Phun Physiology: Is excessive endurance exercise bad for the heart?

Maybe. This according to a study published this past week (June 4) in Mayo Clinic Proceedings by a team of cardiologists that bases its claims on a review of a number of animal and human studies.

Because the blogosphere was quick to pounce on the story (here, here, here, and here), I thought a short commentary might be appropriate. One that addresses the original article and whether it pertains to endurance cycling known as randonneuring.   

First of all, the researchers are not referring to daily, moderately intense workouts. Or to 2-3-mile runs four times a week. Nor are they referring to short intense interval workouts 2-3 times per week. In fact, the researchers acknowledge that these kinds of exercise regimens are extremely beneficial and may even add seven years to one’s life.

So what kind of activities does this particular team of cardiologists believe qualify as “excessive endurance exercise?” According to the article,   

[C]hronic training for and competing in extreme endurance events such as marathons, ultramarathons, ironman distance triathlons, and very long distance bicycle races . . .

Cycling? In an interview, the lead researcher, James O’Keefe, mentions the Tour de France and 200-mile bicycle races as examples of excessive endurance exercise.

Inferring from the article, it seems that for an endurance exercise regimen to qualify as “excessive,” it must be 1) almost daily, 2) hours at a time, 3) intense (racing), and 4) chronic (yearly).

The researchers have hypothesized that over time in some athletes excessive endurance exercise begins to remodel the heart in unhealthy ways. I’ve lifted the types of heart changes and their timelines from the article: 

. . . transient acute volume overload of the atria and right ventricle, with transient reductions in right ventricular ejection fraction and elevations of cardiac biomarkers, all of which return to normal within 1 week.

Over months to years of repetitive injury, this process, in some individuals, may lead to patchy myocardial fibrosis, particularly in the atria, interventricular septum, and right ventricle, creating a substrate for atrial and ventricular arrhythmias.

Additionally, long-term excessive sustained exercise may be associated with coronary artery calcification, diastolic dysfunction, and large-artery wall stiffening.

The phrase “patchy myocardial fibrosis, particularly in the atria” refers to tissue scarring in the heart’s two upper chambers—the atria. The heart’s electrical circuitry known as the pacemaker (SA-node) is located in the right atrium. Consequently, scarring there increases the likelihood of arrhythmias.

One type of arrhythmia known as atrial fibrillation can be particularly problematic, if not diagnosed and treated, since it can lead to sudden death. I shall say more about atrial fibrillation below.

  

It is important to note that the researchers view their thesis regarding the adverse cardiovascular effects of long-term excessive endurance exercise as tentative and that not all individuals may be susceptible to the aforementioned pathologies. In fact, the researchers note that “lifelong vigorous exercisers generally have low mortality rates and excellent functional capacity.”

It is extremely important to keep in mind that the occurrence of SCD [sudden cardiac death] during marathons, triathlons, and collegiate athletic events is rare and should not deter individuals from participating in vigorous ET [exercise training]; the benefits of regular PA [physical activity] to the individual and to society as a whole far outweigh potential risks. At the same time, long-term training for and competing in extreme endurance events may predispose to CV [cardiovascular] issues that are not seen in more moderate forms of PA.

Now the question: What does this study have to do with randonneuring? Nothing, unless randonneurs are also involved in daily, long-distance racing.  

But what about other studies? Of direct concern for randonneurs is the potential for atrial fibrillation, the chance of which increases in some individuals, who may have trained for but never competed in endurance-type races. This is the contention of Dr. Luis Mont, a Spanish physician, who 

reports that atrial fibrillation is more frequent in middle-aged individuals who formerly took part in competitive sports and continue to be active, or simply in those involved in regular endurance training without having actually participated in competitive sports.

Dr. Mont adds that

long-term endurance sport participation may well increase the incidence of cardiac arrhythmias, particularly atrial fibrillation, atrial flutter, sinus node dysfunction, and right ventricular premature beats.

Again, this pertains to a small proportion of the general population of endurance athletes. 

