Miller R G, Moussavi R S, Green A T, Carson P J, Weiner M W
Department of Neurology, California Pacific Medical Center, San Francisco 94118.
Neurology. 1993 Apr;43(4):755-61. doi: 10.1212/wnl.43.4.755.
Normal subjects (n = 7) performed rapid voluntary isometric contractions of the adductor pollicis and the tibialis anterior. Within the first minute of this low-intensity exercise, the speed of tension development slowed, accompanied by a prolongation in EMG burst duration. In contrast, electrically evoked contractions either became more rapid (twitch) or did not change (tetanus), suggesting a fatigue of central origin. 31P NMR measurements of high-energy phosphates showed that the relationship between the fall of maximum force and changes of phosphates and pH was similar to that produced by other high-intensity fatiguing exercise protocols. Thus, rapid movements produce fatigue through two major mechanisms. First, there is slowing of the speed of tension development which appears secondary to central fatigue. Second, the decline of muscle force is primarily attributable to changes in muscle pH or inorganic phosphate, which usually occurs only after high-intensity (but non-rapid) exercise.
正常受试者（n = 7）进行了拇内收肌和胫前肌的快速随意等长收缩。在这种低强度运动的第一分钟内，张力发展速度减慢，同时肌电图爆发持续时间延长。相比之下，电诱发收缩要么变得更快（单收缩），要么没有变化（强直收缩），提示中枢性疲劳。高能磷酸盐的31P核磁共振测量表明，最大力量下降与磷酸盐和pH值变化之间的关系与其他高强度疲劳运动方案所产生的相似。因此，快速运动通过两种主要机制产生疲劳。首先，张力发展速度减慢，这似乎是中枢性疲劳的继发表现。其次，肌肉力量的下降主要归因于肌肉pH值或无机磷酸盐的变化，而这种变化通常仅在高强度（但非快速）运动后才会出现。
