercise dehydrated or normally hydrated; by the end of exercise their core body temperatures, heart rates, blood osmolalities and thirst ratings were the same.

FLUID LOSS AND PERFORMANCE
If fluid loss leads to thirst, why do some of the best competitors finish endurance races in quite advanced states of fluid loss? Time and again, studies, even those by researchers expecting different outcomes, have shown that the runners who are the most dehydrated, as measured by percentage of body weight loss, run the fastest. Two examples that valdiate this conclusion are the results of the 2000 and 2001 South African Ironman triathlons and the 2004 New Zealand Ironman Triathlon.

The largest body weight loss in these studies was 12 percent in an athlete who finished the race in ~720 minutes. The five fastest finishers in the South African Ironman all finished in less than 9 hours and all lost 6 to 8 percent of their body weights during the race. Three years later, this relationship was confirmed in finishers in the 2004 New Zealand Ironman Triathlon.

Why would the fastest endurance performers exhibit the highest percentages of body weight loss during their winning performances? Perhaps clues exist in the phenomenon that has been termed voluntary dehydration. Exercising humans do not drink to maintain a constant body weight every moment of the day. Rather, we develop a water deficit termed voluntary dehydration by drinking less than the amount of weight (assumed to be due entirely to water loss) that we lose as sweat during exercise. Only at mealtimes do humans increase water intakes and so correct exactly the fluid loss developed in the hours between meals.

There are a number of probable explanations for this phenomenon. First, not all the weight lost during exercise is fluid that needs to be replaced immediately. For example, there is an inevitable loss of weight caused by the fuel, either fat or carbohydrate, that must be burned in order to provide the energy needed for the exercise. The analogy would be the fuel in a motor car that is burned as the car travels—the result is that, until it is again filled with fuel, the car loses weight in direct proportion to how far it travels.

An additional factor is not covered by this car analogy. It is that the carbohydrate that is burned during exercise may be stored in the muscle and liver in a complex that includes a substantial mass of bound water. It has been argued for some years that each gram of carbohydrate used during exercise releases up to 3 grams of water. This water acts as a fluid reserve that is restored only when the body's carbohydrate stores are again filled 12 to 36 hours after exercise. Because the body can store 500 grams of carbohydrate (with an associated 1,500 grams of water), this would explain why humans might lose at least 2,000 grams of weight during exercise without any real water loss. Indeed, studies of this problem have shown that exercising humans can lose at least 1,000 grams without a measureable change in their total-body water content.

Thus the term "voluntary dehydration" may not accurately describe what happens in athletes who lose less than 1 kg during exercise because they may not have lost any body water and hence are not dehydrated. But athletes who lose more than 3 kg during prolonged exercise probably do show a reduction in total-body water content and hence are likely to be voluntarily dehydrated to varying degrees. The explanation for this phenomenon is that already given—either they prevent a large change in ECF solute concentration in response to quite large changes in body water content or their brains are less sensitive to a normal increase in ECF osmolality (solute concentration). But either way, the fact that athletes with the greatest levels of weight loss are usually the fastest finishers in endurance events shows that the response of their brains to body water loss has been entirely appropriate, perhaps optimal.

There is no direct evidence that exercise performance is impaired in those who lose weight during exercise, provided they drink to the dictates of thirst and do not become thirsty. In fact, evidence that the best marathon runners have a remarkable capacity to resist high levels of fluid loss has been provided in countless races around the world.
Last edited by: Trev: Jul 15, 15 10:10
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Re: Tim Noakes: we need you back for a moment [Trev] [ In reply to ]
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I must admit I don't recall ever reading anything in that book regarding tips on losing love handles
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Re: Tim Noakes: we need you back for a moment [Trev] [ In reply to ]
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That is my point, we don't know if the other soldiers also drank too much and got away with it, or if they drank optimally.

It probably is a fine line which is actually worrying.

Agreed there may well be other factors.

It is also possible the soldier started over hydrated. Perhaps he was low on sodium at the start, might have been ill recently?

As I said, it isn't as if he drank that much more than the others. \\



As you continue to defend Noakes and his theories, I will just chime in here and add one thing that it appears that no one mentioned. Perhaps different bodies work differently in the heat? Maybe some lose more sodium and magnesium than others? Perhaps there is not a one size fits all formula here? Maybe the soldier did exactly what everyone else did, but his body reacts differently to heat stress?


