Phun Physiology: Does a hot drink cool better than a cold one?

The Cup of Tea, ca. 1879. Mary Cassatt (American, 1844–1926)

 Oil on canvas (Wikimedia public domain)

Now that the dog days of summer are chasing my wheels, I decided to research an astonishing claim I recently read on a cycling listserv about keeping cool. I’ve included links to references for the interested reader.

My search led me to not one but two popular-press articles published a year ago asserting that a cup of hot tea could cool cyclists better than a cold beverage. If there is any merit to the claim, then American cyclists ought to institute afternoon tea not just for propriety, but also for safety and performance.

A team of researchers at the University of Ottawa made the remarkable discovery that drinking a hot beverage triggers a sweat response which is more than able to compensate for the warming effect of the hot beverage.

The finding begs the question of whether turning on the sweat spigots leads to greater cooling in all cases. The lead researcher, Ollie Jay, notes that the cooling effect of drinking a hot beverage does not hold in all situations. He states:

The caveat is that your sweat must fully evaporate in order to produce the desired cooling effect. If you’re exercising hard, or wearing too many clothes, or in a very humid environment, you may produce sweat more quickly than it can evaporate, in which case it’s no longer desirable to ramp up your sweat rate further.

The tell-tale sign of producing too much sweat? When beads of sweat drop to the ground. At this point, evaporative cooling is not occurring. And there is no advantage to increased sweating. Jay states, “if the sweat’s not going to assist in evaporation, go for a cold drink.” Jay notes,

[I]f you’re in a humid locale—for example, anywhere on the East Coast—don’t try drinking hot water. But on a hot day in the desert, a cup of hot tea might actually be the trick to help cool you down.

Other studies support the intuitive notion of drinking cold beverages to stay cool. One study by Lee and Shirreffs (2007), for example, reports that at 25.4C [77.7F] and a relative humidity of 61%, exercising cyclists who drank cold beverages had significantly lower skin temperatures and lower pulse rates than cyclists who drank warm fluids.

Yet another study by Burdon et al. (2010) conducted at 70% relative humidity and 28C [82.4F] reveals that

Consumption of cold beverages during prolonged exercise in the heat improves body temperature measures and performance.

This team of researchers postulated,

Beverages consumed by athletes exercising in the heat should perhaps be cold for performance and safety reasons.

In sum, it is probably safe to assume that the heat and humidity of North Carolina summers warrant cold drinks all around, especially if you are working hard! 

What’s your cup of tea?

Let’s ride!

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: Cycling regularly may make you smarter . . .

Findings of a recent study out of Dartmouth College support the claim that regular, aerobic exercise makes some humans smarter. The recent popular-press article, which alerted me to this fact, states that

in about 60 percent of the population, [exercise] may be responsible for the expression of a gene that floods your cells with “brain derived neurotrophic factor" — or BDNF — a protein that is thought to help with mental acuity, learning and memory.

In terms of their memory of novel objects, subjects who performed moderate aerobic exercise for four weeks, including exercise on the day of the test, performed better than subjects in the other three test groups: 1) those that exercised for four weeks but not on the day of the test, 2) those that exercised only on test day, and 3) those that did not exercise the four weeks prior to the test.

According to the lead researcher, the key is regularity rather than intensity and also exercising more than half of the days of the week.

I'm operating under the assumption that until it’s proven that I don’t have the exercise-makes-me-smarter gene, I’ve got one more “reason” for cycling regularly.  

Let’s ride!

Phun Physiology: Salt-Stain Science

Want to make a fashion statement? What better way of saying, “I’ve been sweating profusely,” than with white salt stains on black lycra!

Salty SweatersJust because someone’s cycling clothes are covered with salt doesn’t necessarily mean they are a heavy or even “salty sweater.” For example, one might expect the clothes of endurance athletes whose events last several hours to be salt encrusted. On the other hand, what about exercises in which athletes participate for the same time duration? In this case, the crusty accretions of salty sweaters are telltale. One report indicates that 10-15% of Florida State University football players are considered salty sweaters. But what does this mean? And is there something about which athletes need to worry?

