Dear Sports Scientists: Will drinking fluids keep me cool?

Another look at fluid ingestion and temperature regulation

First, if you did not catch the NY Velocity interview with Ross, be sure to---Andy Shen and co do a great job over there and produce some excellent interviews.  Their site is a must read for any serious or enthusiastic cyclist, whether or not they reside in NYC.

Back in June I was very fortunate to present two sessions at the National Athletic Trainers Association annual meeting in Philadelphia, PA.  Both talks were about fluid ingestion, temperature regulation, and dehydration, and last week I received the audience feedback from the two sessions.  As usual the sessions produced polarized views on the subjects.  So I thought it might be a good time revisit this topic, one we have written about quite a bit on the site and in The Runner's Body.  After all, it is the end of summer, it is hot and humid, and plenty of people are training and racing in the heat.

The title of this post was not inspired by an email we received, but one of the core junctures where the two sides of this argument split is how much fluid is the right amount and why athletes should ingest it.  Nearly everyone will agree that ingesting fluid does have an effect on one's ability to regulate core temperature.  However one side of the argument is that athletes should try to maintain weight losses or lose less than 2% of their starting mass, while the other side feels ingesting fluid to thirst (which normally results in weight loss and some "dehydration") is the best practice.

Why ingest the fluid to prevent or minimize weight losses?  Well, some might argue that if we do not, we get too hot and this predisposes athletes to "heat illness."  The exact meaning and relevance of "heat-illness" is debatable and probably deserves its own post altogether, but the rationale for warding off dehydration by minimizing weight losses is that dehydration causes a rise in core temperature, and that causes heat illness, and that it might even cause heat stroke according to some.

The lit review (in brief!)


The evidence used to support the practice of replacing all or most of your weight losses comes from studies that control for the workload while asking subjects to run or cycle in hot and humid conditions.  The smaller scale studies measure weight losses (and sweat rates) and core temperature, the larger scale ones look at cardiac output and skin blood flow, among other variables.  This is good science, because if we permit our experimental subjects to speed up and slow down then suddenly we cannot determine what is affecting core temperature because now we have two independent variables (intensity and fluid volume) instead of one (fluid volume).  Therefore I am not slating those studies and authors and accusing them of bad science.  


The conclusions are that dehydration, as measured by weight losses, increases cardiovascular strain and results in an elevated core temperature at the same workload.  Fair enough, and as I mentioned earlier I do not think anyone, us included, will try to say that fluid ingestion has absolutely no effect on core temperature---it does, and these studies all demonstrate this effect.  And in fact their science is good, but it is the application of the conclusions that are bad.  In writing a scientific paper it is quite easy to wander off and begin to speculate about why you found what you found.  And it is at that point in your discussion that the reviewers let rip and often times sharply remind you to remain within the confines of your data and draw conclusions based only on what evidence you have available to you (i.e. your data)!


The issue with this topic of fluid and temperature is that the data are all collected within a strict set of conditions---as dictated by the scientific process--but then applied to every athlete (slow, fast, recreational, competitive, elite) in any situation (practice, race, fun) and any condition (cold, warm, hot).


Size counts


The size and magnitude of this effect is terribly small, however.  I try to teach my students in my stats class the difference between statistical and practical significance, and this is a classical exercise for this.  Take the absolute difference between the core temperatures at the end of a typical study, where the subjects exercise for up to two hours.  It is typically between 0.5-0.8 C, or maybe 38.x C in the fluid trial and <39.5 C in the no fluid trial.  Statistically significant?  Yes, most likely.  Practically significant or meaningful?  You are allowed to disagree, but I say "no."


And to follow up with that conclusion, the advice to replace fluids and prevent dehydration is dished out from this evidence even though none of the subjects in these trials ever report signs or symptoms of "heat illness."  So perhaps the real story is that even when we exercise in hot and humid conditions, our core temperatures rarely reach critical levels, and we cope with the additional stress just fine as evidenced by the lack of symptoms.  To me it begs the question, "Why are we telling people to follow this practice," because although there is a difference in temperature, it is small and not otherwise meaningful.


