Initial events in exercise-induced muscular injury.
Initial events in exercise-induced muscular injury.
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DOI：
10.1249/00005768-199008000-00002
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发表时间：
1990-08
影响因子：
4.1
通讯作者：
Robert B. Armstrong
中科院分区：
文献类型：
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作者：
Robert B. Armstrong
在不习惯的运动，特别是离心收缩后，立即有骨骼肌纤维损伤的证据：a）在一些肌节中正常肌丝结构的破坏，可以用光学和电子显微镜观察到，和B）肌内蛋白质的损失（例如，肌酸激酶）进入血浆，表明对肌膜的损伤。这种病理可能是造成离心运动后肌肉力量暂时下降和延迟性疼痛的原因。这种损伤的机制尚不清楚，但细胞内Ca 2+稳态的丧失可能起主要作用。在其他实验性肌肉损伤模型中，升高的[Ca 2 +]i似乎通过激活磷脂酶A2引起肌肉酶的释放，这反过来又可以通过产生白三烯和白藜芦醇、通过形成自由O2自由基（在随后的脂氧合酶和环氧合酶反应中）和/或通过释放去污剂溶血磷脂诱导对肌膜的损伤。另一方面，[Ca 2 +]i增加导致肌原纤维快速损伤的机制尚不清楚。无论原因如何，损伤过程中的初始和早期事件都是自生的;即，它们是肌细胞固有的并且在吞噬细胞进入损伤部位之前发生。
Immediately following unaccustomed exercise, particularly that with eccentric contractions, there is evidence of injury to skeletal muscle fibers: a) disruption of the normal myofilament structures in some sarcomeres, observable with both light and electron microscope and b) loss of intramuscular proteins (e.g., creatine kinase enzymes) into the plasma, indicating damage to sarcolemma. This pathology is probably responsible for the temporary reductions in muscle force and delayed-onset soreness that can occur following eccentric exercise. The mechanisms underlying this injury are not known, although loss of intracellular Ca2+ homeostasis could play a primary role. In other experimental muscle injury models, elevated [Ca2+]i appears to cause release of muscle enzymes through activation of phospholipase A2, which in turn could induce injury to sarcolemma through production of leukotrienes and prostaglandins, through free O2 radical formation (in the subsequent lipoxygenase and cyclooxygenase reactions), and/or through release of detergent lysophospholipids. On the other hand, the mechanism responsible for the rapid damage to myofibrils caused by increased [Ca2+]i is unknown. Regardless of the cause(s), the initial and early events in the injury process are autogenetic; i.e., they are indigenous to the muscle cells and occur before phagocytic cells enter the injury site.