Sugawara Kenichi, Tanabe Shigeo, Suzuki Tomotaka, Higashi Toshio
a Faculty of Health and Social Work , Kanagawa University of Human Services , Yokosuka , Japan.
b Faculty of Rehabilitation , Fujita Health University , Toyoake , Japan.
Somatosens Mot Res. 2016 Sep-Dec;33(3-4):161-168. doi: 10.1080/08990220.2016.1229177. Epub 2016 Sep 25.
The aim of the present study was to investigate the neurophysiological triggers underlying muscle relaxation from the contracted state, and to examine the mechanisms involved in this process and their subsequent modification by neuromuscular electrical stimulation (NMES). Single-pulse transcranial magnetic stimulation (TMS) was used to produce motor-evoked potentials (MEPs) and short-interval intracortical inhibition (SICI) in 23 healthy participants, wherein motor cortex excitability was examined at the onset of voluntary muscle relaxation following a period of voluntary tonic muscle contraction. In addition, the effects of afferent input on motor cortex excitability, as produced by NMES during muscle contraction, were examined. In particular, two NMES intensities were used for analysis: 1.2 times the sensory threshold and 1.2 times the motor threshold (MT). Participants were directed to execute constant wrist extensions and to release muscle contraction in response to an auditory "GO" signal. MEPs were recorded from the flexor carpi radialis (FCR) and extensor carpi radialis (ECR) muscles, and TMS was applied at three different time intervals (30, 60, and 90 ms) after the "GO" signal. Motor cortex excitability was greater during voluntary ECR and FCR relaxation using high-intensity NMES, and relaxation time was decreased. Each parameter differed significantly between 30 and 60 ms. Moreover, in both muscles, SICI was larger in the presence than in the absence of NMES. Therefore, the present findings suggest that terminating a muscle contraction triggers transient neurophysiological mechanisms that facilitate the NMES-induced modulation of cortical motor excitability in the period prior to muscle relaxation. High-intensity NMES might facilitate motor cortical excitability as a function of increased inhibitory intracortical activity, and therefore serve as a transient trigger for the relaxation of prime mover muscles in a therapeutic context.
本研究的目的是探究肌肉从收缩状态松弛的神经生理触发因素,并研究该过程中涉及的机制以及神经肌肉电刺激(NMES)对其随后的调节作用。在23名健康参与者中,使用单脉冲经颅磁刺激(TMS)来产生运动诱发电位(MEP)和短间隔皮质内抑制(SICI),其中在一段自愿性强直性肌肉收缩后的自愿性肌肉松弛开始时检查运动皮质兴奋性。此外,还研究了肌肉收缩期间NMES产生的传入输入对运动皮质兴奋性的影响。具体而言,使用两种NMES强度进行分析:感觉阈值的1.2倍和运动阈值(MT)的1.2倍。参与者被指示进行持续的腕部伸展,并在听到听觉“开始”信号后放松肌肉收缩。从桡侧腕屈肌(FCR)和桡侧腕伸肌(ECR)记录MEP,并在“开始”信号后的三个不同时间间隔(30、60和90毫秒)施加TMS。使用高强度NMES时,在自愿性ECR和FCR松弛期间运动皮质兴奋性更高,且松弛时间缩短。30毫秒和60毫秒之间的每个参数均有显著差异。此外,在两块肌肉中,存在NMES时的SICI均大于不存在NMES时。因此,本研究结果表明,终止肌肉收缩会触发短暂的神经生理机制,这些机制在肌肉松弛前的时间段内促进NMES诱导的皮质运动兴奋性调节。高强度NMES可能作为皮质内抑制活动增加的函数促进运动皮质兴奋性,因此在治疗背景下可作为原动肌松弛的短暂触发因素。