My answer to all of these questions is yes of course, seems quite logical that since our bodies vary in so many different ways, why not in how we handle heat stress. And if that is the case, then not knowing how the individual you are talking about reacts, well seems like circle jerking around and around, getting no where really. You cannot tell anything at all, except to what eventually happened to him. He might have drank too much water, or he might have drank too little with electrolytes. Either could have caused his death, along with a few other possibilities.


I'm not saying that Noakes is wrong, just wrong for a lot of people. Just like diet people that like to claim that this or that program is optimal for athletes, or you can just minus your age from 220 to get your max heart rate. I have found that more people fit outside the norm than inside on a lot of issues, especially nutrition.
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Re: Tim Noakes: we need you back for a moment [shacking] [ In reply to ]
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Hello shacking and All,

It appears that what is needed is a more accurate method of diagnosing hyponatremia which is a condition that occurs when the level of sodium in the blood is too low.

While using athlete weight changes before and after racing may be useful .... a rapid and more direct method of assessing the condition at the IV tent appears to be warranted.

Devices like the Pixcell that use only one drop of blood (useful for preemies too) might be a useful tool.



http://www.pixcell-medical.com/

"PixCell Medical Technologies develops, produces, and markets portable medical diagnostic products for point of care testing. PixCell's products are based on its innovative Viscoleastic Focusing (VEF) technology and single use cartridges that enable rapid, accurate and simple blood sampling and analysis. Results are displayed within minutes in an easily readable format. PixCell's mission is to make tests currently restricted to the laboratory more accessible, easy to use and affordable."
"HemoScreen™ is a portable, easy to use, and maintenance free Complete Blood Count device , that provides rapid, accurate and easily readable results."

The condition appears to be very common with more than 3 million US cases per year according to the Mayo Clinic.

http://www.nlm.nih.gov/...y/article/000394.htm


.

Cheers, Neal

+1 mph Faster
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Re: Tim Noakes: we need you back for a moment [xtrpickels] [ In reply to ]
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Hello xtrpickels and All,


I agree with you that the other factors of the experiment should be considered .... in particular the core temperature history of the participant immediately prior to death.




Why am I thinking about extra pickle juice as a cure for cramping, dehydration, and heatstroke? ............. just kidding ............

It looks like humans participating in experiments to expand the envelope of human endurance in hot conditions should have internal core monitoring devices installed or provide other non invasive methods of monitoring biological functions near collapse to predict a timely intervention for preventing death.

Research like that below is pointing the way to non invasive devices that will provide early warning to help prevent incapacitation and death in hot conditions.

http://cs.brown.edu/...ratureEstimation.pdf



"Although the current construction of the KF will not correctly model extreme core temperatures above 39.5°C we suggest that with a few refinements this model could
offer a promising new means of real - time thermal injury risk assessment. We suggest that the other parameters of human health state monitoring are ripe for the intelligent application of machine learning techniques. For the military, performance athletes, first responders, etc., health state estimators hydration state, metabolic
state, fatigue, and cognitive state (see Friedl 2004) remain elusive using non - invasive sensors. From a military combat casualty care perspective, lives can be saved if remote monitoring can detect loss of blood (Rickards et al. 2008). Similarly, from a diabetes management point of view, the ability to estimate and guard against hypoglycemic shock is a critical step on the path to an artificial pancreas (Hoshino et al. 2009). "

.

Cheers, Neal

+1 mph Faster
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Re: Tim Noakes: we need you back for a moment [shacking] [ In reply to ]
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shacking wrote:
Noted- thank you. One phrase still haunts me... "drink to thirst". This is a recipe for disaster. It does depend on the athlete, the context. For me, the classic scenario is to dry up like a raisin on the bike, then bonk the run. I am a heavy sweater though. If I "drink to thirst", I will fall apart.


A valid point. I'm prepared to consider my view somewhat having taken on board others opinions here.

I assume Noakes view is that drinking to thirst is safe advice as drinking to thirst will not let you die of dehydration but drinking too much can kill you.

