Exercise-induced muscle damage and adaptation.

Novel, unaccustomed exercise has been shown to result in temporary, repairable skeletal muscle damage. After exhaustive endurance exercise, muscle damage can be produced by metabolic disturbances associated with ischaemia. Extensive disruption of muscle fibres also occurs after relatively short term eccentric exercise where high mechanical forces are generated. Biopsies taken after repetitive eccentric muscle actions have revealed broadening, streaming and, at times, total disruption of Z-discs. Muscles that develop active tension eccentrically also become sore, lose inherent force-producing capability, and show a marked release of muscle proteins into the circulation. Because creatine kinase (CK) is found almost exclusively in muscle tissue, it is the most common plasma marker of muscle damage. Despite the universal use of CK as a marker, several factors with regard to efflux and clearance remain unexplained. Also the large intersubject variability in response to exercise complicates its interpretation. Damage progresses in the postexercise period before tissues are repaired. However, the mechanism to explain exercise-induced muscle damage and repair is not well defined. Among the factors that may influence the damage and repair processes are calcium, lysosomes, connective tissue, free radicals, energy sources, and cytoskeletal and myofibrillar proteins. Physical conditioning results in an adaptation such that all indicators of damage are reduced following repeated bouts of exercise. Recently, investigators have suggested that the prophylactic effect of training may be due to performance of a single initial exercise bout. Following a second bout of exercise performed 1 to 6 weeks after the first bout, there is a reduction in morphological alterations and performance decrements and a profoundly reduced elevation in plasma CK levels. Several hypotheses have been presented to explain the repeated bout or rapid training effect. Stress-susceptible fibres may be eliminated or susceptible areas within a fibre may undergo necrosis and then regenerate. These regenerated fibres, along with adaptations in the connective tissue, may provide greater resistance to further insult.