Here is a personal story—worth reading—of one cyclist who developed atrial fibrillation while on a bike ride and the outcome.

While many athletes use heart monitors as training aids, the usefulness of such devices extends well beyond training to include the detection of abnormal physiological states such as sudden spikes in heart rate—a possible sign of atrial fibrillation.

Should inexplicable heart-rate spikes occur in someone with whom you are riding, he or she should be strongly encouraged to get it checked out. Atrial fibrillation is something that is easily diagnosed and in many cases is treatable.

  

Be aware and be safe.

Let’s ride!

Update: Here is a link to Iron Rider, which has an important and related blogpost on atrial fibrillation in endurance athletes. 

Phun Physiology: Use It or Lose It?

Diagram from Ron's blog

This is dedicated to all my cycling buddies who have noticed that if we are away from the bike for a couple of weeks that our endurance begins to suffer. What’s going on here? Is it anything serious? Is there some point at which all of our previous conditioning goes for naught?

I’m referring here to the effects of complete inactivity on endurance, when a once well-conditioned athlete goes “cold turkey” and does not engage in any type of physical training for a particular time period, regardless of the reason.

Physiologists have studied the effects of training cessation on well-conditioned endurance athletes. The term they’ve coined for this type of inactivity is “detraining.” Detraining is different from either tapering or maintenance, both of which involve purposeful physical activity which guards against performance decline when athletes are not engaged in their normal training routines. Detraining is also different from the type of recovery in which a cyclist may be inactive for a few days following a long, multi-day ride, for example.

Detraining can result in the loss of physiological gains that have accrued in some cases from years of endurance training. Some of the declines begin to occur in as little as two weeks of inactivity. In one particular study that I use as a reference and whose results I report here, most declines begin to plateau at about 56 days of detraining. However, even the fully detrained athlete has greater endurance than a sedentary control who never trained.

What follows is a brief summary of some of the physiological declines affecting performance in endurance athletes and their timeline. Caution should be exercised in generalizing these findings to individual circumstances. As our riding buddy, Lin, so aptly puts it, “Your mileage may vary.”

12 Days of Detraining
In as little as 12 days of detraining, there are perceptible physiological changes affecting performance.

Most notable to athletes themselves is an increase in perceived exertion during sub-maximal exercise accompanied by an increased heart rate.

What’s happening? At the cellular level, there is a decline in the activity of muscle mitochondrial enzymes. These enzymes convert fuel in the presence of oxygen to the high-energy molecule—ATP—which powers muscles. With a decrease in enzyme activity, muscles cannot work as hard, since there is less ATP. The mitochondrial enzymes rather than oxygen have become the limiting factor. It is easy to understand why VO2 max, which is a measure of the peak volume of oxygen the body consumes during a given time period for a given body weight, declines. VO2max is sometimes taken as an indicator of endurance potential.

During this same time period, there are metabolic changes. Muscles begin to shift away from using fat to using carbohydrate for energy. Ironically, however, a muscle’s ability to store carbohydrate—in the form of glycogen—begins to decline with detraining and, unfortunately, returns to baseline levels within just a few weeks of detraining. Moreover, because carbohydrates provide less energy than fats, the athlete who is detraining pays double. One particular study notes the abrupt onset of these latter changes with detraining:

These metabolic changes may take place within 10 d[ays] of training cessation.

21 Days of Detraining
At 21 days of detraining, the aforementioned declines continue, while others become noticeable.

The reduction in fat metabolism has decreased now from 24% of energy utilization to 7%.

The rate of decline in muscle mitochondrial enzyme activity, which was first noticeable after just 10-12 days of detraining, has accelerated.

Ventilation (breathing) has increased significantly from day 12 of detraining.

Other noticeable changes at this time include declines in blood volume (mostly plasma); stroke volume; and VO2max. Meanwhile, peripheral resistance in blood vessels has increased.

What does all this mean? An increase in peripheral resistance means that the heart must pump harder to get blood to the tissues. Because stroke volume (the amount of blood the heart pumps with each contraction) has decreased, heart rate must increase to compensate.

