Gail and Gerald Oppenheimer Family Center for Neurobiology of Stress, Division of Digestive Disease, Department of Medicine, University of California at Los Angeles, CA, USA.
Neuroimage. 2012 Mar;60(1):728-37. doi: 10.1016/j.neuroimage.2011.12.013. Epub 2011 Dec 17.
Fatigue caused by sustaining submaximal-intensity muscle contraction(s) involves increased activation in the brain such as primary motor cortex (M1), primary sensory cortex (S1), premotor and supplementary motor area (PM&SMA) and prefrontal cortex (PFC). The synchronized increases in activation level in these cortical areas suggest fatigue-related strengthening of functional coupling within the motor control network. In the present study, this hypothesis was tested using the cross-correlation based functional connectivity (FC) analysis method. Ten subjects performed a 20-minute intermittent (3.5s ON/6.5s OFF, 120 trials total) handgrip task using the right hand at 50% maximal voluntary contraction (MVC) force level while their brain was scanned by a 3 T Siemens Trio scanner using echo planar imaging (EPI) sequence. A representative signal time course of the left M1 was extracted by averaging the time course data of a 2-mm cluster of neighboring voxels of local maximal activation foci, which was identified by a general linear model. Two FC activation maps were created for each subject by cross-correlating the time course data of the minimal (the first 10 trials) and significant (the last 10 trials) fatigue stages across all the voxels in the brain to the corresponding representative time course. Histogram and quantile regression analysis were used to compare the FC between the minimal and significant fatigue stages and the results showed a significant increase in FC among multiple cortical regions, including right M1 and bilateral PM&SMA, S1 and PFC. This strengthened FC indicates that when muscle fatigue worsens, many brain regions increase their coupling with the left M1, the primary motor output control center for the right handgrip, to compensate for diminished force generating capability of the muscle in a coordinated fashion by enhancing the descending command for greater muscle recruitment to maintain the same force.
由维持亚最大强度肌肉收缩引起的疲劳会导致大脑中出现活动增加,例如初级运动皮层(M1)、初级感觉皮层(S1)、运动前区和辅助运动区(PM&SMA)以及前额叶皮层(PFC)。这些皮质区域的激活水平同步增加表明与疲劳相关的运动控制网络内的功能耦合增强。在本研究中,使用基于互相关的功能连接(FC)分析方法检验了这一假设。十位受试者在 3T 西门子 Trio 扫描仪上使用 EPI 序列进行大脑扫描的同时,使用右手以 50%最大自主收缩(MVC)力水平进行 20 分钟的间歇性(3.5s ON/6.5s OFF,共 120 次试验)握力任务。通过对局部最大激活焦点的相邻体素 2mm 簇的时间过程数据进行平均,提取左 M1 的代表性信号时间过程,该时间过程数据由广义线性模型确定。通过将大脑中所有体素的最小(前 10 次试验)和显著(后 10 次试验)疲劳阶段的时间过程数据与相应的代表性时间过程进行互相关,为每个受试者创建了两个 FC 激活图。对 FC 进行直方图和分位数回归分析,以比较最小和显著疲劳阶段之间的 FC,结果表明,在多个皮质区域之间的 FC 显著增加,包括右侧 M1 和双侧 PM&SMA、S1 和 PFC。这种增强的 FC 表明,当肌肉疲劳加剧时,许多大脑区域增加了与左手 M1 的耦合,左手 M1 是右手握力的主要运动输出控制中心,通过增强对更大肌肉募集的下行命令以协调方式补偿肌肉产生力的能力下降,从而维持相同的力。