While we know that a small percentage of athletes are considered “salty sweaters,” the underlying cause is elusive. Do salty sweaters just sweat more than their counterparts, or does their diet consist of greater sodium intake than their peers? In the absence of specific scientific studies, there is no clear answer. However, many experts believe there may be a correlation between high dietary salt intake and excessively salty sweat. Moreover,

Research is increasingly showing that salty sweaters are at greater risk for muscle cramps and dehydration.

Experts all agree that athletes need to replenish some of their salt loss during endurance events, whether or not they are salty sweaters.

On this note, although, the spokespeople at Hammer Nutrition believe that salt stains are not an indication that an athlete has completely depleted his or her salt reserves, they still believe that electrolyte intake during physical activity is important for promoting fluid and electrolyte balance and proper physiological functioning. They state that:

Salt stains on jerseys and shorts are NOT an indication that the athlete is sodium depleted. Rather it is the body excreting excess amounts due to an over abundance in the body.
The overabundance of dietary sodium theory as the cause of salt stains is echoed by others.

It is hypothesized that salt stains arise as a result of the body attempting to rid itself of excess sodium. Laboratory results seem to support this claim.

We know consuming high sodium converts into high sodium loss in sweat and urine. We know consuming low sodium converts into lesser sodium loss in sweat and urine than high
sodium.


Is Sodium Loading Beneficial?A team of researchers has empirical data supporting the claim that there may be some benefits for sodium loading. Sodium loading as the term suggests refers to the practice of drinking a salt solution prior to exercising. The title of their study published in what is dubbed the Official Journal of the American College of Sports Medicine couldn’t be any clearer on the matter: Sodium Loading Aids Fluid Balance and Reduces Physiological Strain of Trained Men Exercising in the Heat.


High Dietary Sodium Intake is Very UnhealthyIn spite of the fact that the practice of sodium loading appears in the Official Journal of the American College of Sports Medicine, I shall throw a cautionary flag. The practice of sodium loading notwithstanding, the article is not suggesting that a high daily salt intake is healthy for anyone, including athletes.

In fact, when faced with high dietary salt intake, the body responds by increasing blood pressure in an effort to mitigate sodium toxicity. Over time this can lead directly to hypertension and heart disease.

From the mid-1980s to the late 1990s, the amount of salt used by the average American increased by about 55%. It is estimated that Americans eat 5-6 times what a natural diet would provide without salt added.

Serious consideration should be given to reducing dietary sodium, given the causal connection between high-salt consumption and coronary artery disease.

The good news, however, is that lowering sodium intake reduces blood pressure. Additionally, dietary supplementation of a few minerals normally deficient in the American diet—magnesium, potassium, calcium—taken either singly, or in combination, reduce(s) blood pressure.

On this note, it is thought that Americans get only 43% of the recommended daily amount of potassium, only 60% of magnesium, and 35-50% of calcium. Consequently, reducing sodium intake while increasing potassium, magnesium, and calcium intake to normal levels can have a powerful blood-pressure lowering effect.

While some promote dietary supplementation of magnesium, potassium, and calcium, the proper amount of these minerals can be found in non-processed foods, including fruits and vegetables.

RecommendationsIt seems to be clear that proper fluid and electrolyte balance prevents cramping, especially with athletes who are “salty sweaters” when performing in the heat. Regardless of whether one is a salty sweater or not, the recommendations are the same for everyone:
1) Reduce daily sodium intake, if it is high.
2) During endurance events, consume an electrolyte supplement along with fluid and food intake.
3) I’ve argued elsewhere that because of cellular co-transporters, hydration is much more efficient when water is consumed along with both electrolytes and food (i.e., glucose and amino acid sources).
4) There is no reason to believe that so-called salty sweaters should consume more than normal amounts of electrolytes during exercise. In fact, some experts believe that consuming too much salt during exercise may upset the delicate hormonal balance and thus the body’s ability to maintain proper electrolyte balance as the body attempts to rid itself of sodium and, inadvertently, water.


Let’s ride!

