Chronic fatigue is caused by a depletion in glycogen stores. The remedy is eating a diet high in carbohydrates.
Most athletes have experienced burn-out, also known as chronic fatigue, at some point in their athletic careers. Chronic fatigue is when an athlete becomes persistently exhausted during consecutive days or months of strenuous training to the point that their form and performance markedly suffer. Chronic fatigue usually occurs after a dramatic increase in training or late in a season; hence an additional name, overtraining. Chronic fatigue is a phenomenon that is found across many sports. In fact, a study was recently released looking at measures athletic trainers of professional soccer teams took to combat chronic fatigue (Recovery in soccer, 2013. Nedelec M, et al.).
It has long been known that the physiological root of chronic fatigue is a depletion of muscle glycogen stores (Effects of repeated days of intensified training on muscle glycogen and swimming performance, 1988. David L Costill, et al.). The simplest way to combat chronic fatigue is by eating a diet high in carbohydrates during periods of physically taxing training. The aforementioned 1988 study had twelve elite swimmers more than double their daily mileage for ten consecutive days. They found that the swimmers who were unable to complete the training had significantly lower levels of muscle glycogen. Interestingly, the group of swimmers that were unable to complete the training had a low carbohydrate diet to begin with and did not increase their caloric intake despite the increase in training. The differences in glycogen stores of those able to tolerate the training increase (group "B") and unable to tolerate the training increase (group "A") can be seen in figure 1 below.
What is it about glycogen reserves that are so important? Glycogen is the body's primary source of energy for exercise lasting longer than ten seconds up to 20 minutes or longer depending on the exercise intensity. As glcogen stores, found in both the liver and muscle itself, are used up, the body begins shifting over to fats. The problem is that fats require more oxygen to catabolize to an equivalent amount of energy (measured in ATP). When glycogen is used up, exercise capacity is severely limited. To make matters worse, the brain can only utilize blood glucose for energy (under non-fasting conditions). Whatever glucose is left is needed for the brain. The muscles must switch to almost 100% fat. In marathon runners this switch is often referred to as "hitting the wall." It usually occurs in a trained marathon runner around miles 17-20.
Obviously having large glycogen stores is important for marathon runners, but what about athletes whose sports require a much shorter duration of continuous exercise? They are affected as well because even as glycogen begins being used up the body is switching over to more costly fat metabolism; this occurs even with relatively short durations of exercise. For example, a 90 minute soccer match leaves players' glycogen reserves severely depleted (The copenhagen soccer test: physiological response and fatigue development, 2012. Bendisken M, et al.). The way that glycogen depletion creates fatigue may be through restriction of Ca2+release, which causes muscle fiber contraction (Role of glycogen availability in sarcoplasmic reticulum Ca2+ kinetics in human skeletal muscle, 2011. Ortenblad, et al.). As exercise intensity (%VO2max) increases, the body obtains a larger percentage of its energy from carbohydrates (see figure 2). As a side note for those looking to burn weight, while intense exercise burns carbohydrates, moderate exercise is what burns unwanted fat.
Recovery is an energy intensive process. Carbohydrate ingestion aids recovery (The use of recovery methods post-exercise, 2005. Reilly and Ekblom). Most likely the way that depleted glycogen reserves hinder recovery is via reduced energy availability for recovery. There are many companies in the business of selling recovery products. Perhaps this is the reason for the plethora of misinformation on what the body needs to recover. The research suggests that all the body needs is plenty of carbohydrates, sources of which do not necessarily need to be marketed directly to athletes.
Next time you start feeling burnt out, just remember this is your body's way of telling you your glycogen reserves are running low. Time to have pasta for dinner!
Brown fat (pictured on the right) is able to freely burn off excess fat. A team at Harvard found one way to stimulate its production is through exercise.
It seems every month a radical new weight loss method is discovered. So talk of brown adipose tissue (BAT), or simply brown fat, revolutionizing the weight loss industry has to be met with a degree of skepticism. However, brown fat could be important to fighting the obesity epidemic. Brown fat is a specialized type of adipose tissue that catabolizes fat to produce heat. Most adipose tissue store fat to be released when sugar levels are too low. When the liver's glycogen stores become depleted, the body switches to utilizing its fat reserves. The adipocytes that take up, store and release fatty acids are what comprise white fat.