However, there are situations which arise when racing where I can see it being awkward, or tactically disadvantageous to only drink when thirst kicks in. Suppose thirst kicks in, you take a bottle and you get jogged and drop it. Do you lose time and go back for another? Staying a little ahead of thirst would mean you can relax and take a bottle further on with no loss of time.

Suppose a rival makes a break to take distance out of you just as your thirst kicks in and you have to decide to take the drink or go without. Being a little ahead of thirst gives you an option, an insurance policy.

I don't see the harm in some forward planning but you must be careful not to over drink.

Noakes may be going too far to one extreme to combat what he feels is a real danger of drinking too much.

On the other hand would going thirsty for a while be detrimental to performance?

I find it almost impossible to drink when running. I might get a drink in on the bike just before the run. I would rather do that before I'm thirsty, half a pint of liquid isn't going to cause a problem, but taking half a pint every few minutes would, so it's all about common sense and balance.

I still think drink to thirst is best advice for most sports and events and for most people even in an Ironman or a double marathon or 12 hour or 24 hour event. Perhaps if you are looking to shave a few seconds here and there it might be a tactic to take on some liquid on the bike to limit any liquid you need to take on the run which might slow you down.

However the longer the event the more danger of over drinking if you drink ahead of thirst, so Noakes advice to drink to thirst is sound.

On the very rare occasions I have taken on liquid ahead of thirst I've needed to urinate soon afterwards, so thirst works fine for me. All drinking in advance of thirst does is cause discomfort and wasted time urinating.


But I'm prepared to accept drinking to thirst might not work for those who have a genetic fault or have suffered some sort of illness which has damaged their thirst mechanism. Perhaps this is some sort of illness which has gone undiscovered.
Noakes has found the thirst mechanism is highly individual.

But, when people claim their thirst mechanism does not work properly and fails to make them drink enough, are they in reality getting dehydrated to the point performance is affected? Are they so used to, and so conditioned to permanently be slightly over hydrated, they mistake what is perfectly normal and acceptable as dehydration?

I think it is also a mindset. The athlete believes his performance will suffer if he doesn't drink enough so he drinks before he is thirsty. He has become so dependent on gadgets, so dependent on the clock, power meters, heart rate, counting calories, unnecessary quantification of every element of his training, racing, diet and 'fuelling strategy' he has lost confidence in his own brain and body. He has lost the ability to 'feel', lost the ability to trust his thirst mechanism.
Last edited by: Trev: Jul 16, 15 9:17
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Re: Tim Noakes: we need you back for a moment [nealhe] [ In reply to ]
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It appears that what is needed is a more accurate method of diagnosing hyponatremia which is a condition that occurs when the level of sodium in the blood is too low.

I'm pretty sure that the level of sodium isn't the issue, it's the concentration. Then, the rest of this sentence makes sense.






Take a short break from ST and read my blog:
http://tri-banter.blogspot.com/
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Re: Tim Noakes: we need you back for a moment [Trev] [ In reply to ]
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You make some really excellent points here Trev, and they are well taken. You are right too-- overhydration kills, and the worst underhydration usually does it maybe impair performance. I think it is important for athletes to practice and study their own fluid balance, weighing themselves before and after long hot workouts, and getting in touch with how much they should drink. You may find this interesting, although it was pretty in depth...

http://journals.lww.com/cjsportsmed/Fulltext/2015/07000/Statement_of_the_Third_International.2.aspx
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Re: Tim Noakes: we need you back for a moment [shacking] [ In reply to ]
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Hello shacking and All,

Thanks for posting the 'Statement of the Third International Exercise-Associated Hyponatremia Consensus Development Conference, Carlsbad, California, 2015'

http://journals.lww.com/...International.2.aspx

The conference also endorsed the 'drink to thirst' primary recommended fluid intake strategy to prevent symptomatic EAH.