Phun Physiology: Pickle Juice and Muscle Cramps

You’ve probably heard of the latest quick fix for muscle cramps: pickle juice. Is there anything to the claim that a few slurps of the sour brine actually stops muscle cramps? Moreover, what does the science say, if anything, on the matter? Stay tuned.

There have been many anecdotal testimonies claiming that pickle juice not only prevents muscle cramps, but that it relieves muscle cramps faster than anything else on the store shelf. And as randonneurs, we know that the worth of any convenience store is measured by the shelf space allotted to pickles.

The only problem sometimes is deciding which one!

Do you think that maybe some people may not find the mixture of vinegar (acetic acid) and salt (calcium chloride, sodium chloride) in water very appetizing?

Pickle juice has also been commercially packaged. This link to a YouTube video shows someone demonstrating how to drink pickle juice.

Every kid knows that the worst thing about medicine is taking it. But maybe, just maybe, we don’t actually need to drink pickle juice in order to receive its benefit! Read on . . .

Apparently, pickle juice does stop cramping. In controlled experiments, researchers have discovered that drinking pickle juice stops cramping in just over a minute, while water provides no relief from cramping.

However, because cramping ceased immediately, researchers now believe that the positive effects of the sour elixir are not due to its having been absorbed by the body. In other words, while pickle juice contains salt and fluids—which are known to alleviate cramping—they haven’t had time to re-establish proper fluid and electrolyte imbalances in slightly dehydrated human subjects. There goes one hypothesis out the window.

There’s more. Unless you really had your mind set on it, you can actually forego both the pickle and the briny solution, since research has also indicated that drinking vinegar by itself will relieve muscle cramps.

Not appealing, but you’re still in a pickle?

Don’t worry. Apparently, you don’t even have to swallow the vinegar!

In their search for a scientific explanation, researchers have hypothesized that there may be some specialized sensory receptors in the mouth and throat that communicate with nerve cells attached to the spasmed skeletal muscles, telling them to ease up. Or, in the researchers’ own words:

We suspect that the rapid inhibition of the electrically induced cramps reflects a neurally mediated reflex that originates in the oropharyngeal region and acts to inhibit the firing of alpha motor neurons of the cramping muscle.
If this is the case, my advice would be to obtain something with vinegar in it and simply: “Rinse and spit.”

Unless, of course, you’ve been hankering to go a round with “Hot Mama.” In which case, you’re on your own!

A word of caution: while pickle juice may provide an immediate fix for muscle cramping, don’t ignore the underlying causes, which still need to be remedied, including proper fluid and electrolyte balance. And do it as soon as possible!

Let’s ride!

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: Branched-Chain Amino Acids

What are branched-chain amino acids (BCAAs), the claims being made about them as they relate to endurance athletic performance, and the reality?

If the following commercial claims do not provide sufficient incentive for you to want to try BCAAs, arouse a little intellectual curiosity, or make you wonder whether your cycling buddies haven’t intentionally withheld vital information from you in order to retard your development and prevent you from assuming your rightful place on the podium, don’t worry. There’s more!

Ever since the 1970s, when it was first thought that BCAAs were legal performance enhancers, there has been much interest in these three naturally occurring essential amino acids on the part of nutritionists and athletes, not to mention commercial purveyors.

In fact, just this week, I received two different e-mails from a well-known nutrition-supplement chain store touting the alleged benefits of BCAAs. Here is a portion of the claim for one of the products.

Branch Chain Amino Acids (BCAA) – leucine, isoleucine and valine – are critically important for stimulating muscle protein synthesis, reducing protein breakdown and preserving muscle glycogen stores.* The body uses these essential amino acids as fuel during exercise.*

The asterisks of course alert us to the following claim . . .