In contrast, well-conditioned athletes possess the opposite cardiovasculature: low peripheral resistance, low pulse, and high stroke volume. Moreover, conditioned athletes store more glycogen (while burning it more efficiently) and metabolize fat better than detrained athletes.

56 Days of Detraining
At 56 days of detraining, many of the aforementioned declines begin to plateau.

VO2max appears to stabilize as does the activity of mitochondrial enzymes, with values still 50% above those of sedentary controls.

Moreover, there is no reduction in muscle capillarization, the amount of small blood vessels serving the muscles. However, stroke volume and mitochondrial enzyme activity have declined to control, or baseline, levels.

By this time, there is a noticeable change in the type of skeletal muscle fibers (cells) brought about by inactivity. Broadly speaking, skeletal muscles are made up of type I and type II fibers, type I being preferred by endurance athletes due to their resistance to fatigue during aerobic exercise. There are also two types of type II muscle fibers—type IIa and type IIb. Type IIa is preferred over type IIb for the same reason that type I is preferred over type II. While there is no loss of type I muscle fibers, detraining results in the conversion of a percentage of type IIa fibers to the less-preferred type IIb fibers. In fact there was an increase in type IIb fibers from 5% to 19% as a result of detraining

60 Days of Detraining
At 60 days of detraining, there is measurable atrophy (decrease in thickness) of the heart’s muscle wall and, consequently, its ability to pump. This corresponds to the decrease in stroke volume noted earlier, necessitating a faster pulse.

84 Days of Detraining
At 84 days of detraining, the once highly conditioned endurance athlete still has 50% more mitochondrial enzyme activity than the sedentary individual who has never trained.

Additionally, the former still enjoys 22% better lactate dehydrogenase (LDH) enzyme activity over controls.

The more LDH activity an individual has the greater is his or her lactate threshold. An athlete with a high lactate threshold is able to exercise at a higher level aerobically than an athlete with a lower lactate threshold. The lactate threshold is the point at which an athlete begins metabolizing anaerobically. (Anaerobic respiration is incompatible with endurance cycling.) This occurs because lactate, which is a by-product of anaerobic respiration, interferes with other metabolic pathways. LDH removes lactate (or what some refer to as lactic acid). It follows from this that an athlete’s LDH enzyme activity is a good indicator of aerobic or endurance conditioning (capacity).

Summary
It is true that an endurance athlete’s performance begins to suffer as a direct result of inactivity even in the space of ten days. The good news is that performance decline is not progressively linear as a function of time of inactivity. While we may lose our competitive edge quickly, the physiological declines of inactivity begin to plateau at about 56 days with the exceptions of stroke volume and glycogen storage capacity both of which continue to decline to baseline, or control, levels. Consequently, the detrained athlete will still be able to outperform the sedentary individual who has never trained. Even the pumping action of the heart of a fully detrained fifty-year-old male is as strong as that of a much younger male who has never trained.

There are ways that endurance athletes with limited time to condition can stave off the adverse effects of detraining, that is, if they can manage short, intense workouts known as interval training. One possibility for cyclists who wish to maintain their present conditioning level is speed training. According to some:

[S]peed endurance training can maintain muscle oxidative capacity, capillarization, and endurance performance in already trained individuals despite reduction in the amount of training.

Another group maintains that athletes who are able to train as little as once per week at 70% VO2 max are still able to maintain their aerobic conditioning level.

Summary of Physiological Effects of Detraining
Heart rate increases as well as total peripheral resistance
Blood volume decreases (mostly the plasma portion)
Stroke volume decreases to baseline levels
Cardiac output decreases
VO2max decreases
Conversion of some type IIa skeletal muscle fibers to type IIb muscle fibers
Lactate threshold decreases
Ventilatory efficiency decreases while rate increases
Fat metabolism decreases while carbohydrate metabolism increases
Resting muscle glycogen levels decrease
Mitochondrial enzyme activity decreases


Let’s ride!

