Hultman E, Spriet L L, Söderlund K
Biomed Biochim Acta. 1986;45(1-2):S97-106.
Fatigue--or decrease in force generation--is a reduction of simultaneously attached cross-bridges in the force generating state. Two processes are necessary for the force generation: Firstly Ca++ release from the sarcoplasmic reticulum to the sarcoplasm and the binding of Ca++ by the troponin molecule and secondly the turnover of myosin-actin cross-bridges. These processes require energy in at least three different ATPase reactions and can consequently be inhibited when ATP hydrolysis is decreased, i.e. when ATP content is to low or when the reaction products (ADP, Pi and H+) reach inhibiting levels or when muscle pH has decreased to values inhibiting actomyosin ATPase activity (22). Low pH will also decrease Ca++ release and Ca++ affinity by troponin (23). In isometric contraction the force is well preserved as long as ADP phosphorylation can be provided by both PCr degradation and anaerobic glycolysis. When the PCr store is exhausted the force starts to decline and if muscle activation is maintained the force will continue to decrease along with falling glycolytic rate. ADP phosphorylation rate decreases successively and ATP content falls with an at least transient increase in ADP. The ATP decrease, apart from the minor increase in ADP, is balanced by an equimolar increase in IMP. Lactate accumulation produces an increasing acidity with muscle pH values down to 6.25. Early changes in free ADP content cannot be excluded as reason for the initial decrease in force production followed by more pronounced inhibition of ATPase activity during continued contraction due to both substrate lack and product inhibition together with pH effect on the excitation--contraction mechanism. In dynamic exercise with supramaximum work intensity the relation between fatigue development and metabolism is similar. In prolonged dynamic exercise relying on oxidative metabolism without lactate formation the point of fatigue is reached when the glycogen store is exhausted. Again ADP phosphorylation rate is decreased when the energy substrate is changed from carbohydrate to fat with lower maximum rate of ATP resynthesis.
疲劳——即力量产生的下降——是指处于力量产生状态的同时附着的横桥数量减少。力量产生需要两个过程：首先，钙离子从肌浆网释放到肌浆中，并与肌钙蛋白分子结合；其次，肌球蛋白 - 肌动蛋白横桥的周转。这些过程至少需要三种不同的ATP酶反应提供能量，因此当ATP水解减少时，即ATP含量过低、反应产物（ADP、磷酸和氢离子）达到抑制水平或肌肉pH值下降到抑制肌动球蛋白ATP酶活性的值时，这些过程会受到抑制（22）。低pH值也会减少钙离子的释放以及肌钙蛋白对钙离子的亲和力（23）。在等长收缩中，只要磷酸肌酸降解和无氧糖酵解都能提供ADP磷酸化，力量就能很好地维持。当磷酸肌酸储备耗尽时，力量开始下降，如果维持肌肉激活，力量会随着糖酵解速率的下降而继续降低。ADP磷酸化速率相继降低，ATP含量下降，同时ADP至少会有短暂的增加。除了ADP的少量增加外，ATP的减少由IMP等摩尔增加来平衡。乳酸积累会使酸度增加，肌肉pH值降至6.25。不能排除游离ADP含量的早期变化是力量产生最初下降的原因，随后在持续收缩过程中，由于底物缺乏、产物抑制以及pH值对兴奋 - 收缩机制的影响，ATP酶活性会受到更明显的抑制。在超最大工作强度的动态运动中，疲劳发展与代谢之间的关系类似。在依赖氧化代谢且不产生乳酸的长时间动态运动中，当糖原储备耗尽时会达到疲劳点。同样，当能量底物从碳水化合物转变为脂肪，且ATP再合成的最大速率较低时，ADP磷酸化速率会降低。
