Influence of Fitness and Gender on Sweating

sweaty girl


A review of two studies from 2012 looking at the influence of sex and fitness on sweating. One study found that at the the same percent of VO2MAX aerobically fit sweat up to twice as much, while at same power output unfit sweat more inefficiently form their forehead. The other study found evidence suggesting women have a lower maximal sweat output.


Two studies came out this past year looking at the physical characteristics that influence sweating. One of the studies looked at the influence of aerobic fitness.  The other study looked at the influence of gender.  The amount one sweats is based on several physical characteristics.  People with a greater body mass will sweat more simply because they have more metabolic processes going on, thus producing more heat. Body surface area plays a role because a smaller surface area means that more heat must be lost per unit area to generate the same amount of total heat loss. Sudomotor activity is the nervous system’s activation of the sweat glands.

The study that compared sweating of aerobically fit and unfit individuals yielded some interesting results [Cramer, M. N., Bain, A. R. and Jay, O. (2012), Local sweating on the forehead, but not forearm, is influenced by aerobic fitness independently of heat balance requirements during exercise. Experimental Physiology, 97: 572–582].

The study found that at the same power output or evaporation requirement (Ereq) both fit and unfit individuals had approximately the same whole body sweat output. Interestingly, the researchers found that when they looked at specific regions of the body there was significant discrepancy. The unfit individuals had significantly greater sweat levels on the forehead, but no significant difference between fit and unfit individuals on the forearm. The study authors concluded that the sweat efficiency of the aerobically fit individuals was greater. This is because excess sweating on the forehead leads to dripping.  Evaporative cooling is what generates heat loss, dripping sweat is just wasted fluids.  When the study participants exercised at 60% of their VO2MAX, the fit individuals sweated significantly more at all areas of the body. This was expected because more cooling was needed to compensate for the fitter individuals’ greater power output at 60% of their VO2MAX. These results can be seen in the figure below.

The study participants exercised for an hour on recumbent cycling machines.  These exercise machines were chosen so that mechanical efficiency would not be a factor. Because the power output was the same for fit and unfit individuals, the evaporation requirement (Ereq) should be the same in the BAL trial.  In this first study, only men were chosen as participants because of gender differences in sweating. Gender differences were discussed in a second, more recent study.

This second study found that when controlling for all physical variables, women have a lower maximal sweat efficiency [Gagnon D & Kenny GP (2012). Sex differences in thermoeffector responses during exercise at fixed requirements for heat loss. J Appl Physiol 113, 746–757.]

This study compared the thermoeffector responses of males and females during exercise. Females are generally smaller and have a lower VO2MAX than males.  The study authors controlled for this by using males and females with similar fitness and physical size. The onset of heat regulation was the same in both genders, an approximate response time of five minutes.  Therefore, the onset threshold is not significantly different in males or females. As the figure below shows, before the maximal sweat rate any differences in total heat loss can be explained by a difference in metabolic heat production.

Eventually the sweat production reaches a maximum. At this point heat loss from sudomotor activity (scientific name for nervous system control of sweating) is at a plateau even if metabolic rate is increased. The body’s other method of heat loss is vasomotor activity, bringing warm blood to the body surface in dilated blood vessels for cooling. It appears that vasomotor activity is equal in both genders across all ranges of required heat loss.  However, females have a lower maximum sweat production. Female’s lower sweat production is because the individual glands produce less sweat; the same number of glands per unit area are activated in both genders. The authors acknowledge they do not know why there is less sudomotor sensitivity in females at maximum heat loss requirement. In addition, the menstrual cycle affects a woman’s resting body temperature by ~0.3-0.5°C. The effects that the menstrual cycle has on female heat loss during exercise is not known.

In summary, fitness and gender influence an individual’s sweating capability and efficiency. Fit people have a lower sweat-rate on the forehead, but the same whole-body sweat-rate at the same power output. Females have a lower maximal sweat production than males, but appear to have the same vasomotor activity.

Examining the Controversy: Is too much exercise bad for the heart?

swimming in triathlon  

The mainstream media claims recent research may show vigorous exercise is unhealthy. That isn’t the complete picture.