Phun Physiology: Endurance Exercise Performance — Speed or Power

Ever wonder why one endurance athlete—say, cyclist or marathoner—is faster than another, or what it might take to get faster, short of a heart and lung transplant or a new pair of genes (although we might not be able to skip the part about the pain and suffering of hard training)?

Now there is something for us academic types who are completely comfortable sitting on the sideline allegedly exercising our brains while telling other people how they can go faster by invoking pain and suffering on them.

Last year, a couple of physiologists—Joyner and Coyle—at the Mayo Clinic devised a model, which is a review of known factors, how they interact, and their ability to predict endurance performance (i.e., speed or power) in elite athletes. The authors are quick to point out there are still some important unknowns, including genetics, psychology of motivation, and aspects of neuromuscular interactions.

Thus, the model can be thought of more as a summary of current understanding, food for thought, and/or a generator of new ideas, rather than the last word on the subject. Such are models in science.

Regarding the different variables and their interaction as they relate to endurance performance, we’ve known for some time, for example, that there is more to the equation than just VO2•max , since two different athletes with the same VO2•max can possess different levels of endurance. No doubt, lactate threshold (LT) is also an important consideration in endurance performance. While many believe LT to be the most important indicator of endurance performance, this is highly contentious at best. The present model accounts for the relationship between these last two factors, or what Joyner and Coyle call “the oxygen consumption that can be sustained for a given period of time,” a concept the authors have dubbed “performance VO2.”

How other variables such as cardiac output, hemoglobin content, maximum heart rate, and the relative abundance of type I (slow twitch) muscle fibers, for example, affect endurance performance are also discussed.

The authors describe their tripartite model as follows:

VO2•max and lactate threshold interact to determine the ‘performance VO2’ which is the oxygen consumption that can be sustained for a given period of time. Efficiency interacts with the performance VO2 to establish the speed or power that can be generated at this oxygen consumption. This review focuses on what is currently known about how these factors interact, their utility as predictors of elite performance, and areas where there is relatively less information to guide current thinking.

Having been provided the various known factors governing endurance performance, an interested party can do some research to determine which ones can be improved upon and how this might be done through training.

The original article that appeared in the Journal of Physiology is located here with useful hotlinks for many of the reviewed references quoted therein.

He said, she said, NSAIDs: Ibuprofen and Endurance Athletes

Although probably not the last word on the subject, an editorial this year in the British Journal of Sports Medicine (BJSM) sounds a cautionary note concerning the widespread prophylactic use of ibuprofen among endurance athletes. Prophylaxis is the use of ibuprofen for pain prevention: taking it before exercise. The author claims that not only does prophylactic use of ibuprofen not reduce pain but, in fact, slows tissue healing.

The BJSM editorial was picked up by and introduced in a recent New York Times blog article, which provides a section for readers’ comments.

Neither article is a difficult read. Both provide hot links to abstracts or in some cases to the original research they quote.

Phun Physiology: Hydration Science for Endurance Athletes-The Hydration Triangle

It’s that time of year when the thoughts of endurance athletes turn to fluid intake, a topic motivated by the knowledge that too little or too much water is bad. Even slight dehydration amounting to just 1% of body weight loss adversely affects athletic performance. On the other side of the continuum, overhydration can easily lead to life-threatening hyponatremia.

As my title suggests, the emphasis here will be more on hydration science and less on its application. But why would anyone want to write about—much less read—something as esoteric as the science of hydration? Although application may be at the top of the list of things endurance athletes want to know, and although hydration science does not pretend to provide answers for all the specifics of application, it is nonetheless useful for a few good reasons.

First, hydration science may provide a means for adjudicating between some of the opposing claims we endurance athletes encounter on the topic of hydration. Secondly, it serves both as an excellent starting point and solid foundation for developing personal hydration strategies. Third, some of us might well enjoy learning about science and the history and philosophy of science as it relates to hydration. While we might be inclined to agree with this last reason, if only for pure entertainment value, there is more to it than meets the eye.

