title: Muscle damage and endurance events.
abstract: Intensive training for and competition in endurance events like the marathon are accompanied by injury to fibres in the active skeletal muscles. Evidence for the injury comes from the increases in intramuscular enzymes and myoglobin found in the blood following the exercise, from the subjective sensation of soreness in the muscles in the post-exercise period, and from direct histological examination of samples of the damaged muscles. Histological studies demonstrate that some muscle fibres undergo degenerative changes following the exercise; the necrosis is accomplished by macrophages and other phagocytic cells that invade the injured cells and the adjacent interstitium. Following the degeneration the fibers appear to be regenerated so that there is not a net loss of fibres. Precisely what initiates the cellular damage is not known, but hypotheses suggested include, 'metabolic overload' and 'mechanical strain'. Eccentric contractions are known to cause the greater amount of damage in muscles, which suggests that high local tensions in fibres may be more important than metabolic considerations in the aetiology of the injury. Training reduces the magnitude of the damage that occurs in response to a given exercise task, although competitors in endurance events may demonstrate chronic muscle injury because of increasing training intensities. Other than training, there is no compelling evidence that any drug treatment or preventative measures will lessen this form of injury.
mesh_terms: D000818:Animals; D001265:Athletic Injuries / Q000209:etiology* / Q000378:metabolism; D003402:Creatine Kinase / Q000097:blood; D006801:Humans; D009132:Muscles / Q000293:injuries* / Q000378:metabolism; D009212:Myoglobinuria / Q000209:etiology; D010146:Pain / Q000209:etiology; D010807:Physical Endurance; D005082:Physical Exertion; D013314:Stress, Mechanical
chemical_list: D003402:Creatine Kinase