Ingesting fluid keeps does not keep you cool


Long ago, in an exercise lab far, far, away (ok, in Fort Worth, TX), some bored or motivated (or both) students were testing an athlete preparing for the Honolulu Marathon.  At the end of the heat acclimatization period, the runner did a performance run (80 min) at marathon pace (14-15 km/h, or  8.75-9.4 mph) and ingested quite a large volume of fluid (1.75 L) while we measured the rectal temperature response.  He did not ingest quite enough water to prevent weight losses, but came pretty close, losing only 1.6% of his body mass pre to post.
  

And by the way, the conditions in the heat chamber were 27.3 C and 60-65% relative humidity---the expected conditions on race day in December in Hawaii.  

So if the model is that you must prevent or minimize weight losses, and that you must do that to prevent an excessive rise in core temperature, and this model is based on the evidence I mentioned earlier, how does one explain the graph above?  According to that model, this athlete should be no where near 40 C since he lost only 1.6% of his body mass and was only minimally "dehydrated," yet after 80 min he is nearly to 41 C.  And herein lies a problem, because if some data do not support a particular conclusion, said conclusion must be scrapped and we must formulate a new one that incorporates all the available evidence.

Therefore it is not the fluid you ingest that keeps you cool, but as we have written here before it is your metabolic rate, or how hard you are exercising, that really predicts your core temperature during exercise.  Do not mistake what I am saying here, though---fluid plays a role, but only a very small one, and more importantly when we permit athletes to pace themselves they just slow down in the trials where they do not drink or receive very small volumes of fluid.  The result is that they reach the same core temperature at the end of the time trial, but take a little longer to finish.

For me the bigger message is that if performance is a desired outcome, if the runner wants to go as fast as they can, then they should drink to thirst.  Ingesting volumes that are larger than that have not been shown to produce faster performance times.  If performance is not important, the evidence from where I am sitting tells me that ignoring thirst and/or ingesting very small volumes of fluid will result in a miserable day out, but will not cause you to get heat stroke or collapse---two conditions that result from mechanisms other than changes in fluid balance.

If using a "hydration system" and lugging an additional 1-2 kg of mass during training runs makes you feel better, then please continue, but just know that you are not lowering your risk for anything by doing so.  The normal response is to replace less than what we lose, and it is perfectly normal and healthy to drink to thirst.

A look ahead:  Running economy and the marathon WR

Meanwhile, the Fall marathon season is upon us!   Berlin is around the corner and Chicago is boasting a super hot field that, under optimal conditions, is capable of a record.  Earlier we looked at the Joyner paper but left it before discussing what kind of running economy it would take to break two hours, so watch out for that analysis!

Jonathan

Sports drinks, sweat and electrolytes

The actual data from the lab and the field

In the last post we introduced you to Randy, our imaginary 70 kg average male runner, and we created some potential scenarios regarding his fluid and sodium losses and replacement. The biggest take home message was to listen to your body and to drink to thirst, as this has been shown again and again in the field and the lab to keep people from drinking either too little or too much. We have received tons of feedback and discussion, and as we stated in the comments to that post we are pleased that so many of you are participating in the discussion, sharing your stories, and asking relevant and insightful questions.

Just as we will admit that field studies are not the perfect experiment but play an important role, it is the same with prediction equations. We can predict all we want from imaginary scenarios, and some times the equations are pretty accurate, but there is no substitute for the real thing, and many readers wanted to see more actual data and references that demonstrated why sodium ingestion is not necessary, and how both sports drinks and water will can cause a fall in sodium concentration. So while it is important to go through the exercise in the prior post, the next logical step is to look at the actual data.