A flurry of studies  a few years ago suggesting too much exercise is detrimental to one’s health sparked fierce debate over the legitimacy of the claims. The mainstream media jumped into the fray. The Wall Street Journal published an article “One Running Shoe in the Grave” arguing too much exercise stresses the heart enough to erase any physical activity health gains. What did the studies actually find, and is it a cause for concern?

One study tracking 52,000 adults for 15 years found that runners had a 19% decrease in all-cause mortality. However, when it was broken down by mileage a U-shaped curve emerged. Those exercising moderately for 2-5 days a week had the lowest mortality. The extremes had the highest mortality. In fact, the people running more than 25 miles a week had almost as high a mortality rate as those not exercising at all. The figure below shows this “U-curve” from the study (Running and all-cause mortality risk: is more better? 2012. Lee J, et al.)

However this does not give the complete picture. Another study, published in 2011, found that vigorous exercise and moderate exercise had differing amounts of benefit towards reducing mortality risk. The authors found that moderate exercise showed a gentle, increasing curve when plotted against mortality risk.  Meanwhile, vigorous exercise had far higher marginal returns up to about 50-60 minutes a week when it began to plateau. For both vigorous and moderate exercise, diminishing returns was observed as expected. However, no negative relationship was seen with extreme durations of daily exercise. The relationship can be seen in the figure below (Minimum amount of physical activity for reduced mortality and extended life expectancy: a prospective cohort study, 2011. Wen CP, et al.)

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So although the relationship cannot be fully established, if vigorous exercise does cause an increase in mortality risk past a certain point what is the cause?  According to a review by cardiologist James O’Keefe and colleagues, the cause is a problem with heart function.  (Potential Adverse Cardiovascular Effects From Excessive Endurance and Exercise, 2012.  James O’Keefe, et al.). Athletes develop an enlarged left ventricle to enable increased circulation. This remodeling does not disappear for at least several years following retirement from vigorous exercise. Several biomarkers for myocardial damage appear to be elevated following intense, prolonged races such as triathlons or marathons.  Myocardial scarring from vigorous exercise may lead to problems. Endurance athletes have been shown to have a higher rate of electrocardiogram problems.  Endurance athletes may have a five-fold increase in prevalence of atrial fibrillation. The increase in atrial size from endurance training may be responsible for atrial fibrillation.

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Other problems with the cardiovascular system that show up in endurance athletes include coronary artery calcification, diastolic dysfunction, aorta wall stiffening and myocardial fibrosis. Despite all these potential problems the authors add that lifelong vigorous exercisers generally have low mortality and great cardiovascular function; its an interesting paradox.

In conclusion, if health is your sole reason for exercising it may be best to limit exercise to 2-5 days a week of moderate exercise. However, the risks of vigorous exercise are highly speculative until more research comes out. The mainstream media is likely exaggerating the findings of recent studies or drawing hypothetical conclusions. When carefully looking at the data and the papers collectively, the research says vigorous exercise is still good for the body. Regardless of which side ultimately wins the debate, exercise is undoubtedly good for the mind and collective well-being.

Blood Starvation of Muscles During Training

muscle fiber fasicle

Blood flow restriction to muscles during training was shown by a recent study to induce changes in the muscle that increased contractile function. These changes were observed at the cellular and biochemical level.


An exciting field of research right now is how the muscles act when blood flow is constricted. A recent study showed that constricting blood flow during training increased muscle fiber cross sectional area, muscle stem cells and nuclei in the muscle (myonuclei).

The study (Jakob Nielsen, et al. 2012.  Proliferation of myogenic stem cells in human skeletal muscle in response to low-load resistance training with blood flow restriction) assigned twenty healthy males to perform 23 knee extension training bouts for a period of 19 days. Ten subjects performed the training with a pneumatic cuff placed on their thigh to limit blood flow (blood flow restriction or BFR). The other ten subjects served as a control and had no blood flow restriction. Muscle biopsies were taken pre-training, 8 days into the training intervention, 3 days post-training intervention and 10 days post-training intervention.