The fact of the matter is that most of the resources to which endurance athletes turn to obtain advice on hydration omit the greatest discovery of hydration science of the last century. Obviously, lost too is the importance of this discovery for endurance athletes.

Let’s begin with a “fun” one-question, multiple-choice test to see how much you really know about hydration. After reading the question, choose the one best answer from those listed after the question:

What is the most efficient way for an athlete to stay hydrated during an endurance sporting event?

A. Drink water
B. Consume electrolytes
C. Consume carbohydrates
D. Answers A and B
E. Answers A, B, and C

According to hydration science, answer “E” is by far the best answer, although endurance athletes will rarely if ever encounter this direct advice for hydrating. Read on if you are interested in learning why “E” is by far the best answer.

You may already know that answer “A” is wrong, since drinking water without consuming electrolytes may prove fatal by causing hyponatremia. But were you also aware that drinking popular sugar-based sports drinks during endurance events can also lead to hyponatremia? The reason is that the solute concentration they contain is too dilute. What about the practice of athletes diluting these sports drinks simply because they taste too sweet? Isn’t this even worse? Well, of course it is.

If you picked answer “D,” at least you are doing a little better than if you’d picked answer “A.” You’ve avoided hyponatremia. But the bottom line: it’s still a wrong answer, since the question deals with the best way to stay hydrated, not how to avoid hyponatremia. The science of hydration tells us how to do both. But back to answer “D,” which is the advice you are most likely to encounter on most athletic, health related, and nutritional web sites. This mainstream advice on hydration usually assigns one of two roles to electrolytes. You may already know, for example, that endurance athletes must replace electrolytes lost in sweat in order to maintain proper nervous and muscle function. Obviously a good reason to take electrolytes! Additionally, we are advised—rightly so—to ingest sodium (salt, sodium chloride, electrolytes) in order to maintain proper osmotic balance in the blood and extracellular fluid. A few sources may go a step further in suggesting that the electrolyte, sodium, plays an enormous role in maintaining water balance. But a crucial element has been omitted. Without it, hydration suffers.

You may still be wondering how, as the correct answer “E” suggests, the consumption of carbohydrates relates to efficient hydration. The answer is not simply that carbohydrates fuel the hydration process, something they accomplish long after they’ve been absorbed. Carbohydrates in the form of glucose play a more immediate role in hydration, along with sodium, as an obligatory co-transported item. In other words, a sugar-saline solution in the small intestine is absorbed much, much faster than a saline solution alone. Whether the science interests you or not, you can simply memorize what I coin here as the “hydration triangle,” the fact that there are three ingredients that must be present in the small intestine at the same time to ensure efficient hydration: salt, water, and sugar. If you take away the sugar from this mix, then water absorption (i.e., hydration) slows fourfold. Yet, this scientific fact is rarely, if ever, part of the advice given to endurance athletes on hydration. In what follows, I shall ask the reader for indulgence as I present a little of the science of hydration after which I shall finally raise a few important considerations and challenges on the side of application as a reward for that indulgence.

I shall start with a history lesson. Different people in different places independently discovered that drinking a solution of water, salt, and sugar was an excellent antidote for water-loss associated with diarrhea. Almost three millennia ago, for example, Susruta, the father of Ayurvedic medicine in India, advised that warm water into which rock salt and molasses had been mixed was effective for treating diarrhea. Similar recipes were tried over the centuries for combating the life-threatening dehydration associated with cholera. But without the science providing an underlying causal mechanism, successful oral rehydration therapies consisting of water, salt, and sugar never entered mainstream medicine and remained mere historical anecdotes. Once the science became known, however, it provided focus for life-saving treatment. One hydration scientist notes:

There are few more telling examples in the history of medicine where the credibility provided by a firm basic science foundation played a greater role in translational research.

This is in reference to the fact that focused treatment based on the science has saved countless lives from cholera. This lead an editor to write in the prestigious medical journal Lancet that . . .:

The discovery that sodium transport and glucose transport are coupled in the small intestine so that glucose accelerates absorption of solute and water was potentially the most important medical advance this century.