Baker LB, Munce TA, Kenney WL. "Sex differences in voluntary fluid intake by older adults during exercise." Med Sci Sports Exerc. 2005 May;37(5):789-96

This study examined ad libitum fluid ingestion in older adults during intermittent exercise in the heat. Basically, they had continual access to water in one trial and Gatorade in another, and they had to cycle for 15 min and then rest for 15 min. The total time of each trial was two hours (four work/rest bouts) followed by an additional 30 min recovery period. A number of variables were measured, but we will focus on the sodium concentrations. One limitation of this study for our purposes here is that it was performed in older adults, and there is a well-documented effect of age on the thirst mechanism so that as you become older you become less sensitive to thirst. That is, your plasma osmolality rises higher before thirst kicks in.

According to the authors, their main findings were (and we quote):

1. When cool palatable fluids were readily available, active adults aged 54–70 yr drank enough to match sweating rates and maintain their body mass;
2. Their fluid intake behavior was repeatable;
   
3. CES [note: Gatorade] promoted greater voluntary fluid intake and restored PV losses faster than water;
   
4. There were sex differences in the fluid intake behavior of older active adults, with women drinking more water per kilogram of BM than men

As we tried to explain in many of our prior posts, the ingestion of any hypotonic fluid in excess of thirst will cause a fall in the sodium concentration. In this case "in excess" means drinking more than to your thirst. This occurs even though sports drinks contain some sodium because they still have much less when compared to the body fluids. Therefore the end result is a fall in sodium concentration. The data from this study show that these older adults, even when drinking to thirst, experience a fall in sodium concentration when ingesting water or Gatorade:


What we see is the time on the x-axis and the sodium concentration on the y-axis. The black dots represent the Gatorade trial, and the white (open) dots represent the water trial. All the subjects started with a sodium concentration of 142 mM per Liter, and in both trials the average concentration fell over time to approximately 139-140. There were no differences between the groups, and the symbols you see on the graph means that those values are significantly (statistically) different from the baseline value. So water and Gatorade ingestion produced a similar effect, and so Gatorade did not prevent a fall in sodium concentration in these subjects.

However one female subject ingested 2.8 L of water and 2.7 L of Gatorade in the respective trials. She gained weight in both instances, indicating an excessive fluid ingestion, and here are the data that support the conclusion that ingesting Gatorade will not prevent hyponatremia:


The problem is that the authors herald this as proof that ingesting Gatorade is much better than water:

"Furthermore, this woman’s data support the notion that a CES [Gatorade] is superior to water in limiting reductions in serum sodium during exercise-heat stress. During the CES trial, this female subject consumed 2.7 L and had a final serum sodium of 131 mmol per L. Therefore, although she consumed similar amounts of CES and water, serum sodium was maintained above that of symptomatic hyponatremia during the CES trial."

While the authors are entitled to their interpretation of the data, we disagree and conclude that both fluids are producing a steady fall in sodium concentration, and that the 131 value in the Gatorade trial is just marginally outside the symptomatic range (< style="font-weight: bold;">ingesting either water or Gatorade produced a nearly identical fall (~2-3 mmol) in the sodium concentration.

The take-home part: Sports drinks do not prevent hyponatremia

In fact Jonathan tried to apply this finding to a more "real world" situation in a letter to the British Journal of Sports Medicine. In that letter he argued that since the mean finishing time of women marathoners in America is five hours, and if the ingestion of Gatorade at rates similar to those found in the study is advocated by races, coaches, scientist, etc., then there would likely be many women (and probably men, too) presenting with hyponatremia. These data demonstrate that sports drinks do not prevent this condition as their ingestion in these subjects and at these rates causes a fall in sodium concentration.

Again one limitation to this study is it was done on older subjects, who are less sensitive to thirst, and what we might see in younger subjects would be a slight rise in sodium concentration when ingesting Gatorade and a maintenance of sodium concentration when ingesting water. The evidence for that statement comes from a 1992 study by Robert Cade, the inventor of Gatorade who incidentally died this week at the age of 80. In that study three groups of runners completed a marathon. One ingested Gatorade, another "half-Gatorade" (50% water, 50% Gatorade), and the third group water:

So in fact ingesting Gatorade to thirst in younger subjects results in a rise in sodium concentration, which is why you drink more---you never lower your osmolality below the thirst threshold and therefore are thirstier when ingesting a sports drink, whereas with water you maintain the osmolality right around the thirst threshold and drink and abstain as your thirst comes and goes. With sports drinks you instead just get thirstier, which seems kind of ironic since their slogan is "The thirst quencher!"

