Adaptations to exercise training and contraction-induced muscle injury in animal models of muscular dystrophy
Adaptations to exercise training and contraction-induced muscle injury in animal models of muscular dystrophy
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DOI：
10.1097/00002060-200211001-00016
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发表时间：
2002-11-01
影响因子：
3
通讯作者：
Fowler, WM
中科院分区：
文献类型：
--
作者：
Carter, GT;Abresch, RT;Fowler, WM
本文综述了肌肉营养不良动物模型中运动训练和收缩所致肌肉损伤的研究现状。大多数运动训练研究都比较了正常肌肉和营养不良肌肉与运动的适应情况。患病肌肉对运动的适应发生在许多水平上，从细胞外基质开始，但也涉及细胞骨架结构、肌肉收缩能力、修复机制和基因调节。大多数运动损伤研究试图确定肌营养不良蛋白缺乏的肌肉对收缩引起的损伤的易感性。在动物模型中有一些证据表明，患病的肌肉可以适应并对机械压力做出反应。然而，运动损伤研究表明，营养不良的肌肉对高机械力的敏感性增加。大多数涉及运动训练的研究表明，营养不良动物的肌肉适应能力与对照肌肉的适应能力定性上相似。营养不良的有害影响通常只发生在患有晚期肌肉纤维变性的老年动物或经过高阻力的偏心训练后。将这些结论应用于人类的主要限制是人类和基因同源动物模型在表型表达上的差异，以及人类和这些动物模型之间显著的生物力学差异。
This article reviews the current status of exercise training and contraction-induced muscle-Injury investigations in animal models of muscular dystrophy. Most exercise-training studies have compared the adaptations of normal and dystrophic muscles with exercise. Adaptation of diseased muscle to exercise occurs at many levels, starting with the extracellular matrix, but also involves cytoskeletal architecture, muscle contractility, repair mechanisms, and gene regulation. The majority of exercise-injury investigations have attempted to determine the susceptibility of dystrophin-deficient muscles to contraction-induced injury. There is some evidence in animal models that diseased muscle can adapt and respond to mechanical stress. However, exercise-injury studies show that dystrophic muscles have an increased susceptibility to high mechanical forces. Most of the studies involving exercise training have shown that muscle adaptations in dystrophic animals were qualitatively similar to the adaptations observed in control muscle. Deleterious effects of the dystrophy usually occur only in older animals with advanced muscle fiber degeneration or after high-resistive eccentric training. The main limitations in applying these conclusions to humans are the differences in phenotypic expression between humans and genetically homologous animal models and in the significant biomechanical differences between humans and these animal models.