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.

Working out alters DNA

DNA

 

Exercise is found to alter the methylation of cell metabolism related promoter regions in human subjects.

 

DNA expression is a complicated process that has yet to be completely unraveled by geneticists. One way DNA expression is regulated is through methylation. Methylation involves attachment of methyl groups (-CH3) to the DNA, inhibiting its expression. When a promoter region becomes heavily methylated expression of the corresponding gene becomes inhibited.  Methylation plays a role in cell differentiation; specialized cells are methylated in characteristic patterns. Geneticists previously believed that methylation is permanent within an adult cell. However, a recent study first published in Cell Metabolism and featured in Nature found that exercise alters methylation (Acute Exercise Remodels Promoter Methylation in Human Skeletal Muscle, 2012. Romain Barres, et al.).

Exercise was found to demethylate cell metabolism promoter regions in sedentary men and women following acute exercise. In the study muscle biopsies were performed on the subjects following acute exercise at 40% and 80% of maximum. The figure below shows that methylation was significantly reduced in the muscle after acute exercise. In addition, promoters for genes involved in energy metabolism where analyzed in muscle fibers. The figure shows that for all the energy metabolism genes (PGC-1a, TFAM, PPAR, CS and PDK4) methylation was found to be reduced in their respective promoters.  This was not the case for muscle specific genes MEF2A and MYOD1 as well as the muscle “housekeeping” gene GAPDH.

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Acute Exercise Remodels DNA Methylation: (A) Global CpG methylation analysis at rest (REST) and 20 minutes after acute exercise (ACUTE EXERCISE). (B) Ratio of methylation after acute exercise and at rest, dashed line represents no change. *p<0.05, **p<0.01

Similar changes in gene expression were observed following exercise. Exercise increased the gene expression of the demethylated genes as measured by mRNA levels. The intensity of exercise affected the significance of demethylation. Working out at 40% of maximum effort produced less of an effect than at 80% of maximum effort. Within three hours of the exercise effort most of the demethylation effect observed immediately post exercise session had disappeared. Isolated mouse soleus were observed to determine whether exercise-induced factors were needed to cause the methylation changes seen in the human subjects. The mouse muscle fibers contracted ex vivo showed methylation changes as shown by the figure below. This means that external factors are not needed to change the methylation, but the contracting fiber itself causes the changes. Gene expression peaked three hours after the ex vivo muscle contractions. Meanwhile, hypomethylation occurred 45 minutes after ex vivo muscle contractions.

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Muscle Contraction Induces Hypomethylation: Gene expression (A) and promoter methylation (B) in isolated mouse soleus. *P<0.05

 

The study also found that large doses of caffeine induced hypomethylation. The mechanism, the authors believe, is through caffeine-induced calcium release from sarcoplasmic reticulum (the cause of contraction according to the sliding-filament theory). Because the gene expression and methylation patterns differed slightly, gene expression is influenced, but not completely controlled by, DNA methylation.

This study has ramifications beyond exercise. This introduces the novel concept that the environment can influence DNA methylation in non-dividing, somatic, adult cells. Epigenetic marks across the genome are subject to greater disparity than formerly realized.

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.

Fat on the Brain

brain shinyFat literally accrues in the brain of mice consuming a diet high in fat. Exercise was unable to reverse the fat accumulation. The consequences of hypothalamic lipid accumulation may include neural dysfunction and problems with brain regulation.

 

Adipocytes are cells whose specific function is to take up fat. However, fat can also be stored in other cells, a process called lipotoxicity. Excessive fat accumulation in non-adipose tissue can lead to cellular dysfunction and in extreme cases, cell death or apoptosis.

The central nervous system can be affected by lipotoxicity. In a study published this month in the Journal of Physiology, fat content in the hypothalamus region of the brain was observed in mice fed a high-fat diet (Consumption of a high-fat diet, but not regular endurance exercise training, regulates hypothalamic lipid accumulation in mice, 2012, Melissa L Borg, et al.). Fats generally are not a source of fuel for the brain (glucose is the brain’s primary fuel and fat-derived ketone bodies substitute when the body is starved of carbohydrates). Yet, fatty acids can cross the blood-brain barrier and reach the hypothalamus for regulatory purposes. The hypothalamus is the body’s hunger and body weight regulator. In addition to neuronal signals, the hypothalamus receives input from the levels of fatty acids in the cerebral spinal fluid. The hypothalamus has a limited means of oxidizing fatty acids; therefore, high levels of fatty acids result in fat being stored in the hypothalamus.

The study found that a high fat diet resulted in an increased amount of lipotoxicity in the hypothalamus. Surprisingly, exercise did not reduce the amount of lipids in the high fat diet mice. The mice were fed a high fat diet (59% of calories from fat) or low fat diet (5% of calories from fat) for twelve weeks.  Half of the high fat diet mice were exercised six weeks into the study. As the graph below shows, exercise in the high fat diet mice was able to drop most of the added body weight.

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Body weight of mice over a 12 week period as a function of fat content of diet and exercise over the last 6 weeks.

The high fat diet increased a variety of fats in the hypothalamus. Phospholipids, glycerol lipids, saturated fatty acids and monounsaturated fatty acids were all increased in the hypothalamus as a result of a high fat diet. In addition, high fat feeding increased hypothalamic lipid species known to cause insulin resistance. Yet, exercise was unable to reverse the increase in hypothalamus lipids.

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Epididymal fat in the hypothalamus of mice fed a low fat diet, a high fat diet and a high fat diet with a substantial 6 week training program

The figure above demonstrates that a substantial, 6-week exercise program was not able to substantially reduce the hypothalamus lipid content in mice fed a high fat diet. This suggests that the only way to control fat accumulation in the brain is through diet. Since exercise is not a viable means of reversing fat accumulation in the hypothalamus, other means of reducing lipid accumulation, and the harm it may cause to brain regulation, must be sought.

In conclusion, excess lipid accumulation in non-adipose tissue causes cellular dysfunction leading to diseases such as diabetes. Therefore, lipid accumulation in the hypothalamus due to a high fat diet probably harms regulatory processes in the brain. In the study discussed, exercise was found not to reverse hypothalamus lipid accumulation. The fat content of one’s diet should be monitored even in people with a healthy body weight.

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

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.