So those are some of the data that support our conclusions, and we hope that helps to clarify some of our interpretation(s) and conclusions. We will still post a "wrap-up" for the series on cramping in which we will try to briefly summarize the main points but more importantly leave you with some practical advice on this complex topic!

Muscle Cramps: Part II

The electrolyte depletion model of muscle cramps

In part one of this new series we tried to set the scene by providing some history in this area of muscle cramps. At times it might seem like we are a bit heavy on the historical side, but as we mentioned in one of our comments to Part I, understanding the historical record is crucial as often it helps us understand why we think what we do---and this affects one's interpretation of the science. In this post we will focus on the prevailing premise that dehydration and electrolyte disturbances cause muscle cramps.

The first important thing about this area of research is that Professor Martin Schwellnus is hands down the one researcher who has consistently moved this area forward. As a sports physician he has treated many a runner with cramps, and his curiosity and what he was seeing in the medical tents lead him to challenge this paradigm that dehydration and electrolyte problems cause cramps. What he found was that this model was based on not one shred of scientific data, and instead relied heavily on anecdotal evidence. Since 1997 he has published some of the only evidence available that has even attempted to determine what actually is causing the cramps and who is prone to this condition. The first paper he published in 1997 proposed a novel hypothesis for muscle cramps, but we will address that in Part III of this series.

The lab vs. the field

In our series on dehydration we discussed how the lab is not always translatable to the field, and vice versa, but that each has its own important role. Field studies are often cross sectional in nature, and although important we cannot assign direct cause and effect from them. However it is observations and findings from field studies that often lead to the very precise and mechanistic lab studies that are important in advancing our knowledge.

However one major obstacle in this area (cramping), is that no one has yet created a laboratory protocol in which we can reproduce muscle cramps in a controlled manner. Being able to do this is a crucial step in eventually identifying what causes them because it will allow us to make specific interventions to test what the effect is on cramps. So although we are still in the infancy of this area of research, the field studies are a very important starting point and have so far yielded important findings.

One study published in 1990 showed that there was no association between potassium levels and cramps. In that study cyclists rode for up to five hours. Some of the subjects did cramp, but their potassium levels were not uniformly high or low, thus showing no association between that variable and the cramps. However beyond that study (and one more that was presented at a conference but apparently not published) there is little real data out there to support or refute this hypothesis that dehydration or electrolyte disturbances cause cramps.

Study 1: Two Oceans Ultra Marathon

In a 2004 study published in the British Journal of Sports Medicine, Professor Schwellnus and his colleagues examined runners before and after the Two Oceans 56 km marathon in Cape Town. They measured quite a few variables, but since we are discussing changes in electrolytes and hydration, we will talk about those results. Remember that many people, both scientist and personal trainer alike, will profess that cramps are caused by dehydration and/or some disturbance in the electrolytes (sodium, potassium, magnesium, etc.) So the important finding from this 2004 study was that when the crampers were compared to the controls---who were matched for body mass and finishing time---the only differences were that the crampers had lower sodiums and higher magnesiums. The problem with this is that a lower sodium concentration suggests overhydration and not dehydration, and also if magnesium deficiency is meant to cause cramps then surely the crampers should have been lower here?

	Crampers (N = 21)	Controls (N = 22)
Sodium	139.8 ± 2.1	142.3 ± 2.1
Potassium	4.9 ± 0.6	4.7 ± 0.5
Magnesium	0.73 ± 0.1	0.67 ± 0.1
Osmolality	280 ± 6	284 ± 10

The relevance of this study is that if dehydration and electrolyte disturbances really play such a large role in cramps (as they are proposed to), then the crampers should have much higher electrolyte concentrations since they would be losing fluid and causing the concentrations to rise. Yet instead we see something entirely different, first that the crampers had lower sodium concentrations, and second that the crampers were not really different compared to the controls.