Unlike white fat, brown fat takes up fatty acids and turns that fat into heat. Thus, brown fat literally "burns calories". It accomplishes this by uncoupling the dephosphorylation of ATP to ADP. ATP produced by oxidative phosphorylation generates heat rather than powering cellular processes such as muscle fiber contraction. The brown color of brown fat stems from large amounts of mitochondria flecked throughout the adipocyte. Brown fat is interspersed with an abundance of blood vessels that dissipate heat to the rest of the body. Brown fat has been known for many years. It exists in hibernating animals and mammalian infants as a thermoregulator. However, only in the last several years has it been known to exist in adult humans (Human Brown Adipose Tissue, 2010. Sven Enerbäck.). The figure below shows where in the human adult and infant the brown fat is found.
Brown fat has been shown to decrease weight in diet-induced obesity mice. The study put brown fat into obese mice and found that weight gain was severely minimized. Not only was weight lost, but insulin insensitivity was markedly reduced. Brown fat may be able to treat diabetes and obesity (Brown adipose tissue regulates glucose homeostasis and insulin sensitivity, 2013. Kristin I. Stanford, et al.). The question then is how can we get more brown fat? Although the research goes back and forth, the latest research suggests that white adipose tissue (undesired fat) and brown adipose tissue are closely related in development. In fact, scientists have been able to "brown" white fat both in vitro and in vivo with a hormone called irisin. As a hint to its importance, irisin is highly conserved: the sequence is 100% identical in mice and humans (by comparison, insulin is 85% identical in mice and humans).
Last year a team at Harvard found that exercise increased production of irisin in mice through the upregulation of the PGC1-alpha (A PGC1-alpha-dependent myokine that drives brown-fat-like development of white fat and thermogenesis, 2012. Pontus Bostrom, et al.). Humans also increase irisin production during exercise. Through the biochemical pathway is not completely understood, a three fold increase in irisin has notable effects on browning of adipose tissue. Irisin may have undiscovered benefits to other tissues. It seems paradoxical that exercise, which expends energy itself, would generate brown fat. The authors speculate that muscle contraction to bring on shivering may be the evolutionary link between brown fat and exercise.
In summary, brown fat decreases obesity and increases glucose tolerance. Whether doctors are able to harness brown fat to clinically treat obesity or diabetes remains to be seen. Next time you work out, take satisfaction in knowing that exercise continues to burn calories even after you finish.
According to study published this month, aerobic exercise does not hinder one's attempt to gain muscle mass via resistance training.
Within the physical trainer community there is a misconception that aerobic training reduces muscle mass. The belief is that aerobic activity burns muscle and prevents bulking up. It is true that aerobic activity burns fat; so aerobic activity prevents one from bulking up in that sense. However, a Swedish study published this month found that not only does aerobic exercise not prevent muscle gain, it actually helps build muscle mass (Aerobic exercise does not compromise muscle hypertrophy response to short-term resistance training, 2013. Tommy R Lundberg, et al.).
The study had ten, healthy male participants train one leg with just resistance training and the other with both resistance training and aerobic exercise. The training program lasted 5 weeks. The researchers measured physical characteristics, biochemistry and performance of both legs (specifically the quadriceps) before and after the training program. Perhaps most surprising was the finding that the increase in muscle volume in the leg receiving both aerobic training and resistance training was significantly greater than the leg receiving resistance training alone. In addition, MRI scans showed that the cross sectional area of aerobic and resistance trained legs was significantly greater than legs doing resistance training alone. The changes in muscle volume of the quadriceps muscle with pure resistance training (RE) and both aerobic training and resistance training (AE+RE) can be seen in the figure below.
Although muscle volume (hypertrophy) was increased by additional aerobic training, the maximal velocity and power was compromised by aerobic training. The reason for this may be because even though the aerobic training increases muscle fiber size, it recruits type-II (fast-twitch) muscle fibers to type-I (slow-twitch) muscle fibers. It should be noted that the recruitment was not significant, but there was an effect. The progression of maximal power of each leg over the course of the resistance sessions can be seen in the figure below.
Being physiologists, the researchers also analyzed gene expression of VEGF (a growth factor that increases blood vessel proliferation), myostatin (another growth factor that inhibits muscle growth and differentiation), PGC-1alpha (a transcriptional coactivator involved in energy metabolism), and muscle atrophy factors MuRF-1 and atrogin-1. The graph below shows how each training program affected the respective gene expression.
Apparently, if size is all that matters than aerobic exercise is not of consequence. Maximum power was decreased in aerobically trained legs. This presented a paradox: the larger muscles had less maximal power. Thus, aerobic exercise does not compromise muscle hypertrophy (muscle size), but it does reduce maximum power output and velocity.
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.