Exercise-induced muscle damage.
Muscular overuse is associated with structural damage of the contractile elements and reflected in delayed onset muscle soreness (DOMS). Mechanical stress is supposed to be the major contributing factor for inducing muscle damage. The initial damage is followed by an inflammatory response and eventually by regeneration. Calcium is assumed to play an important role in triggering the inflammatory changes. Biopsy data in man indicate that the inflammatory changes in humans do not parallel the soreness ratings, leaving the delayed onset of muscle soreness unexplained. It is a well known phenomenon that one bout of eccentric exercise has a long lasting protective effect against damage induced by a second bout of exercise. Experimental evidence suggests that this adaptation can partly be attributed to an increase in connective tissue. Plasma CK activity has widely been used as a marker for the amount of muscle damage. It has been shown that gender differences in exercise-induced CK release are caused by sex hormones dependent differences in sarcolemmal permeability. Plasma CK activity does not necessarily reflect the amount of structural damage.
Kuipers
H
H
University of Limburg, Maastricht, The Netherlands.
D003402:Creatine Kinase / Q000097:blood; D012090:Cumulative Trauma Disorders / Q000201:enzymology / Q000503:physiopathology*; D015444:Exercise / Q000502:physiology*; D005260:Female; D006801:Humans; D008297:Male; D009132:Muscles / Q000201:enzymology / Q000503:physiopathology*; D012206:Rhabdomyolysis / Q000201:enzymology / Q000503:physiopathology
D003402:Creatine Kinase