Login required to started new threads

Login required to post replies

Prev Next
Tim Noakes: we need you back for a moment
Quote | Reply
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
Quote Reply
Re: Tim Noakes: we need you back for a moment [Slowman] [ In reply to ]
Quote | Reply
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
Quote Reply
Re: Tim Noakes: we need you back for a moment [triguy42] [ In reply to ]
Quote | Reply
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.


Webmaster:
http://www.irondistance.com
http://www.triathloncoach.ca
Quote Reply
Re: Tim Noakes: we need you back for a moment [Slowman] [ In reply to ]
Quote | Reply
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
Quote Reply
Re: Tim Noakes: we need you back for a moment [Slowman] [ In reply to ]
Quote | Reply
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.

Proud member of Fishtwitch and the ST Grammar Police
disclaimer: PhD not MD
Quote Reply
Re: Tim Noakes: we need you back for a moment [Slowman] [ In reply to ]
Quote | Reply
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.
Quote Reply
Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
Quote | Reply
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
Quote Reply
Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
Quote | Reply
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
Quote Reply
Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
Quote | Reply
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.

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

--- Your best is our business. ---
Last edited by: ironguide: Apr 22, 09 5:22
Quote Reply
Re: Tim Noakes: we need you back for a moment [Slowman] [ In reply to ]
Quote | Reply
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
Quote Reply
Re: Tim Noakes: we need you back for a moment [ironguide] [ In reply to ]
Quote | Reply
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
Quote Reply
Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
Quote | Reply
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 ?
Quote Reply
Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
Quote | Reply
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. :-)


--
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
Quote Reply
Re: Tim Noakes: we need you back for a moment [ironguide] [ In reply to ]
Quote | Reply
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.
Quote Reply
Re: Tim Noakes: we need you back for a moment [GregX] [ In reply to ]
Quote | Reply
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
Quote Reply
Re: Tim Noakes: we need you back for a moment [GregX] [ In reply to ]
Quote | Reply
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
Quote Reply
Re: Tim Noakes: we need you back for a moment [big slow mover] [ In reply to ]
Quote | Reply
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
Quote Reply
Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
Quote | Reply
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 ?
Quote Reply
Re: Tim Noakes: we need you back for a moment [GregX] [ In reply to ]
Quote | Reply
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
Quote Reply
Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
Quote | Reply
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



Beta testing this sig line. The old one was so old I can't remember where I got it from. Or maybe I'm so old I can't remember where I got it from. I forget.
Quote Reply
Re: Tim Noakes: we need you back for a moment [Slowman] [ In reply to ]
Quote | Reply
In Reply To:
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...
Quote Reply
Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
Quote | Reply
In Reply To:

....(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/
Quote Reply
Re: Tim Noakes: we need you back for a moment [devashish_paul] [ In reply to ]
Quote | Reply
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 ?
Quote Reply
Re: Tim Noakes: we need you back for a moment [Tim Noakes] [ In reply to ]
Quote | Reply
In Reply To:
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
Quote Reply
Re: Tim Noakes: we need you back for a moment [Tom A.] [ In reply to ]
Quote | Reply
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.
Quote Reply

Prev Next