Excerpts:

"The reported incidence of asymptomatic EAH has ranged from 0%30,53 to 51%54 immediately post-race. In a study of an ultramarathon, 67% of the participants were hyponatremic (asymptomatic) at some point during the race, but only 27% finished the with serum [Na+] <135 mmol/L (40% self-corrected prior to finishing the event).11 The highest reported incidence of asymptomatic hyponatremia post-race has been consistently noted in 161-km ultramarathons, in which the reported incidence of EAH has ranged between 5% and 51%.18,54–56 The incidence of asymptomatic EAH in Ironman triathlons in different environments has been reported to range from negligible10 to as high as 18%57 and 25%.19 In studies on endurance cyclists the incidence of asymptomatic EAH has ranged from 0% in a 720-km race30 to 12% in a 109-km race.15 In a 26.4-km swim, 17% of swimmers developed asymptomatic hyponatremia.32The reported incidences at the standard marathon distance run (42.2 km) have ranged from 0%53 to 12% to 13% of race finishers.28,58Additionally, asymptomatic hyponatremia was observed in 33% of premier league UK rugby players following an 80 minutes rugby competition59 and 70% of elite rowers during a 28-day training camp.60"



"Symptomatic EAH is rare and occurs with considerably less frequency than asymptomatic EAH, but complications associated with EAH have led to at least 14 athlete related deaths since 1981.28,38,47,50,61–69 Symptomatic EAH generally occurs as an isolated case or in small clusters during or following endurance events with participants reporting to the race medical facilities or to hospital emergency departments within 24 hours after participation. In general, participants seek treatment for a constellation of symptoms ranging from feeling unwell to convulsions. Clusters of cases have occurred in military training exercises, marathons, Ironman triathlons and ultramarathons. The incidence of symptomatic EAH has been reported to be as high as 23%57 and 38%70 of athletes seeking medical care in an Ironman Triathlon and an ultramarathon, respectively, but most endurance events report no cases of symptomatic EAH, especially at the marathon distance and below.


Two studies have examined large compilations of data to help define the incidence of symptomatic and asymptomatic EAH. 55,71 In the first study of 2135 athletes from 8 endurance events ranging in length from 42.2 to 161 km,71 the incidence of symptomatic EAH was 1% (compared to 6% with asymptomatic EAH) among study participants. In the second study of 669&#8201;161-km ultramarathon runners,55,72 only one case (0.1% among study participants) of symptomatic EAH presented during the 5-year sampling period (compared to 13% with asymptomatic EAH), but considering the total number of race participants over this time period, the actual incidence of symptomatic EAH was approximately 0.06%.Symptomatic EAH has also been reported in hikers73–75 and military personnel. 75–77 Symptomatic EAH accounted for 16% of Grand Canyon hikers seeking medical care for exercise-associated collapse or exhaustion from May 31, 1993 through September 31, 1993 providing an estimated incidence rate between 2 and 4 per 100,000 persons. 73,78 Furthermore, suspected hyponatremia was found to account for 19% of non-fatal suspected heat-related incidents in the Grand Canyon National Park from April through September during 2004 through 2009 hiking seasons. 74 In the US active duty military, the annual incidence rate of hyponatremia from 1999 through 2012 has ranged from &#8764;4 to 13 cases per 100,000 person-years (averaged 6.7 cases per 100&#8201;000 person-years). 77


However, this incidence is probably inflated as the data were derived from a medical coded database that does not have a specific designation for EAH and likely includes hyponatremia from both exercise and non-exercise related conditions. Alarmingly, symptomatic EAH is now being reported in a more diverse set of sporting activities. For instance, symptomatic EAH has been reported in shorter distance endurance competitions, such as a half marathon79 with slower finishers completing the distance in 2 to 3 hours and a sprint triathlon with slower finishers taking approximately 2 hours to complete.80 In addition, EAH has been reported in US professional and college American rules football players40,41 and has led to the deaths of 3 US high school football players between 2008 and 2014.63,64,69 Symptomatic hyponatremia has also been reported in a 48 year old lawn bowler who was heterozygous for the Delta F508 cystic fibrosis (CF) mutation, although it is unclear if complete genetic analysis for all possible CF mutations was performed,81 a 34 year old woman following a Bikram Yoga session82 and in a 39 year old woman following a 2 hour workout including tennis and weightlifting.83 Cases of symptomatic EAH have also been induced in 2 separate laboratory studies involving low intensity exercise conducted in high ambient temperatures.84,85 Deaths from symptomatic EAH have occurred in a 25 year old male police officer participating in a 19-km bicycle training ride68 and at least partially contributed to a case of fraternity hazing involving a male pledge performing calisthenics.67 It is likely that other cases of symptomatic hyponatremia have either not been recognized or reported."

