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.

Winding Up Your Body’s Clock

clock of circadian rhythm

Scheduled physical activity is found to help regulate and amplify the body’s circadian rhythm. This suggests a way for curing defective circadian rhythms and a multitude of diseases that have been linked to malfunctioning circadian rhythms. 

 

Animals, including humans, utilize clocks called circadian rhythms to keep the body aligned with nature’s daily night and day cycle. The circadian rhythm is controlled by the suprachiasmatic nucleus in the brain. The circadian rhythm is a daily cycle of behavioral and physiological functions regulated by fluctuating levels of hormones. Malfunctions in the circadian rhythm often develop in the elderly and a recent study found these malfunctions in the circadian rhythm may be to blame for a myriad of diseases including diabetes, cancer, cardiovascular disease and mood disorders [Arendt J (2010). Occup Med (Lond) 60, 10–20.]. A study published in the December 2012 Journal of Applied Physiology found that scheduled physical activity strengthens and regulates the circadian rhythm (Voluntary scheduled exercise alters diurnal rhythms of behavior, physiology and gene expression in wild-type and vasoactive intestinal peptide-deficient mice, 2012. Analyne M. Schroeder, et al.).

In the study mice were given varying levels of access to a running wheel: no access, free access, late night access and early night access. By measuring ambulatory activity, body temperature, heart rate and circadian rhythm hormones the researchers found that having scheduled access had a strong control over their circadian rhythm. Even free access versus no access had an effect. Mice are naturally active at night. The figure below shows how varying access to running wheels affected their ambulatory activity.

Ambulatory activity in wild-type mice as a function of time of day in response to no, free, early night and late night access to running wheels.

Even more interesting was the effect of the running wheel access variable in vasointestinal polypeptide (VIP) deficient mice. VIP deficiency leads to circadian rhythm loss of function. Late night running wheel access was able to restore many of circadian physiological and behavior cycles to those seen in the wild type (VIP normal) mice. One of the molecular clocks measured was PER2 and Luciferase, the ratio of which corresponds to different points in the circadian rhythm. The figure below compares this molecular clock with wild type mice.

A measurement of PER2::Luc ratios in VIP deficient mice (VIP -/-) as a result of varying access to a running wheel. The dotted lines represent the levels seen in the wild-type mice.

What this study shows is that not only can exercise be important for therapy, but the time that exercise is performed is also important. For people who perform exercise on a daily basis, maintaining a standard workout schedule is beneficial because our bodies are “ready to go”at the workout time each day. Apparently, this readiness does not require our normal circadian rhythm machinery as evident by the VIP deficient mice’s ability to get on a schedule. Further research is needed to show that scheduled physical activity can help elderly patients suffering from a loss of circadian rhythm function.

Resistance Training vs Aerobic Training for Weight Loss

resistance training newport beach 

A large study finds that resistance training is not as effective for reducing body weight as aerobic training.

 

 

A recent study conducted by researchers at Duke University looked at the weight loss efficiency of aerobic training, resistance training and a combination of the two (Effects of aerobic and/or resistance training on body mass and fat mass in overweight or obese adults, 2012. Leslie Willis, et al.). As expected, the study found that the training strategies have very different affects on the body.

Resistance training involves any type of exercise where the joint performs a full motion with a force opposed to that motion. With elastic bands the opposing force increases as the motion is extended. In hydraulic resistance training the opposing force increases as the speed of motion increases.  Aerobic training includes repetitive motions such as cycling, swimming and running. For this particular study weight lifting was used for resistance training. A cycling machine, elliptical machine and treadmill were used for the aerobic training.

Those subjects participating strictly in resistance training saw no decrease in body mass. However, this was because any decrease in fat was offset by an increase in  lean body mass. The fat composition was reduced by resistance training participants. On the other hand, aerobic training participants saw a significant drop in both fat composition and total body mass. When time is considered, the aerobic training is even more efficient. Aerobic training in this study took 133 minutes a week compared to the 180 minutes a week spent by the resistance training group.

The effect of different modes of exercise on change in body mass and body composition. ††P < 0.05, †P < 0.10 Post Hoc Test compared with resistance training. ‡‡P < 0.05 Post Hoc Test compared with aerobic training.

Interestingly, no increase in weight loss was observed when resistance training was added to aerobic training, but there was a significant drop in fat percent.  Waist circumference has been found by some studies to be a better predictor of cardiovascular health than BMI. Although resistance training by itself did not decrease waist circumference, it created a significant drop when added to aerobic training relative to aerobic training by itself.