Stanley Schultz illustrates the problem posed by water loss due to cholera and the miraculous role played by the applied science:

Death is the result of dehydration and circulatory collapse complicated by metabolic acidosis and can occur within hours of the onset of symptoms. Indeed, one of the terrifying aspects of the disease is that an individual in the pink of health in the morning might turn into a shriveled corpse by the evening.

The point I’m trying to make here regarding the effectiveness of hydration in the presence of sugar is illustrated by this last example. Still used in the treatment of cholera, oral rehydration therapy is sufficiently effective not only to catch up with but get ahead of and finally reverse the effects of even extreme dehydration. The small intestine is capable of absorbing 8L of fluid in a single day!

Now that the important medical history lesson is behind us, let’s wade a little bit into the history of science, the philosophy of science and, while we’re at it, why not a little bit of science, itself?

First up is a lesson in the history of science. Scientists have known for some time that living organisms have no direct way of pumping water into and out of cells in spite of the fact that such water movement is vital to life. Additionally, scientists knew that water moves across cell membranes by following solutes, a process called “osmosis.” But osmosis is a slow, passive process. By the early 1960s, scientists became aware of sodium “pumps,” which we now know occur in great numbers in all cells of all organisms. These pumps actively move ions across cell membranes, creating ionic gradients which water then follows. Because this sodium-potassium ATPase pump is able to create ionic gradients, it uses energy—ATP—which is obtained by the oxidation of glucose inside cellular organelles called “mitochondria.” While the presence of these sodium pumps accounts for much of the water movement at the cellular level, they cannot account for the much more rapid water movement that occurs in the small intestine in the presence of sugar-saline solutions. Could this mean that another type of pump exists, one that can account for the rapid water movement (i.e., hydration) that occurs in the presence of a sugar-saline solution in the small intestine?

Now it’s time for the philosophy of science lesson. This allows an explanation of what I mean by the term hydration “science.” Isn’t science based on observation? If so, isn’t knowledge of the observed fact that water absorption increases fourfold in the small intestine in the presence of sugar enough to satisfy scientists? Isn’t this the scientific discovery alluded to above by Shultz that placed oral rehydration therapies on solid footing? Not really. This is not science in the manner scientists understand science.

Science seeks to explain how the world works. It does so by developing and testing explanatory theories to describe visible events. Here science sought to learn what mechanism was behind, or causing, the observed fact that sugar speeds the rate of water absorption in the small intestine. Science advances by proposing the existence of novel entities and process in order to explain a particular event. Such descriptions are called “theories.” By their very nature, scientific theories deal in speculation. This entails postulating hypothetical—or, yet to be discovered—entities responsible for visible events. Hydration science took a huge leap in 1964 when Schultz proposed the existence of a co-transporter molecule in the small intestine to explain how sugar might be involved in rapid intestinal water absorption. The hypothetical model proposed a new type of transporter molecule, one that simultaneously ferries sodium and glucose. Experiments designed to rule out alternative explanations—such as glucose being used as an immediate energy source, rather than acting simply as an obligatory co-transported item—provided strong evidence for the existence of the sodium-glucose co-transporter. Eventually, the actual existence of the co-transporter was established and its molecular nature was determined. In other words, the sodium-sugar co-transporter had been discovered by science. Here Schultz explains the science behind the discovery:

. . . our model could readily explain the observation that fluid absorption is increased by glucose. We now know that for every glucose molecule absorbed, two sodium ions and two counterions (mainly chloride) must also be absorbed; thus, glucose augments total solute (and, therefore, water) absorption approximately fourfold.

Furthermore, he explains corroboration of the discovery, the evidence that the sodium-sugar co-transporter actually exists . . .

. . . the Na-coupled sugar carrier . . . first cloned and sequenced by Ernst Wright and coworkers, is [now] referred to as [the] Na-coupled glucose transporter (SGLT1).

