Boulton Daniel, Taylor Chloe E, Macefield Vaughan G, Green Simon
School of Science and Health, Western Sydney University Sydney NSW, Australia.
School of Science and Health, Western Sydney UniversitySydney NSW, Australia; School of Medicine, Western Sydney UniversitySydney NSW, Australia.
Front Physiol. 2016 May 13;7:163. doi: 10.3389/fphys.2016.00163. eCollection 2016.
During voluntary contractions, muscle sympathetic nerve activity (MSNA) to contracting muscles increases in proportion to force but the underlying mechanisms are not clear. To shed light on these mechanisms, particularly the influences of central command and muscle afferent feedback, the present study tested the hypothesis that MSNA is greater during voluntary compared with electrically-evoked contractions. Seven male subjects performed a series of 1-min isometric dorsiflexion contractions (left leg) separated by 2-min rest periods, alternating between voluntary and electrically-evoked contractions at similar forces (5-10% of maximum). MSNA was recorded continuously (microneurography) from the left peroneal nerve and quantified from cardiac-synchronized, negative-going spikes in the neurogram. Compared with pre-contraction values, MSNA increased by 51 ± 34% (P < 0.01) during voluntary contractions but did not change significantly during electrically-evoked contractions (-8 ± 12%, P > 0.05). MSNA analyzed at 15-s intervals revealed that this effect of voluntary contraction appeared 15-30 s after contraction onset (P < 0.01), remained elevated until the end of contraction, and disappeared within 15 s after contraction. These findings suggest that central command, and not feedback from contracting muscle, is the primary mechanism responsible for the increase in MSNA to contracting muscle. The time-course of MSNA suggests that there is a longer delay in the onset of this effect compared with its cessation after contraction.
在自主收缩过程中,收缩肌肉的肌肉交感神经活动(MSNA)随力量增加而按比例升高,但其潜在机制尚不清楚。为了阐明这些机制,特别是中枢指令和肌肉传入反馈的影响,本研究检验了以下假设:与电诱发收缩相比,自主收缩时MSNA更高。7名男性受试者进行了一系列1分钟的等长背屈收缩(左腿),每次收缩间隔2分钟休息,在相似力量(最大力量的5 - 10%)下交替进行自主收缩和电诱发收缩。通过微神经ography从左腓神经连续记录MSNA,并根据神经图中心脏同步的负向尖峰进行量化。与收缩前值相比,自主收缩时MSNA增加了51±34%(P < 0.01),而电诱发收缩时未显著变化(-8±12%,P > 0.05)。以15秒间隔分析的MSNA显示,自主收缩的这种效应在收缩开始后15 - 30秒出现(P < 0.01),在收缩结束前一直升高,并在收缩后15秒内消失。这些发现表明,中枢指令而非收缩肌肉的反馈是导致收缩肌肉MSNA增加的主要机制。MSNA的时间进程表明,这种效应的起始延迟比收缩后停止的延迟更长。