Interestingly, the subjects who had their blood flow restricted retained an increase in strength 5 days and 10 days post training intervention. The control subjects’ strength returned to pre-intervention levels 10 days post-training intervention. The cause of this sustained strength increase in the experimental group can be explained at the cellular and biochemical level.

Subjects who had their blood flow restricted saw increases in muscle stem cells, muscle nuclei, and muscle fiber cross sectional area. The differences were measured by muscle type as well.  Type I fibers are slow twitch fibers, responsible for aerobic work. Type II fibers are fast twitch and provide anaerobic work. Both mucle fiber types saw a large increase in Pax7+ expressing stem cells in subjects who had blood flow constricted. As the figure below shows, both muscle fiber types saw an increase in myonuclei when the subject had blood flow to the muscle constricted (blood flow restriction or BFR). The BFR change in type II muscle is surprising given the low intensity (normally aerobic) exercise. No change in either muscle fiber type was seen post-training in the control group (CON).

The muscle fiber cross-sectional area increased in both groups of subjects during training. However, the control group lost virtually all gains post-training. The blood flow restriction group maintained gains in muscle fiber cross sectional area 3 and 10 days post training. The authors suggest that hypoxia-induced protein synthesis is responsible for the gains seen in muscle fiber cross-sectional area in the blood flow restricted muscles.

In conclusion, blood flow restriction during training appeared to strengthen muscle function even after the cessation of the training program. The muscle achieved an increase in contractile power through increases in muscle fiber cross-sectional area, muscle stem cells, and myonuclei.  The discussed results have clinical significance: blood flow restriction may help patients regain lost or damaged muscle.

However, blood flow restriction likely does not extend beyond potential clinical applications to elite training programs.  Both groups followed the same training sequence. It would be reasonable to believe that training performance would be hurt by blood flow restriction. Thus, for a healthy, elite athlete doing high-intensity training, blood flow restriction would hamper their ability in a workout.

Heat, the Brain and Fatigue

sun hot heat sweat 

Heat limits athletic performance. The way heat causes fatigue may be through an elevated brain temperature.



Our bodies do not perform as well in hot conditions. Hyperthermia is when the body gets overheated resulting in a decrease in maximal power output. Most of us have experienced the fatigue that occurs with heat while exercising or during labor. Personal experience tells us that heat creates fatigue, but what is the physiologically basis of this heat-induced fatigue?

Before looking at how heat affects performance it is important to understand fatigue. There is much debate among today’s exercise physiologists about what actually limits performance during maximal-effort exercise. It is a muscles versus brain dissension. Do the muscles tire, signaling fatigue to the brain or does the brain, in an effort to avoid injuring muscle tissue, signal fatigue to the muscles? The idea that the brain is actually responsible for limiting performance was first introduced in the late 19th century, but has not yet been proven.

A hot environment makes it harder for the body to regulate its body temperature during exercise for several reasons. Blood cools off muscle tissue by moving into the body’s core and out to the skin. A hot environment means that the skin is unable to dissipate heat easily due to a reduced temperature gradient. The elevated temperature of the skin also lowers the temperature gradient between the body’s core and skin. During exercise in a hot environment, blood is simultaneously needed to deliver oxygen to the muscles and to thermoregulate by going to the skin. To make matters worse, blood pressure is reduced because water is being lost as sweat. This strain on available blood is why dehydration is so detrimental to athletic performance in hot environments.

One study found that regardless of the temperature of the exterior environment fatigue always sets in at the same core body temperature [Walters, et al. (2000). Exercise in the heat is limited by a critical internal temperature.]. The authors reasoned that a warm environment simply means that the “critical” core body temperature is reached sooner. However, this critical core body temperature theory has been challenged recently by studies showing ways of altering the critical core body temperature. Dopamine and caffeine were both shown to increase the core body temperature that fatigue sets in. Dehydration, on the other hand, lowered the core body temperature at which fatigue set in. Therefore, not only does being dehydrated mean that your body has a harder time regulating its body temperature, but the body temperature at which fatigue comes on is lower.

Force exerted as a function of time and hyperthermia condition. Four electrical stimulations (EL) were done demonstrating that the muscle was capable of greater exertion from the EL than brain stimulation. Hyperthermia had less effect on muscle contraction during electrical stimulation than brain stimulation.