In conclusion, despite what resistance bands manufacturers or resellers claim, resistance training does not burn fat or decrease body weight according to this study. From this study it appears that the best method of losing fat is aerobic training. If time allows, resistance training can be added on.

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.

Screen Shot 2012-12-15 at 8.40.29 AM

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.

Screen Shot 2012-12-17 at 11.24.22 PM

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.

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.)

Screen Shot 2012-12-09 at 3.08.14 PM

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.

Screen Shot 2012-12-09 at 4.29.45 PM

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.

Concussions in the NFL lead to Depression

football

 

Professional football players who suffer from a concussion are more likely to develop long-term mental health episodes such as depression.

 

The prevalence of concussions in football has significant mental health ramifications. One concussion occurs every 2.44 NFL games. A study published in the American Journal of Sports Medicine looked at correlations between concussion incidences and depression (Nine-Year Risk of Depression Diagnosis Increases With Increasing Self-Reported Concussions in Retired Professional Football Players, 2012. Zachary Y. Kerr, et al.).

The study used a 2001 General Health Survey sent to the 3,729 members of the NFL Retired Players Association. A second General Health Survey was sent nine years later in 2010. The surveys asked questions regarding the respondents physical and mental health as well as the number of concussions suffered during their professional careers. Those exhibiting depression in the first survey were not used in the study.

Of the players who reported never having a concussion, only 3.0% were diagnosed with depression. Of those who reported suffering from 10 or more concussions, 26.8% were found to suffer from depression. The relationship between number of self-reported concussions and likelihood of suffering from depression was a linear relationship. Those who reported suffering from 3 or more concussions were twice as likely to suffer from depression as those reporting 1-2 concussions over their career and three times more likely than retired professional football players who did not suffer any concussions over their professional career.

Work on depression in US soldiers in Iraq has suggested there may be a link between tauopathies, tau protein deposits in the brain, and depression. Repeated head impacts elevate tau protein levels causing neural breakdown. The physical blow to the head could directly cause neuron death or breakage of neuron connections. Lesions in neural tissue could release harmful biochemical agents.

Concussions often go unreported, especially at the amateur level. This study highlights the importance of monitoring the accumulation of concussions. Other studies have found that concussions can lead to negative personality and cognitive changes. Although the dangers of concussions cannot be underscored enough, with regards to this study on concussions in former NFL players there are several limitations. Most significantly, it is likely that there are many lurking variables that this study could not account for. For example, risky behavior that leads to concussions may be favored in those prone to depression. Career-ending concussion accumulation may lead to depression. Nonetheless, the number of concussions suffered is a significant predictor of depression later in life.

Most likely, a positive relationship between concussions and depression would apply across sports, competition levels as well as to the military and other non-athletic instances.

Playing on Turf increases Injuries in the NFL

football 

A recent study found that NFL games played on turf showed significantly higher rates of lower-leg injuries.

 

 

Across sports and competition levels, playing surfaces have been switching from natural grass to artificial turf. This has several health ramifications. Some researchers have speculated that the rubber polymers used in artificial turf cause cancer. Although turf’s carcinogenic properties have not been proven, a recent study of NFL players showed that the incidence of knee and ankle injuries is significantly higher in games played on turf.

The first NFL stadium to use an artificial playing surface was the Houston Astrodome in 1966. The surface, called AstroTurf, was manufactured by Monsanto and consisted of a padded-carpet over asphalt. In the 1990’s infill surfaces became popular and are widespread today. Infill surfaces consist of an interwoven mat of polyethylene fibers filled with rubber particles. The frequency of NFL games played on turf has been increasing over the years as more NFL stadiums adopt turf. The figure below demonstrates this trend over the previous decade.

Screen Shot 2012-11-25 at 10.03.26 PM

Several studies have looked at injury rates in football players based on field surface. A study done in the early 2000s found that ACL injury rates of high school players are higher in games played on turf. However, the same study found college players were more likely to sustain an injury on grass than turf. A recent study looked at several different lower leg injuries in NFL players using extensive data collected by the injury surveillance system maintained by NFL trainers (An Analysis of Specific Lower Extremity Injury Rates on Grass and FieldTurf Playing Surfaces in National Football League Games : 2000-2009 Seasons; 2012. Elliot B. Hershman, et al.). The study used data from NFL seasons from 2000 to 2009.