*These statements have not been evaluated by the Food and Drug Administration.
Another BCAA product marketed by the same retailer comes with a slightly different set of claims, also accompanied with an asterisk:

BCAA's [sic] enter your bloodstream and attach directly to muscle where they repair damaged muscle tissue. This process helps ensure maximum muscle recovery and growth!*
I then searched for the claims by a competitor regarding its BCAA formulation:

· Decreases perception of fatigue and increase cognitive performance.
· Helps build, maintain, and repair lean muscle mass.
In all, I’ve been able to compile a list of ten (10) alleged benefits of BCAAs by commercial vendors that I wish to discuss. The claims include: 1) performance enhancement as a third energy source after carbohydrates and lipids, 2) glycogen preservation, 3) faster muscle recovery, 4) reduced muscle damage, 5) reduced muscle soreness post-exercise, 6) reduced mental fatigue, 7) increased cognitive capacity post-exercise, 8) decreased muscle wasting, 9) performance enhancement in heat, at altitude, and in other situations, and 10) immune system support.

Before getting down to the business of addressing each of these claims vis-à-vis the scientific literature, I shall provide some background information on BCAAs and amino acids in general.

No doubt humans require protein. Dietary protein is digested enzymatically by our body into smaller molecules known as amino acids, which in turn are immediately absorbed by the small intestine. After entering each of our body’s cells, the amino acids are then used as building blocks for the manufacture of tens of thousands of different human proteins, including muscle tissue, which is largely protein.

Twenty types of amino acids are required by the body. Our cells have the ability to synthesize all but eight of the 20 amino acids. The eight we cannot synthesize are called “essential” amino acids, because they can only be obtained from our diet. The BCAAs—valine, leucine, and isoleucine—are three of the eight essential amino acids the body requires but cannot synthesize.

Why are BCAAs important to athletes? It is true that BCAAs, particularly leucine, play an important role in muscle synthesis. Not only do BCAAs take their place alongside other amino acids as raw materials in protein synthesis, but leucine acts uniquely as a signaling molecule that initiates post-exercise protein synthesis.

The importance of ingesting leucine post-exercise becomes abundantly clear when we learn that its intracellular concentration diminishes as a direct function of the duration of endurance exercise. The longer we exercise the less leucine there is to trigger post-exercise muscle protein synthesis.

Where do BCAAs get their name? All amino acids have the same general structure:
Note that the central carbon (C) atom has four bonds depicted as lines radiating out like points on a compass to four different groups called “side chains.” Three of the side chains are invariable. The variable fourth side chain (in green) determines the particular amino acid, in this case glycine. The BCAAs get their name from the fact that the variable fourth side chain is branched.
Locate the branched side chain located on the “south” side of each of the three BCAAs. Imagine valine as an aerodynamic Tour rider on a road bike, leucine as an upright randonneur, and isoleucine as a trick rider doing a wheelie.

Now it is time to unveil my list of ten alleged benefits of BCAAs followed by critical commentary:

1. Since the 1970s, assertions keep popping up that BCAAs act as fuel during exercise in addition to carbohydrate and fat. To the contrary, BCAAs are not performance enhancing in the sense that they provide a significant or “third” energy source for endurance athletes. Thus, the commercial claim quoted above that, “The body uses these essential amino acids as fuel during exercise,” is highly misleading. While it is true that amino acid breakdown during exercise may result in some energy production, it is trivially true.

According to one expert, a Tour de France cyclist consumes only twice the amount of BCAAs during competition as a sedentary individual. Compare this to both carbohydrate and fat consumption, where detailed studies have shown that

the oxidation of BCAAs only increases 2- to 3-fold during exercise, whereas the oxidation of carbohydrate and fat increases 10- to 20-fold.

Moreover, the same researcher argues that when athletes fuel primarily with carbohydrates as they normally do, BCAA oxidation slows.

[C]arbohydrate ingestion during exercise can prevent the increase in BCAA oxidation. BCAAs, therefore, do not seem to play a major role as a fuel during exercise, and from this point of view, the supplementation of BCAAs during exercise is unnecessary.
Yet another research team concludes that

Leucine oxidation increases in proportion to energy expenditure, but the total contribution of BCAA to fuel provision during exercise is minor and insufficient to increase dietary protein requirements.
2. The claim made by the first commercial provider above, that BCAAs play a role in “preserving muscle glycogen stores” is also misleading, again, because it is only trivially true.

We just noted above that during exercise the relationship between BCAAs and carbohydrates is the reverse of this last claim; that is, carbohydrate ingestion during exercise slows BCAA oxidation. But since BCAAs are gradually depleted as a function of exercise duration, it is not altogether clear how they could preserve muscle glycogen as claimed.