What is also noteworthy from this study was that the crampers had an average loss of body weight of 2.9%, compared to 3.6% for the non-cramping controls. In otherwords, the people who DID NOT cramp lost more weight than the people who did. It goes further than this, because Schwellnus et al were able to measure the change in plasma volume as well - a more direct measure for what is happening to fluids. Here, they found that the crampers actually gained a small amount of 0.2% during the race. The non-cramping control subjects LOST 0.7%. So the sum effect of this data is that it suggests very strongly that cramping is not associated with dehydration, or with lower serum electrolyte levels, which is what we have had drilled into us for many years!

The follow-up study from Iron Man - further evidence against serum electrolytes

The next year they published a study in Medicine and Science in Sports and Exercise, and instead of runners it was Ironman triathletes. According to what most of us hear day in and day out, it is these ultra-distance athletes who are exercising for 10+ hours at a time that must be most susceptible to dehydration and electrolyte deficiencies. After all, they are sweating for hours on end, and the numbers tell us that with so many liters of sweat lost then they must also be losing grams and grams of "essential electrolytes" such as sodium. Below you will see the basic data on these athletes, and the important finding here is that we see the crampers and controls were the same age and were similar in mass, had similar pre to post cahnges in mass, and also finished the Ironman in similar times:

	Crampers (N = 11)	Controls (N = 9)
Age (years)	33.5 ± 8.8	35.4 ± 8.1
Pre-race mass (kg)	79.1 ± 5.9	77.7 ± 6.4
Post race mass (kg)	76.3 ± 5.6	74.6 ± 6.5
Body mass loss (%)	3.4 ± 1.3	3.9 ± 2.0
Total race time (min)	660.8 ± 77.9	685.7 ± 48.5

So the two groups were essentially the same in that the crampers did not spend longer in the course or lose more weight (a crude measure of dehydration). Yet again the crampers and the controls looked remarkably similar on paper---except as in the 2004 study the crampers again had a statistically significant lower sodium concentration, and, we will repeat this, that suggests they were more hydrated compared to the controls. . .yet they were cramping. Here are the data from the electrolytes in the two groups:

	Crampers (N = 11)	Controls (N = 9)
Sodium	140 ± 2	143 ± 3
Potassium	4.4 ± 0.06	4.2 ± 0.5
Magnesium	0.9 ± 0.2	0.8 ± 0.1

Recall that what is most often put forward as the cause of cramps is either dehydration or some electrolyte disturbance, but the data from these two studies do not support that hypothesis. Although these are field studies and we cannot assign a cause and effect relationship, this available evidence suggests that these (normal) levels of dehydration do not appear to cause cramps. If these levels of dehydration did cause cramps and were largely responsible for cramps, then what we should see is a very high incidence of cramps in all of the race finishers with the same physiological characteristics as these subjects----or in other words, the vast majority of the race finishers.

Rejecting the old models

In science when the available evidence does not support the hypothesis, we must change the model. Based on this available evidence we see clearly that dehydration and electrolyte levels are not associated with muscle cramping during or after exercise, and therefore we must adopt a different model to explain what is causing them. We cannot just ignore the data we have shown here and keep on telling people that it is dehydration and electrolytes when new evidence suggests otherwise.

So in Part III of this short series we will lay out the newest hypothesis that tries to explain the "why" and the "how" of muscle cramps. It is novel and, as you might have guessed already, has nothing to do with electrolytes and dehydration! So come back and join us for Part III of this series, and then join us for the comments and debate!

See also:
Part I: Theories and fallacies of muscle cramps

References:
Brouns F et al., "Ammonia accumulation during highly intensive long-lasting cycling: individual observations." International Journal of Sports Medicine. 1990 May;11 Suppl 2:S78-84.

Schwellnus MP et al., "Aetiology of skeletal muscle 'cramps' during exercise: a novel hypothesis." Journal of Sports Sciences. 1997 Jun;15(3):277-85.

