Hainaut K, Duchateau J
Laboratory of Biology University of Brussels, Belgium.
Muscle Nerve. 1989 Aug;12(8):660-9. doi: 10.1002/mus.880120807.
The study of muscle fatigue started about a century ago, when it was proposed that the observed decrease in force during prolonged voluntary contractions resulted from changes in central processes which reduced the motor drive. In the middle of this century it was noticed that this loss of force could not be restored by maximal electrical stimulation of the motor nerve, and thus the importance of peripheral mechanisms, located beyond the motoneuron, was emphasized. However, it was not clear which peripheral site was most important in decreasing the muscle mechanical capacity during fatigue. More recently, the comparison between peripheral failures during sustained and intermittent contractions indicated that recorded mechanical changes underwent deterioration which was not closely related to the recorded electrical changes. It was thus proposed that muscle intracellular processes dominate the force decrease during muscle fatigue. This concept has been substantiated by the study of standard fatigue tests performed in control, trained, and disused human muscles, as reviewed in this paper.
肌肉疲劳的研究始于大约一个世纪前，当时有人提出，长时间自愿收缩过程中观察到的力量下降是由中枢过程的变化导致的，这些变化减少了运动驱动。在本世纪中叶，人们注意到通过对运动神经进行最大程度的电刺激无法恢复这种力量损失，因此强调了位于运动神经元之外的外周机制的重要性。然而，尚不清楚在疲劳过程中哪个外周部位对降低肌肉机械能力最为重要。最近，持续收缩和间歇收缩期间外周衰竭的比较表明，记录到的机械变化出现了恶化，这与记录到的电变化没有密切关系。因此有人提出，肌肉细胞内过程在肌肉疲劳期间主导着力量下降。如本文所综述的，这一概念已通过对在对照、训练和废用的人体肌肉中进行的标准疲劳试验的研究得到证实。
