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The fatigue that results from physical exercise is a multifactorial phenomenon that is comprised of complex interactions between physiological and psychological factors. Fatigue is assumed to be an inability to maintain the required force or power or an increasing difficulty to continue the work rate at a given exercise intensity. Taking into account that homeostasis disturbances may be harmful, fatigue should be considered a defense mechanism that prevents tissue damage by reducing the intensity of or even interrupting physical activity. Fatigue is known to have peripheral and/or central origins. Although most studies focus peripheral factors, which include circulatory, metabolic, muscular, nutritional and thermoregulatory disorders, exercise-induced cerebral metabolism and neurohumoral or neurotransmitter turnover are also implicated in fatigue genesis. “Central fatigue” refers to these central nervous system alterations that may prevent muscular and neural damage by failing to drive the muscles appropriately. Most authors consider central fatigue during prolonged exercise to be a consequence of the accumulation or depletion of neurotransmitters, serotonin in particular. Although the role of serotonergic neural trafficking on exercise performance has been well documented, dopamine and noradrenaline neurotransmissions also contribute to central fatigue. In addition to having their activity modified by exercise, all of these brain monoamines exhibit relevant thermoregulatory effects. These amines play an important role in the function of thermoregulatory centers, such as the preoptic area and the anterior hypothalamus, and it is hypothesized that changes in their turnover are associated with the development of fatigue as a consequence of heat imbalances. The brain is especially endangered by hyperthermia. For this reason, the exacerbation of exercise-induced hyperthermia appears to diminish the central nervous system drive to the working muscles; this protects the brain from thermal damage while causing a detriment to physical endurance. This effect is more pronounced when hyperthermia occurs simultaneously with inhibitory signals from the central nervous system, as in the case of altered neurotransmitter metabolisms. Even though it has been stated that central fatigue

The Involvement of Brain Monoamines in the Onset of Hyperthermic Central Fatigue