The brain’s ability to regulate its temperature is stressed during exercise. Cerebral metabolism increases during exercise. Yet, the brain must deal with reduced cerebral blood flow because blood is being diverted to active muscles and thermoregulating skin. It is hard to determine if the core body temperature or brain temperature is responsible for fatigue. Because the brain gets arterial blood from the body core their temperatures are closely linked. Thus, a hot body core results in a hot brain. The brain is typically a fifth of a degree Celsius above the core body temperature. One recent study used experimental techniques to selectively heat the brain during exercise (Lars Nybo, 2012. Brain temperature and exercise performance). The results suggest that the brain’s temperature has a significant impact on performance. However, other studies have concluded that the skin’s temperature sensors are responsible for hyperthermia fatigue [Sawka et al. (2012). High skin temperature and hypohydration impair aerobic performance].

In conclusion, it appears that hyperthermia causes fatigue by elevating the brain’s temperature. Much debate still remains regarding the source of fatigue and the role that hyperthermia plays on fatigue. Understanding the way that heat decreases performance will provide avenues for increasing athletic capability in warm environments.

Rebuilding Muscle Protein

myosin structureMuscle protein synthesis is activated through exercise and nutrition. This myosin molecule (right) is one of many muscle proteins that are generated during muscle protein synthesis following exercise or an amino acid rich meal.


For a competitive athlete, one of the primary goals of working out is to stimulate muscle protein synthesis.  Muscle protein synthesis drives muscle hypertrophy, an increase in muscle mass.  There are two ways to drive muscle protein synthesis: nutrition and exercise.  Foods with essential amino acids stimulate muscle protein synthesis. Muscle protein synthesis is especially important after resistance training like lifting weights, but is also at play following endurance activities such as swimming or cycling.

If essential amino acid intake stimulates muscle growth why can’t someone build muscle mass by eating lots of protein? The reason is the “muscle full” response.  According to a 2012 review by PJ Atherton and K Smith entitled Muscle Protein synthesis in response to nutrition and exercise (Issue 590 of The Journal of Physiology) the “muscle full” response halts amino acid uptake. Muscles will take up amino acids for about 90 minutes before the muscle full point is reached.  Following resistance training, the muscle will take up amino acids for an extended period of time. Interestingly, this exercise-induced extension of the muscle full response occurs up to 24 hours post-exercise bout.

Muscles continue to take up essential amino acids for an extended duration 24 hours post exercise.

Following exercise the body uses the amino acid equivalent of 20 grams of protein. In addition, the way in which the body stores amino acids for muscle protein synthesis suggests that a greater frequency of small protein meals trumps one large meal. While amino acids trigger muscle protein synthesis, insulin decreases muscle protein breakdown. Insulin controls sugar levels in the blood by lowering blood sugar levels following a meal. However, insulin also rises following a meal that is carbohydrate free in order to halt catabolic muscle protein breakdown.

A trained athlete will have a specific muscle protein synthesis response. Due to increased efficiency, the trained athlete will spend less time doing muscle protein synthesis following exercise. This specificity means that an endurance athlete will build mitochondrial protein (mitochondria power aerobic work), but not myofibrillar protein. Resistance trained athletes will have post-exercise myofibrillar synthesis, but not mitochondrial protein synthesis.  An elegant study demonstrated this by having athletes exercise one leg on a cycle bike and another leg on a resistance machine (Wilkinson et al 2008). A person who rarely exercises will have a less specific and efficient muscle protein synthesis response following a workout.

In conclusion, nutrition and exercise have an overlapping role in regulating muscle protein synthesis. Determining the optimal conditions of muscle protein synthesis would aid athletes interested in bettering their performance.

The Physiology of Icing Sore Muscles

meb marathon new york


Meb Keflezighi (left, winning the 2009 NYC marathon) credits much of his success to icing.



