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通过大鼠比目鱼肌体外实验，探讨牵拉负荷导致的肌肉损伤与肌细胞内酶的流出，骨骼肌细胞线粒体钙浓度（ＭＣＣ）以及细胞脂质过氧化反应之间的关系。４ｈ培养和牵拉后发现，牵拉负荷使肌肉ＭＣＣ显著性增高（Ｐ＜０．０１），且比对照组高６７．９％。脂质过氧化反应终产物丙二醛（ＭＤＡ）和肌酸激酶（ＣＫ）的释放无显著性变化（与对照组比较，Ｐ＞０．０５）。结果提示，骨骼肌细胞ＭＣＣ的增接与肌肉损伤有密切关系，并且可能是肌肉损伤的始发因素，介导一系列肌肉损伤机制的发生；脂质过氧化反应也可能发生在ＭＣＣ变化之后；ＣＫ的流出与牵拉损伤似无直接关系
The rat soleus muscle in vitro experiments to explore the tensile load induced muscle damage and intracellular enzyme efflux, skeletal muscle mitochondrial calcium concentration (MCC) and the relationship between lipid peroxidation. After 4 h of culture and stretching, the muscle MCC was significantly increased (P <0.01) by pulling load and 67.9% higher than that of the control group. There was no significant difference in the release of malondialdehyde (MDA) and creatine kinase (CK) from the end products of lipid peroxidation (P> 0.05). The results suggest that MCC in skeletal muscle cells is closely related to muscle damage and may be the initiating factor of muscle injury and mediate a series of muscle injury mechanisms. Lipid peroxidation may also occur after MCC changes. CK outflow and pull injury does not seem to have a direct relationship