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!

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Ego numquam pronuncio mendacium,
sed sum homo salvaticus

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.

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Frank,
An original Ironman and the Inventor of PowerCranks

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.

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Frank,
An original Ironman and the Inventor of PowerCranks

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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<If you're gonna be dumb, you gotta be tough>
Get Fitter!
Proud member of the Smartasscrew, MONSTER CLUB
Get your FIX today?

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.

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float , hammer , and jog

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?
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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.

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.

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.

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Steve Fleck @stevefleck | Blog

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

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Ego numquam pronuncio mendacium,
sed sum homo salvaticus

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?

 
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

"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.

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Dan Empfield
aka Slowman

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

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.

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.

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?

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.

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 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!

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.

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Dick

Take everything I say with a grain of salt. I know nothing.

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.

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Steve

http://www.PeaksCoachingGroup.com

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.

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Steve

http://www.PeaksCoachingGroup.com

I'm sorry but this is absurd. I can't believe that I am agreeing with Frank... 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.

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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."

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Scott, totally off topic, but are either of your two brothers still in the sport at all?

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Where would you want to swim ?