About a year ago I met Meb Keflezighi, one of the greatest American marathon runners of all-time, while training at Mammoth Mountain in California. Since then the 37 year-old stud has had a very successful season culminating in a fourth place finish at the 2012 London Olympics. During our meeting he stressed the importance of icing on his success. Therefore, I was not too surprised that Meb emphasized his devotion to icing during media interviews after winning the 2012 American Olympic marathon trials. Meb is unquestionably one of the world’s most elite marathon runners. However, the question remains: What part has icing played on Meb’s running career?

Although studies looking at the effects of icing, or cryotherapy, have had somewhat conflicting results, most studies have found icing following exercise-induced muscle damage to be beneficial. The extent of muscle damage peaks between 24 and 72 hours following strenuous exercise. Exercise-induced muscle damage includes sarcolemma disruption, fragmentation of the sarcoplasmic reticulum, lesions of the plasma membrane cytoskeletal damage and swollen mitochondria. Outside the muscle fiber there may be swelling due to an increase in blood flow and capillary permeability.

One study looked at the multi-day effects of icing on exercise-induced muscle damage (Effects of cold water immersion on the symptoms of exercise-induced muscle damage, 1999, Roger Eston and Daniel Peters). The study used 15 female subjects and endurance exercised their biceps. The cryotherapy group submerged their exercised arm into a tub of 15 degrees Celsius  water for 15 minutes. This treatment was administered immediately after the bout of exercise and every 12 hours thereafter for 3 days.

The study results show that creatine kinase activity, a predictor of muscle damage, was lower in the cryotherapy treated group two and three days after the bout of exercise. The graph below shows these results.

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Eston and Peters also showed that the arm circumference and tenderness were not significantly affected. However, arm strength returned to baseline much faster in the cryotherapy group. This is of particular interest to athletes who often are expected to complete consecutive workouts in a 72 hour timeframe.  The difference was significant: after 72 hours the control group had a mean isometric strength that was 86% of baseline while the cryotherapy group had a mean isometric strength that was 111% of baseline.

A more recent study on the subject of icing measured blood flow, temperature and muscle endurance in cryotherapy treated and control groups (Changes in Blood Flow, Temperature and Muscle Endurance in Association with Cryotherapy, 2009, Masahiro Utsunomiya, et al.). In this Japanese study three groups were established: resting group (10 minute rest), 2-minute cooling group (2 minute icing and 8 minutes of rest) and 10-minute cooling group (10 minutes of icing).  Endurance was significantly boosted by icing. After ten minutes of rest the resting group performed at 59.2% of the initial test, the 2-minute cooling group 73.1% of initial test and the 10-minute cooling group 80.7% of the initial test. This suggests that the effects of icing are immediate.  Decreases in deep part temperature and tissue circulating volume were also observed as duration of icing increased.

The authors suggested that the cooling decreased oxygen consumption and cellular metabolism. This would potentially increase muscle endurance.  However,  an EMG signal processed with Fast Fourier Transformation saw no significant differences between the groups during the second bout of training. The authors hypothesized that the lack of significance means differences in endurance could have been the result of lowering myogenic pain instead of an increase in physiological fatigue.

The Running Mechanics of Elite African and Caucasian Marathoners

Hall Ryan olympics

Ryan Hall, one of the greatest marathoners not of African descent. Although his form contributed to his running efficiency, he was forced into retirement from injuries.


The mechanics of the perfect running form we should all strive for…


An interesting video comparing the running mechanics of some of the fastest African and Caucasian marathon runners including Ryan Hall and Meb. Meb is still chasing medals in the 2016 Rio Olympics, while Ryan Hall retired after injuries derailed his career. This video offers suggestions for enhancing performance and preventing injuries. Brought to  you by Somax Performance Institute, a renowned sports science center just north of San Francisco. Enjoy!

Exercise and Heart Physiology

heart physiology 

A 2011 paper uses MRI technique to challenge a hypothesis developed in 1975. The study found that endurance training increases left ventricular mass by increasing ventricular wall thickness and volume. Resistance training produced no affect on the heart.  


The body adapts to exercise by changing the physiological parameters of the heart. Changes are observed in the left ventricle, the chamber responsible for pumping blood throughout the body (as opposed to the right ventricle, which pumps blood through the pulmonary circuit). The left ventricular end-diastolic volume is the volume of the left ventricle just before contraction (systole).