"When fluid intake matches or even slightly exceeds sweat losses, the ingestion of sodium-containing sports drinks can attenuate the rate of fall of [Na+] over the course of 2 hours of continuous174 or intermittent85 cycling and ˇ&shy;4 hours of running.89,175 However, it is critical to emphasize that sodium containing sports drinks, which are hypotonic, will not prevent EAH in athletes who overdrink during exercise, as all sports drinks have a significantly lower [Na+] (10-38 mmol/L) than serum (ˇ&shy;140 mmol/L). The dilutional effect of volume excess overwhelms any positive effect of sodium and electrolytes in sports drinks.90 Therefore, while modest salt replacement is likely not harmful and has been associated with significant increases176 or no change14,177 in serum [Na+] during competitive field events it will be of modest to no benefit in situations where excess fluids are being consumed. The potential detrimental effects of excessive sodium supplementation are not clear.72,178"


[Emphasis added]


I previously incorrectly believed that drinking a sports drink with a large measure of salt provided some protection against EAH (exercise associated hyponatremia) ....

....... based on this report I will review and modify (as required) my hydration and nutrition procedures ...... and be very careful to not over hydrate during exercise .......... or for a day or so afterward.

Next gadget might be a serum Na realtime read out next to the Watts and cadence.

.







Cheers, Neal

+1 mph Faster
Last edited by: nealhe: Jul 18, 15 18:13
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Re: Tim Noakes: we need you back for a moment [nealhe] [ In reply to ]
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I appreciate everyone's enthusiasm and expertise. There is one take home message that I want to make sure everyone understands. We as a whole do not need to concern ourselves with hyponatremia that is asymptomatic. Also, hypovolemic hyponatremia (dehydration) is easily correctible (oral and IV fluid replacement). Yes, I also realize people can die from dehydration too. Our main danger we need to address in terms of education is hypervolemic hyponatremia, which causes brain swelling, pulmonary edema, and sometimes death when not recognized.
Too often, the conversation turns to a discussion of all three scenarios simultaneously which confounds the important safety issue. Also, journalists and lay people without a proper understanding of physiology confuse the 3 repeatedly. This is frustrating.
We know one thing-- that drinking to thirst will prevent fluid overload. This is a great recommendation for recreational athletes, and even marathoners whose race will end in under 3 hours. It may even suffice for a significant proportion of ultrarunners based upon their own body characteristics (weight, sweat rate, etc) Unfortunately, drinking to thirst is not an appropriate strategy for competitive amateur and professional athletes who compete in hot conditions for over 4 hours at a time, such as in an Ironman race.
Luckily, learning how much and how often to hydrate is a learnable skill set obtained through practicing in the heat, by weighing before and after, and noting how conditions and hydration strategies affect weight. What continues to irk me is the idea that we are all cast of the same mold, and that there is only one truth that we can apply to everyone. I am glad Dr. Noakes has run ultras and has had his boots on the ground, but I reject the idea that "drink to thirst" is an undeniable, universal law.

