EXERCISE-INDUCED MUSCLE DAMAGE
EXERCISE-INDUCED MUSCLE DAMAGE
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DOI：
10.1055/s-2007-1021034
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发表时间：
1994-04-01
影响因子：
2.5
通讯作者：
KUIPERS, H
中科院分区：
文献类型：
--
作者：
KUIPERS, H
肌肉过度使用与收缩元件的结构损伤相关，并反映在延迟性肌肉酸痛（DOMS）中。机械应力被认为是导致肌肉损伤的主要因素。最初的损伤之后是炎症反应，最终是再生。钙被认为在引发炎症变化中起重要作用。人类的活检数据表明，人类的炎症变化与疼痛等级并不平行，这使得肌肉疼痛的延迟发作无法解释。众所周知的现象是，一轮离心运动对第二轮运动引起的损伤具有长期持久的保护作用。实验证据表明，这种适应可以部分归因于结缔组织的增加。血浆CK活性已被广泛用作肌肉损伤量的标志物。研究表明，运动诱导CK释放的性别差异是由性激素依赖的肌膜通透性差异引起的。血浆CK活性不一定反映结构损伤的程度。
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.