In 1975 the Morganroth Hypothesis was proposed (Comparative Left Ventricular Dimensions in Trained Athletes, 1975, Joel Morganroth, et al.). Morganroth and team studied the hearts of varsity college athletes in the sports of wrestling, swimming and endurance running as well as world-class track and field athletes.  The hearts were studied echocardiographically, a revolutionary, non-invasive technique at the time, but primitive compared to today’s MRI instruments. They found that the athletes involved in isotonic exercise (swimming and running) had a greater left ventricular mass due to a greater left ventricular end-diastolic volume. However, their ventricular wall thickness was no different than non-athletes. The athletes involved in isometric exercise (shot put and wrestling) were found to have a greater left-ventricular wall thickness than non-athletes. However, no difference in left ventricular end-diastole volume was observed.  The increase in ventricular volume in isotonic athletes and ventricular wall thickness in ventricular wall thickness in isometric athletes independently resulted in an increase in left ventricular mass as the figure below demonstrates.

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The Morganroth hypothesis was challenged by a paper released in 2011 (A prospective randomised longitudinal MRI study of left ventricular adaptation to endurance and resistance exercise training in humans, 2011, Spence AL, et al.).  Study participants were put through a 24-week training program. The training program came in two flavors: endurance or resistance. The longitudinal study measured heart parameters using MRI at baseline, at the end of the training program and after a detraining period. The study found no significant difference in the heart physiology in the resistance trained group. However, the endurance trained group showed an increase in both left ventricle volume and ventricular wall thickness. As the figure below shows, after the detraining period the left ventricle wall thickness decreased, but the left ventricular volume did not change in the endurance trained participants.

Impact of exercise training and detraining on MRI derived measures of cardiac mass, volume and wall thickness. Bars represent percentage change from baseline after training (filled bars) and detraining (open bars) values in the endurance (upper panel) and resistance-trained (lower panel) groups. *P < 0.05 post-training vs. baseline, †P < 0.05 post-detraining vs. baseline. For measures of IVS, PWT, LVIDd and LVIDs, n= 7 for endurance group. EDV, end-diastolic volume; ESV, end-systolic volume; LVM, left ventricular mass; LVMi, left ventricular mass index; LVIDd, left ventricular internal diameter during diastole; LVIDs, left ventricular internal diameter during systole; IVS, interventricular septal thickness; PWT, posterior wall thickness.

In the endurance trained group left ventricular mass increased an average of 8%. Some other interesting findings from the study include the fact that fitness was retained in the resistance group and endurance group as measured by bench press, push-ups and squats after detraining. Leanness was conserved in the resistance group, but not the endurance group, after detraining.

In summary, advances in MRI imaging of the heart allow more precise measurements of changes in the heart. Using MRI, researchers found that left ventricular mass increased via volume and thickness in endurance trained athletes. However, no physiological changes in the heart were seen in the resistance trained group.

Muscle Fiber Influence on Motor Neurons



A team of Harvard researchers found that muscle fibers have retrograde influence on motor neurons.


Athletes generally refer to muscle fibers as “fast twitch” and “slow twitch” depending on muscle contraction speed. From slowest to fastest, the muscles are designated type I, IIA, IIX, IIB. Studies have shown that each motor neuron is homogenous for the muscle fibers it operates. Thus, a slow motoneuron would operate a bundle of slow twitch motor muscle fibers.

Muscle fibers can be converted to a different muscle fiber type by attachment to a alternate motoneuron. For example, a slow twitch muscle fiber can be converted to a fast twitch muscle fiber via attachment to a fast motoneuron. The question then becomes can this mechanism operate in reverse?  In other words, can muscle fibers cause the motoneurons to change from fast to slow and vice versa?

This is the question a team of Harvard researchers sought to address (Retrograde influence of muscle fibers on their innervation revealed by a novel marker for slow motor neurons, 2010, Joe V. Chakkalakal, et al.).

