Bodybuilding

During prolonged exercise, athletes become fatigued. For many years, exercise scientists believed that fatigue was simply related to peripheral muscle glycogen depletion and perhaps the hypoglycemia which may occur during prolonged exercise. However, more recent studies indicated that athletes fatigue even though blood glucose levels were maintained during exercise and a sufficient amount of glycogen was available in the muscle. These findings suggested that fatigue could not simply be explained by peripheral adaptations but that other factors may be involved in the fatigue process during prolonged exercise. The potential role that central fatigue may play in overtraining, and dietary strategies that may help delay central fatigue.

Central Fatigue Hypothesis

Newsholme, Blomstrand, and colleagues initially advanced the theory that fatigue during prolonged exercise may be partly related to exercise-induced alterations in the central nervous system. The theory suggests that as muscle glycogen levels decline during exercise, there is an increased oxidation of fat and the branched-chain amino acids (BCAAs) leucine, isoleucine, and valine as fuel substrates. As a result, free fatty acid (FFA) levels in the blood gradually increase while the availability of BCAAs in the blood decreases. The increase in FFA levels in the blood is accompanied by a release of the amino acid tryptophan from albumin, serving to increase the level of free tryptophan in the blood. The result is that as one exercises, the ratio of free tryptophan to BCAA steadily increases.

Increases in the ratio of free tryptophan to BCAA have been shown to increase the entry of tryptophan into the brain. Increased concentrations of tryptophan in the brain have been reported to promote the formation of the neurotransmitter beta-hydroxytryptamine (serotonin). Increased levels of serotonin in the brain and peripheral tissues have been reported to induce sleep, depress motor neuron excitability, influence autonomic and endocrine function, and suppress appetite in animal and human studies. Consequently, an exercise-induced imbalance in the ratio of free tryptophan to BCAA has been implicated as a possible cause of acute physiological and psychological fatigue (central fatigue). It has also been hypothesized that chronic elevations in serotonin levels, which may occur in athletes who overtrain, may explain some of the reported signs and symptoms of the overtraining.

Although the central fatigue theory seems straightfor­ward, there has been debate in the scientific community regarding the validity of the hypothesis. Segura and Ventura hypothesized that the increase in the free tryptophan to BCAA ratio may help to decrease the perception of pain, thus improving exercise performance by increasing the pain threshold. However, given the most recent research there is more sound scientific evidence to support the theory that central influences during exercise may play a role in the onset of fatigue under certain conditions. However, because the potential causes of overtraining are multifaceted and have yet to be fully understood, the degree to which central fatigue may contribute to overreaching and/or overtraining remains to be determined.

Nutritional Needs of the Immune System:

Although moderate exercise has been reported to enhance immunity, intense prolonged exercise has been found to temporarily suppress the immune system. For example, research has indicated that following intense exercise, the immune system may be depressed for as long as 6 hours. This open window of suppressed immune function may allow the body to be more susceptible to acquiring host infections. To support this theory, several studies have reported that following intense exercise like a marathon, athletes have a greater incidence of upper respiratory tract infections (URTIs) for several weeks following the event. Additionally, athletes who overreach and/or overtrain often get URTIs, ear infections, and/or colds. This suggests that athletes who train too often or too intensely may experience a chronically suppressed immune system.

The primary metabolic fuel for the lymphocyte is glutamine. The availability of glutamine affects lymphocytic function. In this regard, in vitro and in vivo, evidence suggests that increasing the availability of glutamine enhances immune function while decreasing glutamine levels suppresses immune function. During high­intensity intermittent and prolonged exercise, it has been suggested that glutamine levels decline in the blood. The reason for this is that glutamine, like BCAAs, readily serves as a metabolic substrate during exercise. The exercise-induced hypoglutaminia has been reported to last up to 6 hours following high-intensity intermittent exercise. Moreover, some overtrained athletes have been reported to have chronically low glutamine levels Consequently, one theory of exercise-induced immuno-suppression is that decreased glutamine availability following exercise may serve to suppress lymphocytic function, making it more difficult to respond to immune challenges. Athletes involved in periods of intensified training that often involves training more than once per day may therefore be more susceptible to a hypoglutaminia-induced immunosuppression.