While it is true that BCAAs do cause glucose synthesis and subsequent gluconeogenesis (glycogen synthesis), it is difficult to understand the significance of these events in the grand scheme of muscle energetics in light of each of the previous comments.

3. There is good evidence that BCAAs aid muscle recovery. In fact, the mechanism by which leucine is thought to initiate post-exercise protein synthesis is well known.

And although researchers tell us that

endurance exercise reduces the rate of muscle protein synthesis in proportion to the duration and intensity of activity,
they remind us that the post-exercise ingestion of a combination of leucine and carbohydrate allows maximum stimulation of protein synthesis.

4. BCAAs do seem to reduce muscle damage that results from exercise, according to many experts, one of which notes:

BCAA supplementation before and after exercise has beneficial effects for decreasing exercise-induced muscle damage and promoting muscle-protein synthesis.
5. In some situations, BCAAs may reduce post-exercise muscle soreness and fatigue. One group of researchers found that delayed-onset muscle soreness (DOMS) that results from resistance exercise is attenuated by BCAA supplementation.

BCAA supplementation prior to squat exercise decreased DOMS and muscle fatigue occurring for a few days after exercise.

6. There seems to be good evidence that BCAAs can reduce mental fatigue, and that

7. BCAAs improve cognitive function post-exercise. First a note on what is meant by physical fatigue.

There are two components of physical fatigue that affect endurance athletic performance, that is, the ability to maintain power output. These are the peripheral and central (mental) components.

Peripheral factors affecting physical fatigue include failure in neuromuscular signaling, waste buildup, and muscle energy store depletion, for example.

Central (mental) factors of physical fatigue are less well known. Central fatigue however can be demonstrated by the fact that willful maximal muscle effort is less than that which can be achieved when the motor nerve to the same muscle is electrically stimulated.

According to a well respected study by a Swedish researcher,

[W]hen BCAAs were supplied to human subjects during a standardized cycle ergometer exercise their ratings of perceived exertion and mental fatigue were reduced, and, during a competitive 30-km cross country race, their performance on different cognitive tasks was improved after the race.
Part of the reason researchers believe that BCAAs reduce mental fatigue is that they seem to have cornered a mechanism for its action. In short, it is thought that BCAAs block the uptake of a particular serotonin precursor (the amino acid tryptophan) in the brain. Serotonin (5-HT) is thought to play a role in causing central fatigue.

8. BCAAs are currently being studied as a way to slow muscle wasting in the elderly. Although this has little to do with endurance athletes in their prime, muscle wasting known as sarcopenia is a direct function of aging processes. Medical researchers assert:

[L]ong-term essential amino acid supplementation may be a useful tool for the prevention and treatment of sarcopenia, particularly if excess leucine is provided in the supplement.
9. Finally, the claim that arises from time to time regarding the alleged performance enhancing nature of BCAAs. Although some have suggested that BCAAs help athletes perform at moderate levels (40% VO2max) in the heat (34° C/ 93.2° F), the evidence is equivocal. So too is the suggestion that athletes perform better at altitude after ingesting BCAAs.

Generally speaking, no study so far suggesting a performance enhancing effect of BCAAs for endurance athletes has been able to withstand criticisms concerning methodology. One team of researchers reports that

A number of research groups examined whether BCAA supplementation might have a beneficial effect on endurance performance, but the results are inconsistent.

10. Although controversial, at least one study suggests that BCAAs decrease the negative effects of long-term strenuous exercise on the immune response. While exercise generally bolsters the immune response, long-term strenuous exercise as a stressor can have the opposite effect. Whether BCAAs benefit those who over train is currently debatable.

In sum, there are indeed great benefits that BCAAs provide for endurance athletes, in particular, benefits relating to muscle recovery, maintenance, and growth, but also cognitive function and reduced physical fatigue caused by mental factors. On the other hand, claims regarding muscle energetics and increased performance are generally viewed by most experts as dubious at best.