My “hydration triangle” entails not only the discovery of the co-transport molecule but its successful translation. The stepped-up hydration afforded by the sodium-glucose pump requires a sugar-saline solution in the small intestine. Neither a water solution nor a saline solution is sufficient to activate the sodium-sugar transporter. According to the hydration triangle, the only things an athlete must supply during an endurance event are water, sodium, and glucose, given that the sodium-glucose transporter is already in place and that chloride ions usually accompany sodium ions in most food sources.

One last philosophy of science lesson is needed before I turn to application. There is a reason why scientific laws, principles, theories, even models, are difficult to apply to the real world. Scientific models like the sodium-sugar transporter do not mirror reality. They are simplifications of reality, representing only those aspects of reality we wish to consider at any given time. As such, simplified working models cannot perfectly predict outcomes in the real world, which is incredibly more complex. This implies that prediction is only one of several goals of good theories and models, but certainly not their main goal. In other words, scientific models work perfectly in their perfect worlds, not in the real world where other influences, many of them unaccounted for, influence outcomes. This is one of the paradoxes of scientific understanding regarding the relationship between scientific laws and the observable world which do not always match. Richard Feynman suggested:

There is . . . a rhythm and a pattern between the phenomenon of nature which is not apparent to the eye, but only to the eye of analysis; and it is these rhythms and patterns which we call the Physical Laws . . .

Try to envision the point this way. One may have a good, bad, or indiferent experience with a particular sports drink which is a sugar-saline solution. Either way, the experience neither adds to nor subtracts from the basic science of hydration. Each application of science comes with its own complex set of special circumstances whether known, unknown, or even knowable. I’m ready now to present a shopping list of run-on considerations when applying hydration science.

One must be careful not to attribute too much to or to the exclusivity of the sodium-sugar model. First, there are several means by which water is absorbed in the small intestine, including amino-acid co-transport pumps, although the SGLT1 pump presented here is by far dominant. Second, the model presented here does not account for the fact that glucose may not be the only sugar transported with sodium, although it is the most important sugar. None of this changes the validity of the hydration triangle—water, salt, and sugar—a model that is supported by the following comment by an international team of researchers:

In the human intestine we estimate about half of the 8 liters absorbed each day occurs by cotransport and the other half occurs by osmosis through cotransporters. This would account for the intimate link between sugar, salt and water transport . . .

Further, the fact that the obligatory co-transported sugar is glucose in no way obligates athletes to directly consume glucose. Many types of carbohydrates, including sugar sources like maltodextrin, are enzymatically digested to glucose when they reach the small intestine. The model also does not account for the fact that other sugars besides glucose are absorbed by their own transporters. The claim has been made that a 2:1 ratio of glucose to fructose is absorbed faster than glucose alone. Another study indicates that a glucose-fructose-sucrose sugar combination is absorbed even faster. Critics of simple-sugar formulations contend that while this may be true, the studies which included these findings indicate that exertion was only at 50-55% maximum power. These same critics contend that the absorption rate provided by a blend of sugars is insufficient for either higher energy output or for endurance sports.

Another application consideration has to do with the concentration of sugar solutions in the stomach, which directly affects stomach emptying and the subsequent rate of intestinal absorption. If the sugar solution introduced to the stomach is too concentrated—estimates put the upper limit between 6-8%—gastric emptying is delayed. If the athlete continues drinking overly concentrated sugar solutions, the chances of stomach discomfiture increase, including nausea, and vomiting. If, on the other hand, athletes drink formulations with lower sugar concentrations, they may run up against other problems. One problem is caloric intake. Many sports drinks containing simple sugars do not provide sufficient calories for endurance athletes. Taste is not always a sufficient determiner of sugar concentration. Late in endurance events, the taste threshold for sweets decreases, meaning that sports drinks containing simple sugars taste even sweeter. Athletes who dilute what was already a dilute drink obtain even fewer calories. The practice of athletes diluting sugar-based sports drinks poses a second potential problem. Many popular sugar-based sports drinks do not contain sufficient amounts of sodium for endurance athletes. Diluting them further exacerbates the problem and may even lead to dilutional hyponatremia. According to one source,

The Endurance Formula, introduced in 2004, contains twice the sodium and three times the potassium than the typical Gatorade formula, as well as chloride, magnesium, and calcium to better replace what athletes lose while training and competing.

