超微结构变化及其与肌肉疲劳、损伤的关系

Ultrastructural Changes and the Relationships Between Muscle Fatigue and Muscle Injury

近年来有大量文献综述讨论这一专题。运动时肌肉损伤使输出功率减低,肌肉疲劳。运动后即刻超微结构变化最常见的表现涉及肌小节损伤,肌质网和线粒体颗粒肿胀。超微结构的变化程度参与肌肉疲劳的发生现未知。最可能的机制涉及直接抑制肌质网Ca^(2+)释放通道和在某种场合因兴奋收缩偶联阻断,但钙如何促使细胞损伤也仍未解决。钙激活蛋白酶类,磷脂酶A可能促进肌肉损伤,由于肌膜和亚细胞器膜结构降解,力竭运动后自由基增加,导致脂质过氧化增加和肌细胞完整性丧失。自由基能促进疲劳尤其显得重要,自由基防护剂可预期在一定程度上保护肌细胞。

In recent years, there have been a number of reviews discussing ' ultrastructural changes and the relationships between muscle fatigue and muscle injury' . The reduced power output caused post-exercise ultrastructural changes most commonly involve sarcomere disruptions, swollen SR and mitochondrial vesicles. The extent of ultrastructural changes participate in the development of fatigue is unknown. The most likely mechanism involves a direct inhibition of the SR Ca2+ releasing channel and in certain situation a block in E-C coupling, but how Ca2+ triggering cell injury remains unresolved. Ca2+-activated proteinas, phospholipase A could intitate muscle injury by degrading the sarcolemma and internal membrane structures. Free radicals increased following exhaustive exercise result in increased lipid peroxidation and loss of muscle cell integrity. Free radicals' increasing fatigue is especially important. Free radical protectors may be expected to protect muscle cell in a certain extent.