What about the toxicity of BCAAs? Most athletes are aware of the problems associated with ingesting too much protein: kidney damage, arteriosclerosis, and dehydration, for example. The same prohibitions apply to BCAAs, although there don’t seem to be any problems inherent to them. One researcher notes that

Acute intake of BCAA supplements of about 10-30 g/d seem to be without ill effect.
Finally, one group of researchers assures us that

There are no reports concerning BCAA toxicity in relation to exercise and sports.

What about cost and availability of BCAAs? One can easily compare costs of supplements on the one hand with natural foods on the other. One researcher notes
a typical BCAA supplement sold in tablet form contains 100 mg of valine, 50 mg isoleucine, and 100 mg leucine. A chicken breast (100 g) contains ~470 mg valine, 375 mg isoleucine, and 656 mg leucine, the equivalent of about 7 BCAA tablets.

Plant products also contain BCAAs. The previous researcher reports that in fact,

One quarter cup of peanuts (60 g) contains even more BCAA and is equivalent to 11 tablets.

Endurance athletes need more protein than non-athletes but not as much as body builders. Most of us probably get as much protein as we need. The amount of protein we consume on a daily basis can easily be calculated and compared with recommended amounts.

The best time to consume complete proteins (along with carbohydrates to ensure maximal protein synthesis) is immediately after exercise, when the machinery of protein synthesis is literally waiting in the wings for raw material, a pool of exogenous amino acids. Complete proteins contain all 20 amino acids, including ample amounts of BCAAs. Examples include beans and rice or food of animal origin.

A little protein ingested during exercise may also help with sundry physiological processes like hydration given the fact that there are amino acid transporters whose activity aids intestinal water absorption, thereby aiding quick and maximal hydration.

Regarding the purchase of BCAAs, one can obtain powders of complete proteins that contain sufficient amounts of BCAAs at grocery stores or online and which generally cost much less than commercially supplied BCAA caplets.

The amounts of BCAAs in everyday foods, including plants material, can be found at web sites like this. Some of the highest levels of leucine are found, for example, in soy protein and spirulina, a sea weed. The optimal ratios of BCAAs occur naturally in food.

As parting advice, I wouldn’t become too anxious about BCAAs as long as I knew that I was getting sufficient amounts of (complete) protein in my diet. Researchers note that BCAAs consumed in excess are simply excreted by the body.

We’ll get a meal as soon as we finish, but for now just grab a burger or a pack of peanuts and . . .

Let’s ride!

Phun Physiology: How Cold Is It? Check Your Humoral Thermometers

Boys on bicycles in village of Cheremshanka, eastern Siberia, February 2002. Photo by Oleg Nikishin.

Randonneuring blogs this time of year have a certain fascination with and well-placed respect for temperature.

When one of our local riders, Jerry, noted that the sweat in the sleeves on his jacket was frozen at the conclusion of an early-January ride, it caused me to think about how cold it must have been.

His comment reminded me of the classic children’s story by Jack London, “To Start a Fire,” in which spittle froze before reaching the snow-covered ground.

As he turned to go on, he spat speculatively. There was a sharp, explosive crackle that startled him. He spat again. And again, in the air, before it could fall to the snow, the spittle crackled. He knew that at fifty below spittle crackled on the snow, but this spittle had crackled in the air. Undoubtedly it was colder than fifty below—how much colder he did not know.

The scenario hints at a well-known aspect of science: different solutions freeze at different temperatures. We all know, for example, that water freezes at 32° F, while antifreeze freezes at a much lower temperature.

We use this type of information instinctively when we see a frozen puddle of water alongside the road and surmise that the ambient temperature is probably 32°F or lower.

The temperatures at which many other solutions freeze, including body fluids called “humors,” have been cataloged. Some of this information might be interesting, if not useful, to a cyclist. The one exception might be blood, which freezes between -2 and -3 °C (28.4 and 26.6 °F), since it may be difficult to distinguish between freezing and coagulation, I’m not sure.

Before answering how cold it must have been in order for Jerry’s sweat to freeze in the sleeves on his jacket on that January-cold 200km bicycle ride, our customary science lesson is in order.

