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80年代中期，许多研究证明，运动中乳酸的产生与体内是否缺氧无关，并指出“氧债”、“氧亏”、和“无氧阈”是3个错误概念，提出了“运动后过量氧耗”的概念。近年来提出的疲劳控制链或运动性疲劳突变理论，都力图从多方面说明疲劳的发生原因。运动可使骨骼肌纤维胞浆钙离子浓度升高；大负荷运动后骨骼肌延迟性结构变化，与胞浆Ca2＋浓度的延迟性升高在时间上具有一致性；运动可使自由基生成增加，自由基可造成组织损伤。研究表明，运动员肌纤维的机能对运动成绩的影响大于心肺功能，在这方面的研究已深到细胞、分子水平。
In the mid-1980s, many studies demonstrated that lactate production during exercise was not related to hypoxia in vivo and pointed out that “oxybital debt”, “oxygen deficiency” and “anaerobic threshold” were three incorrect concepts and proposed “post-exercise excess Oxygen consumption ”concept. In recent years, the proposed fatigue control chain or sports fatigue mutation theory, all trying to illustrate the causes of fatigue in many ways. Exercise can increase skeletal muscle fiber cytoplasmic Ca2 + concentration; post-exercise skeletal muscle delayed structural changes, and delayed cytoplasmic Ca2 + consistency in time; exercise can increase free radical generation, freedom Bases can cause tissue damage. Research shows that the function of athlete’s muscle fiber has more influence on exercise performance than that of cardiopulmonary function, and the research in this aspect has deep to the cell and molecular level.