The aforementioned study looked at several different lower leg injuries in NFL players: knee sprains, MCL and ACL injuries, ankle sprains, inversions and eversions. Although all injury categories demonstrated a higher frequency in turf than grass, MCL (median collateral ligament) injuries and inversions (an ankle sprain where the ankle is twisted inwards) both did not show significance. The injuries that did show significantly higher prevalence on turf were knee sprains, ACL injuries, ankle sprains and eversions. The figure below shows the injury rates in NFL players based on a density ratio of turf over grass injury rates.

Screen Shot 2012-11-25 at 10.24.27 PM

ACL sprains occurred at a rate 67% higher on turf than grass. Eversion ankle sprains occurred at a rate 31% higher on turf than grass. Despite the significantly higher rates of injury on turf, this study was limited because it did not suggest any mechanisms by which turf causes higher lower-leg injury rates nor a means to make artificial surfaces safer.

Aging, Physical Activity and Blood Flow

quadriceps muscle anatomy 

Physical activity diminishes age’s affect on the reduction of the potent vasodilator NO. Elevated NO in the blood results from or causes a reduction in the amount of dangerous radical oxygen species in the blood.

 

Many physiology studies have shown that reactive oxygen species increase in humans with age. Reactive oxygen species have been impacted in the age-related deterioration of the brain. Fortunately, physical activity has been shown to decrease the concentration of reactive oxygen species. The role that physical activity has on preventing Alzheimer’s Disease through reactive oxygen species reduction was discussed in a previous post on ExerciseMed.org. The focus here is the effect that physical activity has on the concentration of reactive oxygen species in the skeletal muscle.

Nitric oxide (NO) is a key regulator of vasodilation in blood vessels feeding the skeletal muscles. When reactive oxygen species are present, nitric oxide gets catabolized. One of the reasons antioxidants are so popular in the health food industry is because, as their name suggests, antioxidants eliminate reactive oxygen species. Older sedentary humans should show the greatest increase in NO following treatment with antioxidants because antioxidants are more prevalent in older patients who abstain from physical activity. One recent Danish study tested this hypothesis by treating subjects with the antioxidant N-acetylcysteine (Lifelong physical activity prevents an age-related reduction in arterial and skeletal muscle nitric oxide bioavailability in humans, 2012.  Michael Nyberg, et al.).

The study placed 8 subjects into each group: a sedentary youth group (mean age: 23), a sedentary older group (mean age: 66) and a physically active older group (mean age: 62). The subjects performed knee extensions for the exercise variable. The study found that the sedentary youth group had the highest concentration of NO metabolites, NOx. The physically active older group, although lower than the youth group, had a higher concentration of NOx in muscle tissue than the sedentary older group. When the older sedentary group was provided with antioxidant N-acetylcysteine (NAC) their NOx levels rose to the active older group with out antioxidants (Control, CON). Both older groups saw a significant increase in NOx concentration, suggesting that NO was compromised by radical oxygen species. At 45% of maximum power output only the older sedentary group saw increases in muscle interstitial NOx concentration following injection of antioxidant NAC. The results can be seen in the figure below.

Screen Shot 2012-11-12 at 8.29.10 AM

Figure 1. Muscle interstitial NOx at rest and during 12 W and 45% Wmax without and with infusion of NAC. Exercise was performed at the same absolute workload of 12 watts and at a relative workload corresponding to 45% Wmax without (CON) or with (NAC) infusion of N-acetylcysteine in young sedentary, older sedentary and older active subjects. †Significantly different from young sedentary within same condition, P < 0.05; ∗significantly different from control conditions, P < 0.05; #significantly different from rest within same condition, P < 0.05.

The older active group showed no decrease in NO2 in their arteries when treated with antioxidant NAC. The young and old sedentary groups both saw increases in arterial NO2 (as shown in the figure below only the older sedentary group saw a significant increase in arterial NO2). This means that only the older active group was able to contain the radical oxygen species.

Screen Shot 2012-11-12 at 4.16.55 PM

Figure 2. Plasma NO2− and NOx at rest without and with infusion of NAC. Femoral arterial blood samples collected during rest without (CON) or with (NAC) infusion of N-acetylcysteine in young sedentary, older sedentary and older active subjects. ∗Significantly different from control conditions, P<0.05

Although antioxidants increased the amount of NO in the blood, the blood flow to the legs did not increase following antioxidant administration. The increase in NO concentration did not cause an increase in leg muscle blood flow. This result is surprising because NO is known to be a potent vasodilator. Thus, exercise-induced hyperemia (increased blood flow) must occur through a pathway other than NO in the legs.

