CHANGES IN MUSCLE CONTRACTILE PROPERTIES AND NEURAL CONTROL DURING HUMAN MUSCULAR FATIGUE
CHANGES IN MUSCLE CONTRACTILE PROPERTIES AND NEURAL CONTROL DURING HUMAN MUSCULAR FATIGUE
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DOI：
10.1002/mus.880070902
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发表时间：
1984-01-01
期刊：
影响因子：
3.4
通讯作者：
WOODS, JJ
中科院分区：
文献类型：
--
作者：
BIGLANDRITCHIE, B;WOODS, JJ
简要描述了限制力量产生和运动耐力时间的因素，以及肌肉和中枢神经系统内不同部位发生的一些变化。有证据表明，在疲劳的持续最大自主收缩（MVC）执行良好的动机主体，力产生能力的减少不需要是由于在中枢神经系统电机驱动或失败的神经肌肉传输的下降，但可以完全归因于收缩失败的肌肉参与。尽管如此，在持续的MVC过程中，单个运动单位的综合肌电图和平均放电率确实逐渐下降。这不一定导致力的损失，因为肌肉收缩速度的平行减慢降低了强直融合频率。由自主努力引起的运动神经元放电率的范围被调节并限制在每块肌肉产生最大力所需的最小值，从而防止神经肌肉传递失败并优化运动控制。这样的中枢神经系统调节机制可能需要来自肌肉的一些反射反馈。
The factors limiting force production and exercise endurance time were briefly described, together with some of the changes occurring at various sites within the muscle and CNS. Evidence is presented that, in fatigue of sustained maximal voluntary contractions (MVC) executed by well-motivated subjects, the reduction in force generating capacity need not be due to a decline in CNS motor drive or to failing neuromuscular transmission, but can be attributed solely to contractile failure of the muscles involved. Despite this conclusion, both the integrated electromyogram and the mean firing rate of individual motor units do decline progressively during sustained MVC. This, does not necessarily result in loss of force since the parallel slowing of muscle contractile speed reduces tetanic fusion frequency. The range of motoneuron firing rates elicited by voluntary effort is regulated and limited for each muscle to the minimum required for maximum force generation, preventing neuromuscular transmission failure and optimizing motor control. Such a CNS regulating mechanism would probably require some reflex feedback from the muscle.