延迟性肌肉酸痛的发生机制与防治研究

Study on the Mechanism and Prevention of Delayed-onset Muscle Soreness

文章采用文献资料法和逻辑分析法对延迟性肌肉酸痛的发生机制及防治成果进行分析整理。发现延迟性肌肉酸痛并不是单一因素作用的结果,而是机体自我保护和恢复的一种多因素综合机制。其表现为机械性肌纤维损伤,局部组织缺血、缺氧、ATP供应不足,一方面致使肌小结产生痉挛,引发炎症,使神经末梢产生疼痛;另一方面引起酶系失活,导致ATP依赖性离子泵功能下降,致使细胞内Ca^(2+)、Na^+、K^+离子异常,而线粒体内Ca^(2+)的堆积会抑制线粒体的呼吸,致使无氧耗能增加,使线粒体内自由基产生率显著上升,氧自由基攻击细胞器导致细胞坏死,最终产生延迟性肌肉酸痛。

The mechanism of delayed muscle soreness and its prevention and treatment were analyzed by literature data and logic analysis.The study found that delayed muscle soreness is not a single factor effect of the results, but the body＇s self-protection and recovery of a multi-factor integrated mechanism.The performance of mechanical muscle damage, local tissue ischemia, hypoxia, ATP supply, on the one hand resulting in muscle spasms, causing inflammation, nerve endings to produce pain;On the other hand it is caused by enzyme inactivation, resulting in ATP-dependent ion pump function decreased, resulting in intracellular Ca^2 ＋, Na^ ＋, K ^＋ ion abnormalities, and mitochondrial Ca^2 ＋ accumulation will inhibit mitochondrial respiration, resulting in increased oxygen-free energy, the have the mitochondria free radicals produce a significant increase in oxygen free radicals attack organelles, lead to cell necrosis, and ultimately produce delayed muscle soreness.