Schwellnus MP et al., "Serum electrolyte concentrations and hydration status are not associated with exercise associated muscle cramping (EAMC) in distance runners." British Journal of Sports Medicine. 2004 Aug;38(4):488-92.

Schwellnus MP. "Muscle cramping in the marathon : aetiology and risk factors." Sports Medicine. 2007;37(4-5):364-7

Sulzer NU et al., "Serum electrolytes in Ironman triathletes with exercise-associated muscle cramping." Medicine and Science in Sports and Exercise. 2005 Jul;37(7):1081-5.

Muscle cramp 'teasers'. . .

Apologies for the absence...and some muscle cramp 'teasers'

Ah, the joys of the University calendar! We must apologize for our somewhat lengthy absence - it has been 5 days since we last did a post, which I think is the longest break we've had since we began The Science of Sport in April earlier this year!

But we have good reason, for both Jonathan and I are both deep into marking and examination of undergraduate and post-graduate exams and theses at our respective universities. Though Jonathan and I both enjoy lecturing and find it very rewarding, when we reach mid to late-November, our disposition towards teaching changes somewhat, as hundreds of exam scripts and thesis work suddenly land on our desks for us to plough through! And funnily enough, the other work doesn't seem to realise it and let up!

So we do apologize for the break, but we're back now, hopefully with a bang, as we get stuck into a new series, this one on Muscle Cramps - Science and Fiction.

A follow on from fluids and dehydration

The series on muscle cramps is really an extension of our last series - Fluid Intake and Dehydration. In that series, we tried to explode some of the myths around drinking during exercise, describing how the prevalent "scientific" advice was in fact flawed (sadly, it's often fatally flawed). We looked at the claims and counter-claims and ultimately encouraged everyone to do the wise thing - listen to your body, and when it says you're thirsty, drink! But only then...don't let the fluid companies tell you that you're the only mammal too stupid to know when to drink by itself!

Introducing muscle cramps - some points to ponder

The muscle cramp story is similar, sadly. In South Africa, we have a host of companies who produce cures, preventative tablets, creams and liquids to help you avoid cramp. The premise, as was the case with fluids and dehydration, is that a cramp is caused by a depletion of some electrolyte - sodium, potassium, calcium or magnesium. All have been mentioned, and most often, it's sodium and magnesium that take the brunt of the blame.

We'll take a step by step journey through muscle cramps in the series. We'll tackle it in three parts:

1. What is a cramp? Very brief history and overview of what we know, and how we know it.
2. The electrolyte-dehydration-heat theory for muscle cramps
3. An alternative view - evaluating the gaps in the theory

So that is what you can look forward to (or with dread, as the case may be!) over the next week.

Until then, here are some issues to ponder:

• Despite the theory that muscle cramps are caused by electrolyte and fluid depletion, it has yet to be shown that people who cramp have lower electrolyte levels or are more dehydrated than those who do not. In fact, the studies have found that "Crampers" and "Non-crampers" have similar electrolyte and dehydration levels. Something wrong with that picture...

• If cramps are caused by electrolyte and fluid depletion, which muscles would be most likely to cramp? Would it not be ALL the muscles, because you're losing electrolytes and fluid through sweat, so then all the muscle groups should be vulnerable...yet for some reason, we cramp in the muscles we actually USE. Again, something out of place there.

(Some of you may already have a counter to these points, saying that what is happening in the muscle is not necessarily what is happening in the blood - we'll tackle that one for sure)

• And then finally, if you are reading this before heading off to bed, we hope that you don't experience the dreaded "Night cramp", which we're sure most of you have had at some stage. You wake up in the night, and feel a slight twinge, usually in the calf. Your first impulse is to point your toe, and when you do that, what happens? You may know that if you do this, you'll be writhing in agony instantly! Instead, what should you have done? The answer is you should stretch the muscle - stretching is the quickest way to get rid of cramp. Now, how do we explain that one according to a heat-electrolyte theory?

The answers to follow, so join us then!

Ross