Some critics argue that in spite of reformulation the sugar concentration issue still lingers. These same critics believe that the only way endurance athletes can get sufficient calories is to consume solutions containing carbohydrates that can pass quickly through the stomach but that do not increase the osmolar concentration in the stomach above the tolerable limit. This means that the upper limits of osmolar concentrations of maltodextrin translate to 15-20% solution concentrations which can also provide up to three times the calories as compared to simple-sugar solutions. Also, because they don’t taste as sweet as simple sugars, athletes can tolerate higher concentrations of complex carbohydrates in their drink formulas.

The scientific models I present here do not directly address the ongoing debates focusing on how much fluid and electrolytes an endurance athlete should consume. The opposing camps base their recommendations on different sets of assumptions. One side argues that what is lost in sweat must be replaced. Others argue that because the maximum rates of absorption for water, sugar, and electrolytes are less than the rates at which they are used or lost, it is impossible to try to replace them at these higher rates, since it may unnecessarily trigger compensatory mechanisms. Both sides of the issue offer replacement guidelines.

Application is also made more difficult by the fact that as some research suggests not only conditioning but heat acclimation decrease perspiration rate and sodium loss in sweat.

We must also consider the fact that because the sodium-sugar transporter is a protein, there may be a genetic component to an individual’s ability to hydrate efficiently.

The list of considerations goes on.

I need to state a cautionary note. Although all the talk here has been about water, salt, and sugar, there is absolutely nothing wrong with consuming regular food during endurance events for either or both electrolyte and carbohydrate sources. Another corollary: don’t attempt to fix that which isn’t broken. In other words, if you are having no great problems with hydration, don’t change something just because you read this article. Many of the food items athletes might normally consume during endurance events are compatible with the hydration triangle. It doesn’t matter whether the food is solid or in liquid form. It’s personal preference that matters.

Consider, for example, a can of V8 juice. One can supplies 29% and 19% of the daily values of sodium and potassium respectively, not to mention almost 12 ounces of water and 14 grams of carbohydrates. Plus, it can be purchased cold, which increases absorption! Do you want carbohydrates with salt? Try a small bag of pretzels washed down with your favorite beverage. Normally, I avoid soft drinks, which are at the high end of the tolerable absorptive limit for sugar solutions. But hours into an event, I’ve been known to consume them, perhaps for the sugar, the salt, the caffeine, the fluid, the taste? Otherwise, I generally prefer maltodextrin-based formulations in my drink bottle in combination with electrolyte supplements all washed down with cold water from my hydration pack. This does not mean that I won’t have a regular sit-down meal with riding buddies during an event, something that I personally find extremely satisfying.

In summary, the hydration triangle introduced here represents, I believe, a good translation of basic hydration science. It notes the three items endurance athletes must ingest during an endurance event to ensure maximal hydration: water, salt, and glucose source. The availability of glucose in the small intestine—in addition to water and sodium chloride—ensures a fourfold increase in hydration above that if glucose were not available. This is due to the utilization of the Na-coupled glucose transporter (SGLT1). We need to be reminded that there are many ways to satisfy the hydration triangle based on personal preference and need. This obviously entails some knowledge of the nutritional content of available food during endurance events and one’s responses to these foods in view of our own physiology and the physical challenges we confront and accept. Because science provides information in ideal settings, it becomes the responsibility of each endurance athlete to develop a suitable, tailor-made personal hydration strategy based on individual needs.

The ideas presented here go beyond the typically stated reasons for utilizing carbohydrates as fuel and electrolytes for maintaining ionic balance and muscle and nervous function, however important. The science tells us that efficient hydration during endurance events calls for a sugar-saline solution in the small intestine in part to activate the sodium-glucose transporter first discovered in the mid-1960s. I believe both the science and its application are captured by what I’ve termed here the hydration triangle.