Pagala M K, Venkatachari S A, Nandakumar N V, Ravindran K, Kerstein J, Namba T, Grob D
Department of Medicine, Maimonides Medical Center, Brooklyn, NY 11219.
Neuromuscul Disord. 1991;1(4):287-98. doi: 10.1016/0960-8966(91)90103-y.
We evaluated the contribution of different processes to fatigue of normal and dystrophic mouse muscles using an in vitro electromyography chamber. Fatigue was induced by repetitive nerve stimulation at 30 Hz for 0.5 s, every 2.5 s until tension decreased by about 50%. We monitored the compound nerve action potential (AP), compound muscle AP, and isometric tension responses to nerve stimulation, and compound muscle AP and tension responses to direct muscle stimulation. In normal mice, about 50% reduction in nerve-evoked tension occurred by 2.4 min in extensor digitorum longus (EDL), 4.8 min in diaphragm, and 9 min in soleus. Analysis of the responses revealed that the fatigue was caused by failure of more than one process in all muscles, and failure of nerve conduction did not contribute to fatigue in any muscle. Failure of neuromuscular transmission, muscle membrane excitation, and excitation-contraction (E-C) coupling and contractility accounted for 55, 45, and 0%, respectively, of the fatigue in EDL, for 21, 74, and 5% of the fatigue in diaphragm, and for 2, 54, and 44% of the fatigue in soleus. In dystrophic mice, while about 50% reduction in nerve-evoked tension occurred by 8.1 min in EDL and 5.6 min in diaphragm, only 29% reduction in tension occurred by 80 min in soleus. Failure of neuromuscular transmission, muscle membrane excitation, E-C coupling and contractility accounted for 22, 63 and 15% of the fatigue in EDL, for 21, 79, and 0% of the fatigue in diaphragm, and for 15, 59, and 26% of the fatigue in soleus. The proportion of slow-twitch oxidative fibers was more than normal in dystrophic EDL, but the same as normal in dystrophic diaphragm and soleus. The slower onset of fatigue was attributable to lesser failure of neuromuscular transmission in dystrophic EDL, and to lesser failure of E-C coupling and contractility in dystrophic soleus.
我们使用体外肌电图室评估了不同过程对正常和营养不良小鼠肌肉疲劳的影响。通过每2.5秒以30 Hz重复神经刺激0.5秒来诱导疲劳，直至张力降低约50%。我们监测了复合神经动作电位（AP）、复合肌肉AP以及对神经刺激的等长张力反应，以及对直接肌肉刺激的复合肌肉AP和张力反应。在正常小鼠中，趾长伸肌（EDL）在2.4分钟时神经诱发张力降低约50%，膈肌在4.8分钟时，比目鱼肌在9分钟时。对反应的分析表明，所有肌肉的疲劳都是由多个过程的失败引起的，并且神经传导的失败在任何肌肉中都不会导致疲劳。神经肌肉传递失败、肌肉膜兴奋以及兴奋-收缩（E-C）偶联和收缩性分别占EDL疲劳的55%、45%和0%，占膈肌疲劳的21%、74%和5%，占比目鱼肌疲劳的2%、54%和44%。在营养不良小鼠中，EDL在8.1分钟时神经诱发张力降低约50%，膈肌在5.6分钟时，而比目鱼肌在80分钟时张力仅降低29%。神经肌肉传递失败、肌肉膜兴奋、E-C偶联和收缩性分别占EDL疲劳的22%、63%和15%，占膈肌疲劳的21%、79%和0%，占比目鱼肌疲劳的15%、59%和26%。营养不良的EDL中慢肌氧化纤维的比例高于正常，但营养不良的膈肌和比目鱼肌中与正常相同。疲劳发作较慢归因于营养不良的EDL中神经肌肉传递失败较少，以及营养不良的比目鱼肌中E-C偶联和收缩性失败较少。