An excerpt from the 2015 Consensus Guidelines states:
For those doubting the protective effect of our thirst sensation or concerned about the risk for dehydration, another simple protective strategy is to estimate hourly sweat losses during exercise and avoid consuming amounts that are greater than this amount during endurance or other athletic events.13 This is facilitated by serial measurements of weights during and after exercise with the goal to maintain weight or even finish exercise with a slighter lower weight. A concern is that this technique may be more time consuming and less likely to be followed by casual athletes. This strategy may be particularly attractive to certain sporting events such as football where sideline scales can easily be available to guide fluid intake.
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Re: Tim Noakes: we need you back for a moment [shacking] [ In reply to ]
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shacking wrote:
I appreciate everyone's enthusiasm and expertise. There is one take home message that I want to make sure everyone understands. We as a whole do not need to concern ourselves with hyponatremia that is asymptomatic. Also, hypovolemic hyponatremia (dehydration) is easily correctible (oral and IV fluid replacement). Yes, I also realize people can die from dehydration too. Our main danger we need to address in terms of education is hypervolemic hyponatremia, which causes brain swelling, pulmonary edema, and sometimes death when not recognized.
Too often, the conversation turns to a discussion of all three scenarios simultaneously which confounds the important safety issue. Also, journalists and lay people without a proper understanding of physiology confuse the 3 repeatedly. This is frustrating.
We know one thing-- that drinking to thirst will prevent fluid overload. This is a great recommendation for recreational athletes, and even marathoners whose race will end in under 3 hours. It may even suffice for a significant proportion of ultrarunners based upon their own body characteristics (weight, sweat rate, etc) Unfortunately, drinking to thirst is not an appropriate strategy for competitive amateur and professional athletes who compete in hot conditions for over 4 hours at a time, such as in an Ironman race.
Luckily, learning how much and how often to hydrate is a learnable skill set obtained through practicing in the heat, by weighing before and after, and noting how conditions and hydration strategies affect weight. What continues to irk me is the idea that we are all cast of the same mold, and that there is only one truth that we can apply to everyone. I am glad Dr. Noakes has run ultras and has had his boots on the ground, but I reject the idea that "drink to thirst" is an undeniable, universal law.

An excerpt from the 2015 Consensus Guidelines states:
For those doubting the protective effect of our thirst sensation or concerned about the risk for dehydration, another simple protective strategy is to estimate hourly sweat losses during exercise and avoid consuming amounts that are greater than this amount during endurance or other athletic events.13 This is facilitated by serial measurements of weights during and after exercise with the goal to maintain weight or even finish exercise with a slighter lower weight. A concern is that this technique may be more time consuming and less likely to be followed by casual athletes. This strategy may be particularly attractive to certain sporting events such as football where sideline scales can easily be available to guide fluid intake.

This is basically what I wrote in my first post on the front page article about the Frankfurt athlete death.

During today's workout I weighed in before the ride in 32C heat and 70% humidity. Starting weight was 140 lbs. Drank 750 mL during the hard 3 hour ride (~2900 ft vertical) and ended the ride at 138.5 lbs. drank 200 mL more of water and ran 5K by which point the temps had gotten a touch hotter. In only 25 minutes on the run trail which had turned to a sauna I lost one more lb on top of the half pound I would have "gained" from the 200 mL water intake. So ended up at 137.5 lbs off 3.5 hours of training with 1L intake. The quick math on that is 1L intake (which would be 1 kilo or 2.2 lbs), so lost a total of 4.7 lbs in this temp given the intake. Also keep in mind that 2 lbs should be automatically lost because as I am working through the glycogen stored on my body I should lose a few lbs anyway with no safety issue....so really it's only around 2.5 lbs of fluid actually lost over 3.5 hours on a crazy humid day. So the replacement rate is around 350 mL per hour, maybe 400 mL but not that much more.

Going through this exercise in a variety of conditions and you kind of end up with the safe range that you can operate in without overdrinking and it takes out some of the guesswork on 'drink to thirst'. If you know your loss rate, you can safely stay 'close enough' and not go too far over or under.

Personally my thirst mechanism is not that great especially in the first 2.5 to 3 hours of any outing (training or racing) on the bike. On the run, I'll notice thirst much earlier.
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Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
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Excellent writing and an excellent contribution-- Thank you!
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Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
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very timely article today on cbc.ca:

http://www.cbc.ca/news/health/hydration-myths-debunked-in-5-easy-sips-1.3155705
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Re: Tim Noakes: we need you back for a moment [ija.z] [ In reply to ]
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http://www.brocku.ca/brock-news/?p=33651

This particular research involved 11 trained racing cyclists who wore IV drips while riding stationary bikes under competition-like conditions. Some cyclists had IV drips containing a saline solution to replenish fluids lost through sweat, but others had IV drips that were shams, providing no rehydration at all. - See more at: http://www.brocku.ca/...-news/?p=33651#.dpuf

“What we’ve found was really novel. Even at up to three per cent body mass dehydration, no impairment was seen in exercise in the heat.” - See more at: http://www.brocku.ca/...-news/?p=33651#.dpuf

If power output is not affected at up to 3% dehydration, then you will go faster when dehydrated up to 3%, because you weigh up to 3% less.
Last edited by: Trev: Jul 20, 15 14:19
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