人类肘屈肌收缩后增强的可能神经机制

Tomoya Ishii, S. Sasada, T. Komiyama
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引用次数: 1

摘要

精确和顺序的运动任务需要艰苦和精细的力控制,涉及不同的,复杂的神经机制,没有这些机制,他们将难以执行。先前的一项研究表明,剧烈用力会引起活动肌肉的增强(收缩后增强,PCP)。然而,PCP的发病机制尚不清楚。我们利用表面肌电活动的频谱分析来研究PCP的神经机制。14名健康参与者被要求在测试1之前和测试2之后执行肌电图匹配任务(最大自愿收缩的2%,MVC),他们施加了短暂的50% MVC(条件反射收缩,CC)。在试验2中施加的力明显低于试验1,表明PCP确实发生了。此外,在测试2中,经常观察到平均频率为~ 10hz的尖峰样肌电反应。功率谱分析表明,CC后α和β波段的峰值功率均增加,且试验2中α和β波段的峰值功率变化与力的变化呈负相关。这些发现表明,主动运动单元的同步解释了PCP。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Possible neural mechanisms underlying post-contraction potentiation in elbow flexor muscle in humans
Precise and sequential motor tasks that require strenuous and fine force control involve distinct, complex neural mechanisms without which they would be difficult to perform. A previous study showed that strenuous force exertion gives rise to potentiation of active muscles (post-contraction potentiation, PCP). However, the mechanisms underlying PCP remain unclear. We investigated the neural mechanisms underlying PCP using spectral analyses of surface EMG activity. Fourteen healthy participants were asked to perform an EMG matching task (2% of maximum voluntary contraction, MVC) before (Test 1) and after (Test 2) they exerted a brief 50% MVC (conditioning contraction, CC). The exerted force was significantly lower during Test 2 than Test 1, indicating that PCP did occur. In addition, spike-like EMG responses with a mean frequency of ~10 Hz were frequently observed during Test 2. Power spectrum analysis demonstrated that the peak power of both α and β bands increased after CC, and that changes in the peak power of both bands during Test 2 negatively correlated with changes in force. These findings suggest that the synchronization of active motor units accounted for PCP.
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审稿时长
18 weeks
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