Figure 3. Leg haemodynamics at rest and during 12 W and 45% Wmax. Exercise and rest without (CON) or with (NAC) antioxidant in young sedentary, older sedentary and older active subjects. †Significantly different from young sedentary within same condition; #significantly different from rest, ‡significantly different from older sedentary within same condition.

This study showed that one mechanism by which NO is increased in physically active elders is through a decrease in radical oxygen species. Another mechanism is an increase in Nitric Oxide Synthase (NOS), a protein that synthesizes NO. The physically active older subjects were found to have a significantly higher amount of endothelial NOS and neural NOS. The authors suggest that the elevated amount of NOS in active older subjects could act as a radical oxygen species scavenger. The increase in NO production may compensate for the age-related increase in radical oxygen species.

In conclusion, the discussed study found that physical activity decreased age’s affect on nitric oxide (NO) decline in the blood. NO is a vasodilator, it opens up blood vessels. The concentration of radical oxygen species was lower in the physically active older subjects than the sedentary older active subjects. The older active subjects had the highest amount of nitric oxide synthase (NOS).  Since radical oxygen species decrease NO concentration, NO concentration may be elevated in the physically active because the combined effects of lower radical oxygen species and higher NOS. Another possibility is that NO scavenges radical oxygen species. This means that the low concentration of radical oxygen species is the product, rather than the cause, of high NO levels in the blood. In addition, nitric oxide was found to play no role in hyperemia during physical activity. Regardless, physical activity is important for maintaining vascular health by maintaining nitric oxide levels with aging.

Brain Plasticity through Resistance Training

boy running

A study finds that resistance training generates memory gains in mice greater than those seen in resistance-free endurance training. The biochemical pathway appears to be a neurotrophic factor, BDNF.

 

 

In a recent post on Exercisemed.org, the effects of endurance training on memory was discussed. That paper, released in the spring of 2012, discussed the impact that brain derived neurotrophic factor (BDNF) had on memory in middle aged mice (Running throughout Middle-Age Improves Memory function, Hippocampal Neurogenesis, and BDNF Levels in Female C57BI/6J Mice, 2012; Michael W. Marlatt, et al.). The study found that the release of BDNF through endurance exercise improved the memory of middle-aged, female mice. The mechanism is likely brain plasticity, the ability of neurons to form new connections and pathways. A Japanese study published this month found that mice participating in a high-load resistance training program had an even stronger improvement in memory (Voluntary resistance running with short distance enhances spatial memory related to hippocampal BDNF signaling, 2012. Min Chul Lee, et al.).

The study used running wheels to exercise the mice. The mice were assigned to three groups: a sedentary control group (Sed), voluntary wheel running with no resistance (WR) and voluntary wheel running with increasing resistance.  The mice were maintained with these controls for 30 days. As the figure below shows, the mice with resistance-free running wheels ran a greater distance than their counterparts with resistance running wheels. However, the work performed was higher in the resistance wheel group. Resistance is given as a percentage of body weight.

Screen Shot 2012-10-29 at 3.02.10 PM

The mice were tested for memory capacity and general cognitive function with a water maze. The water maze has a hidden platform that the mice must find.  The mice were placed in the maze four days in a row.  On average, the mice became more efficient at finding the hidden platform each day. As the figure below demonstrates, the mice with running wheels performed better than the sedentary mice (Sed) regardless of whether or not they had resistance (RWR) or no resistance (WR) on their running wheels. The mice that did resistance training spent more time in the target quadrant, quadrant P (graph C).

Screen Shot 2012-10-29 at 3.19.49 PM

Like other studies, the neurotropic factor BDNF was found to be higher in the wheel running groups. In addition, the protein p-CREB was found to be higher in the wheel running groups and significantly higher in the resistance wheel running group. BDNF and p-CREB have both been implicated by previous studies in brain plasticity and memory. The authors speculated that the gains in resistance training were observed because the training was voluntary. Thus, the negative affects of stress on the brain did not occur. This is the first study to suggest that quality over quantity is the rule for brain plasticity.

Exercise’s effect on brain plasticity is a very “hot” research subject right now.  However, no research has been done on the biochemical affects of exercise in human subjects. While other studies have been focused on endurance training’s effect on brain plasticity, this is the first to look at how shorter resistance training affects the brain.

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.