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人体肌肉疲劳期间肌肉收缩特性和神经控制的变化。

Changes in muscle contractile properties and neural control during human muscular fatigue.

作者信息

Bigland-Ritchie B, Woods J J

出版信息

Muscle Nerve. 1984 Nov-Dec;7(9):691-9. doi: 10.1002/mus.880070902.

Abstract

The factors limiting force production and exercise endurance time have been briefly described, together with some of the changes occurring at various sites within the muscle and central nervous system. 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 central nervous system (CNS) motor drive or to failing neuromuscular transmission, but can be attributed solely to contractile failure of the muscles involved. However, despite this conclusion, both the integrated electromyogram (EMG) and the mean firing rate of individual motor units do decline progressively during sustained MVC. This, however, does not necessarily result in loss of force since the parallel slowing of muscle contractile speed reduces tetanic fusion frequency. It is suggested that 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, thus preventing neuromuscular transmission failure and optimizing motor control. Such a CNS regulating mechanism would probably require some reflex feedback from the muscle.

摘要

限制力量产生和运动耐力时间的因素已被简要描述,同时还介绍了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,在积极性高的受试者进行持续最大自主收缩(MVC)疲劳时,力量产生能力的下降不一定是由于中枢神经系统(CNS)运动驱动的下降或神经肌肉传递的失败,而可能完全归因于所涉及肌肉的收缩失败。然而,尽管有这个结论,在持续的MVC过程中,整合肌电图(EMG)和单个运动单位的平均放电率都会逐渐下降。然而,这不一定会导致力量损失,因为肌肉收缩速度的平行减慢会降低强直融合频率。有人提出,自愿努力引起的运动神经元放电率范围对于每块肌肉来说都被调节并限制在产生最大力量所需的最小值,从而防止神经肌肉传递失败并优化运动控制。这样一种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。

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