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: 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: 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.

Phun Physiology: Mental Fatigue Impairs Cycling Performance

Ever been engaged in some mentally demanding activity and couldn’t wait to take your bike out for a spin? Well it may not be so easy to leave your work at work. In fact, your mentally demanding job could affect your bicycle commute home, according to an article published this year in the Journal of Applied Physiology.

The purpose of the study in the researchers’ own words . . .

Although the impact of mental fatigue on cognitive and skilled performance is well known, its effect on physical performance has not been thoroughly investigated.
Of note, the researchers suggest that mentally fatigued cyclists experience greater “perceived effort” during exercise and quit sooner.

The accompanying study press release provides a summary of the study.

When participants performed a mentally fatiguing task prior to a difficult exercise test, they reached exhaustion more quickly than when they did the same exercise when mentally rested . . .
What was the nature of the mentally fatiguing exercise?

The mental fatigue sessions began with a challenging 90-minute mental task that required close attention, memory, quick reaction and an ability to inhibit a response. After undergoing this session, participants reported being tired and lacking energy. The control session consisted of watching neutral documentaries for 90 minutes and was not mentally fatiguing.

What was the nature of the physical exercise?

After each of the 90-minute sessions – mentally fatiguing or non-fatiguing – the participants did an intense bout of exercise on a stationary bicycle. They rode until exhaustion, defined as the point when they could not maintain a cadence of at least 60 revolutions per minute for more than five seconds.

Importantly, the researchers claim that the limiting factors on performance were mental rather than relating to other physiological systems. They write:

Our study provides experimental evidence that mental fatigue limits exercise tolerance in humans through higher perception of effort rather than cardiorespiratory and musculoenergetic mechanisms.
Does this mean that cyclists should give up their after-work commute? Definitely not, according to the researchers, who assert that

. . . the study suggests that people doing high intensity training, such as competitive athletes, should do their training while mentally rested. However, people who exercise after work should continue doing so, even if mentally fatigued. Most people work out at a moderate intensity, which still gives plenty of physiological and psychological benefit, including relief from stress and improved mental performance.

In fact, a workout after a mentally demanding day at the office may be exactly what we need!

(Photo courtesy of sagittandy)

Phun Physiology: Ever Thought of Having Your Own VO2 Max Tested?

Now you can. I lifted portions of two advertisements directly from this December’s issue of the Triangle edition of “Endurance Magazine.” Apparently, triangle residents (Raleigh-Durham-Chapel Hill) have a couple of choices for VO2 max testing at local universities.

First, brought to you by our friends in Chapel Hill:

Beginning in 2009, the UNC Wellness Performance Center will offer VO2 Max Testing! Results of VO2 max testing allow you to maximize training efficiency and benefit. Get the information you need to Take Your Training to Your MAX!

Direct expired gas analysis will provide you with precise measurement of oxygen uptake, while 12-lead electrocardiography will be used to monitor cardiac function. Anaerobic, ventilatory, and lactate thresholds will be calculated along with specific training heart rate ranges.

ACSM-certified Exercise Specialists and ACLS-trained nurses will administer maximal effort treadmill or cycle ergometer tests. Physician-supervised tests are also available.

VO2 Pricing
Treadmill or bike test $200
Physician-supervised test $250
Computrainer testing is available, utilizing your own bike . . .
Second, brought to you by our friends in Durham:

LET’S FIND OUT WHAT YOU’RE MADE OF.

The K-lab is a state of the art performance testing facility at Duke’s world class Sports Medicine Center. But we don’t just test Duke athletes. Whether you’re a weekend warrior or an elite athlete, we’ll assess your current fitness level, target your proper training zones and show you how to maximize performance while preventing injury. As a leader in the study of athletic performance, we can take you and your body to the next level. . .

Sport Specific Training
VO2 Max
Blood Lactate Testing
Body Composition Analysis . . .

No pricing was provided, although mention of the ad qualifies individuals or teams for 15% off the regular rate.
Since my original post, an anonymous commenter (see below) alerted me to something I completely missed: there is at least a third institution of higher learning involved in VO2 max testing in the Triangle! My apologies! And now, brought to you from our friends here in Raleigh:




Beginner to Elite Fitness/Performance Testing
Fitness Counseling
Resting Metabolic Rate
Body Composition
Heart Rate/Power Training Zones
VO2 Max
Blood Lactate Threshold . . .
Their website (in comments below) includes prices for various services and packages.

Phun Physiology: The Young at Heart, by Dean Furbish

The conversation in the parking lot at the conclusion of Saturday’s “Showdown in Black Creek” Permanent was delightfully animated (see Mike D's previous post). I mention this because we’d spent the day under overcast, melatonin skies and had battled a slight inbound headwind. No dreary moods here, though. The group of nine riders engaged in mild banter, self deprecation, and story-telling over coffee, pastry, and post-ride picture posing. It can be said that these riders are literally some of the young at heart. Read on.

The topic of this post occurred to me when a couple of riders shared hilarious anecdotes about how their normally slow heart rates had raised eyebrows during annual health checkups. Slow heart rates aside, it’s a fact that endurance training makes hearts young.

One indication of a “young” heart is its ability to metabolize glucose as an energy source during exercise. An aged heart loses its ability to utilize glucose during exercise. The good news is that endurance exercise reverses this aspect of aging.

Moreover, exercise benefits even the elderly, including those who previously have led inactive lives.

Exercise turns aged hearts into “young” hearts metabolically, according to a recent study out of Washington University School of Medicine in St. Louis, because it reverses the aged heart’s inability to metabolize glucose during exercise. In fact, exercise training enables the hearts of older people to double their glucose utilization during high-energy-demand exercise just like the hearts of younger people.

Women’s hearts benefit doubly metabolically as the result of endurance training. In addition to increasing cardiac glucose metabolism, it turns out that cardiac fatty acid metabolism increases as well in women. The same cannot be said for men.

I include some of the specifics of the 11-month study to point out that people do not need to be randonneurs or RAAM types or even train for years in order to obtain this anti-aging heart benefit of regular exercise.

In fact, endurance training was defined in the Washington University study as hour-long exercise sessions 3-5 times per week consisting of walking, running, or cycling. Participants began at 65% of maximum capacity for three months increasing to 75% for the next eight months. The six men and six women in the study were between the ages of 60 and 75. Although they were non-obese, participants had previously lived inactive lives.

Phun physiology advice: Keep riding!

The reference is here: Soto PF, Herrero P, Schechtman KB, Waggoner AD, Baumstark JM, Ehsani AA, Gropler RJ. Exercise training impacts myocardial metabolism of older individuals in a gender-specific manner. American Journal of Physiology. Heart and Circulatory Physiology. June 20, 2008 (advance online publication).