The researchers introduced a novel marker of slow motoneurons, SV2A. Using immunofluorescence staining the researchers could mark slow motoneurons.  Fast twitch muscle fibers were converted to slow twitch muscle fibers using the transcriptional cofactor PGC-1alpha (discussed in this post on smoking). It was found that an increase in slow twitch muscle fibers led to an increase in slow motoneurons. The possible mechanisms by which an increase in slow-twitch muscle fibers (via PGC-1alpha) increases slow motoneurons synaptic connections is shown below.

Three possible mechanisms by which PGC-1alpha can increase the amount of slow motor neuron terminals. This study confirms that the mechanism is conversion.

The increase in slow motoneurons demonstrates that the mechanism increasing slow synaptic connections is the conversion of motoneurons from fast to slow.  Motoneurons ability to undergo conversion suggests that they have some postnatal plasticity. The authors suggest that there may be a combination of prenatal and postnatal determinants of motoneuron type.

The physiology of motoneurons and their relationship with muscle fibers may have interesting ramifications on the way we look at training. Evidently more than muscle fiber type and capillary proliferation are at play during training.

Glycogen Starvation in Muscle Training

glycogenGlycogen efficiently stores glucose in a branched, dense polymer. A study released in 2004 suggests that glycogen starvation during training increases endurance performance.

Glycogen is polymerized glucose. For athletes, glycogen has many advantages. When glycogen is broken down into pyruvate during glycolysis it results in a net gain of 3 ATPs. ATP is our body’s and muscle’s high-energy delivering molecule. When glucose is broken down during glycolysis it produces just 2 ATP. Thus, glycogen produces 50% more ATP during glycolysis than glucose. When the cell is in hypoxia (oxygen depletion) it is unable to break down the glycolysis product, pyruvate, further. Thus, for anaerobic exercise, glycogen breakdown results in a considerable energy benefit. In addition, as the image above shows, glycogen is branched every ten glucose monomers. This allows more glucose molecules to be available for glycolysis (only glucose molecules at the end of a chain can be cleaved). Over the course of animal evolution, glycogen has developed into the primary energy-storage molecule because of its denseness and efficient energy-release.

Glycogen has long been known to be beneficial to athletes; hence carbohydrate loading (carbo loading’s affect on performance is debatable, but that is another story). Is glycogen beneficial during training?  That is the question an elegant Danish study sought to answer. The study found that carbohydrate depletion during training was beneficial to performance (Skeletal Muscle Adaptation: training twice every second day vs training once daily; 2004; Anne K. Hansen, et al.)

The study took 7 healthy, untrained men and put them on a strict training schedule for ten weeks.  The training consisted of leg extensions. Each participant worked out both legs for an hour, wait two hours under a fast, and workout one of the legs (low-glycogen protocol) for an hour. The next day, the participant would workout the other leg (high-glycogen protocol) for an hour. On this two-day sequence both legs got two hours of work, but one at lower levels of glycogen than the other. This is because following the first hour bout of exercise, glycogen levels in the muscle drop. The two-day sequence was repeated for ten weeks.  The experimental sequence can be seen in the diagram below.

Schematic overview showing the design of the study.

In response to 10 weeks of training, maximum power output increased significantly, being the same in the two legs. The endurance at 90% of this new maximum power output was markedly increased for both legs, but time until exhaustion was twice as long for low-glucose protocol trained legs compared with high-glucose protocol trained legs. In accordance, the actual work performed by low-glucose protocol trained legs was also markedly larger compared with high-glucose protocol trained legs. The results can be seen in the table below.

Maximal power output and time until exhaustion at 90% of maximal power output before and after 10 weeks of training and total work before and after 10 weeks of training.

Muscle glycogen levels were raised significantly in low-glycogen protocol trained legs at the conclusion of 10 weeks of training. The authors of the study speculated that this may have been the result of a change in GS enzyme, a regulator of glycogen production. Mitochondria enzymes CS and HAD were both significantly higher in low-glycogen protocol trained legs.

The results of this study seem to support this hypothesis regarding glycogen: train low, perform high. However, these results must be treated with caution when applied to athletes. Other factors could be at play; training twice every other day compared to once daily may affect other pathways besides glycogen. In addition, glycogen starvation would potentially limit the amount of training one could conceivably do.

In summary, this study suggests, but does not prove, that glycogen starvation during training may increase endurance.