Neural control of force output during maximal and submaximal exercise

A common belief in exercise physiology is that fatigue during exercise is c aused by changes in skeletal muscle metabolism. This 'peripheral' fatigue r esults either from substrate depletion during submaximal exercise or metabo lite accumulation during maximal exercise in the exercising muscles. Howeve r, if substrate depletion alone caused fatigue, intracellular ATP levels wo uld decrease and lead to rigor and cellular death. Alternatively, metabolit e accumulation would prevent any increase in exercise intensity near the en d of exercise. At present, neither of these effects has been shown to occur , which suggests that fatigue may be controlled by changes in efferent neur al command, generally described as 'central' fatigue. In this review, we examine neural efferent command mechanisms involved in f atigue, including the concepts of muscle wisdom during short term maximal a ctivity, and muscle unit rotation and teleoanticipation during submaximal e ndurance activity. We propose that neural strategies exist to maintain musc le reserve, and inhibit exercise activity before any irreparable damage to muscles and organs occurs. The finding that symptoms of fatigue occur in th e nonexercising state in individuals with chronic fatigue syndrome indicate s that fatigue is probably not a physiological entity, but rather a sensory manifestation of these neural regulatory mechanisms.