Returning to our previous example, we know that water in its purest form freezes at 32° Fahrenheit (F) or 0° Canadian, otherwise known as Celsius (C). But if water has other items dissolved in it, ions and/or non-water molecules, then the freezing point— of what’s now considered a water solution—is lowered directly in proportion to the amount of the dissolved items (solutes).

The lowering of the freezing point of a solution to which solutes have been added is referred to as “freezing point depression.” That salt water freezes at a lower temperature than pure water illustrates this principle.

Consequently, we might correctly predict that body fluids, which contain mostly water, freeze at temperatures below 32 °F, since they include ingredients in addition to water.

Applying our present understanding (thereby demonstrating we have true knowledge and making Socrates very happy), we know that for Jerry’s sweat to have frozen, the ambient temperature on his sleeve must have been below 32 °F. Luckily for inquiring minds, the temperature range at which sweat freezes is known. We would expect a temperature range, since the composition of sweat varies for an assortment of reasons.

That range, -0.08 °C to -1.00 °C (31.86 °F and 30.2 °F), is consistent with the temperatures on the day that Jerry rode. But remember that this only tells us the temperatures at which sweat freezes; it could have been much colder than that. And in this case, it was.

What about the freezing point of saliva? Well that, too, is known (0.07 to 0.34 °C, or 31.87 to 31.39 °F), although, unlike the Jack London short story, unless you are willing to venture to the top of Grandfather Mountain, for example, you probably will not get a chance to determine the “crackling point” temperature of saliva in mid-air.

If you should go to Grandfather Mountain where it is not only cold (record -32 °F) but clothes-flapping windy (record 107 mph), here is some good advice from Jim Croce on experimental design you might want to consider.

While we are at it, how cold must it be for urine to freeze? Well, believe it or not, this has also been worked out by scientists _ _ _ _ -ing away their time in the lab (the correct missing word is “whiling”). Urine freezes between -0.45 °C and -2.5 °C (31.19 °F and 27.5 °F), which is a few degrees below the freezing point of saliva, perhaps useful information to a cyclist.

What about frozen eyeballs? After all, isn’t there watery stuff in the eyes? Some time ago, I read something about eyeballs freezing during an outdoor motorcycle race on the ice in Siberia, although I can’t seem to lay my hands on the article now. Perhaps it was nothing more than figurative speech.

Aside from the drinks with the same name, by most accounts, frozen eyeballs are not something about which cyclists need to worry. The eyeball does have a watery fluid (aqueous humor) in its anterior (front) chamber just behind the front outer clear cornea on which you place your contact lens. But the eye, located in the eye socket, is surrounded and protected by warming tissues including an ample blood supply. If in doubt, one could don protective goggles.

Although not really a body fluid—unless of course you are a Russian who binges or an American who downs too many frozen eyeballs—vodka has a really low freezing point.

80 proof vodka will freeze at approximately -26.95 °C or -16.51 °F.

100 proof vodka will freeze at approximately -40.43 °C or -40.78 °F.

Pure ethanol, the active ingredient in vodka, freezes at −114.3 °C.

It goes without saying that if your vodka should freeze on a bike ride, you are in really big trouble.

He travels fastest who travels alone . . . but not after the frost has dropped below zero fifty degrees or more.—Yukon Code
From a literary perspective, should you wish to compose a Londonesque short story for children about the north woods, you should probably try using another body humor in reference to the cold, since saliva is no longer considered novel. And stylistically, you might substitute a suitable onomatopoeic word for “crackle,” now inextricably linked with saliva. You could choose a perfectly good children’s word.

In summary, here’s your cycling-survivalist’s cheat sheet, with body fluids listed in descending order according to freezing point.

Body Humors
and
Reference Points Freezing Point (°F)
Water/ 32
Saliva/ 31.9 — 31.4
Sweat/ 31.9 — 30.2
Urine/ 31.2 — 27.5
Blood/ 28.4 — 26.6
Vodka (80/100 proof) -16.5/-40.8

Oh, yeah, I almost forgot. One more piece of advice. When it gets really cold, try to remember not to lick your steel touring bike . . .

Let’s ride (in Florida)!