运动性肌肉疲劳的主动肌拮抗肌肌电与脑电关联研究
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摘要
研究目的
     主动肌与拮抗肌的协同收缩是实现人体运动中肢体协调的最重要生理过程之一,目前对运动性肌肉疲劳中主动肌与拮抗肌活动及其中枢调控等问题的认识存在争议。本研究的主要目的是了解静态负荷诱发主动肌疲劳对主动肌、拮抗肌表面肌电信号(sEMG)与脑电信号(EEG)时、频、相位关联关系的影响作用及拮抗肌疲劳对肌肉收缩中主动肌、拮抗肌活动及共神经输入的影响作用,探索静态负荷诱发肌肉疲劳的主动肌、拮抗肌功能联系和中枢控制关系,并从生物电信号关联角度印证拮抗肌中枢神经系统支配的“共驱动”或“异驱动”理论。
     研究方法
     以15名男性青年志愿者为研究对象,记录受试者以20%MVC(最大自主收缩力,Maximal Voluntary Contraction)和60%MVC静态屈肘诱发屈肘肌疲劳过程中肱桡肌、肱二头肌、肱三头肌的sEMG和EEG。此外,分别测试屈肘肌疲劳前、后伸肘肌收缩中测试肌肉sEMG和EEG。通过观察疲劳负荷实验前、后半段主动肌、拮抗肌sEMG与EEG之间的时域互相关关系、相位同步关系、频率一致性关系,了解运动性肌肉疲劳对主动肌与拮抗肌中枢神经系统共神经输入同步支配的影响作用及主动肌、拮抗肌与运动皮层中枢的耦合关系;对比分析屈肘肌疲劳前、后伸肘肌收缩过程中sEMG、EEG指标的差异,了解拮抗肌疲劳对肌肉收缩中主动肌、拮抗肌活动及共神经输入的影响作用。
     研究结果
     (1)两种负荷静态屈肘疲劳负荷实验中,不同脑区运动后半段内肱桡肌、肱二头肌、肱三头肌sEMG及EEG能量在Theta、Alpha、Beta频段内的值相对于运动前半段皆出现显著性的增加,其中sEMG及EEG在Beta频段内能量的平均值及能量相对值皆出现显著性的增加。
     (2)在20%MVC静态屈肘疲劳负荷中,运动后半段肱桡肌、肱二头肌、肱三头肌sEMG与左脑区导联记录EEG信号在Alpha频段内的相干函数值要明显大于运动前半段。
     (3)在20%MVC静态屈肘疲劳负荷实验后半段肱桡肌sEMG与EEG在beta频段,肱二头肌sEMG与EEG在Theta和Alpha频段,肱三头肌sEMG与Theta、Alpha、gamma频段内的相位同步指数显著高于运动前半段,在60%MVC疲劳负荷实验中肱桡肌sEMG与EEG在Gamma频段、肱二头肌sEMG与EEG在Theta频段,肱三头肌sEMG与EEG在Theta、Beta和Gamma频段内的相位同步指数显著高于运动前半段。
     (4)在20%MVC静态屈肘疲劳负荷实验后半段测试肌肉在Alpha和Beta频段内的相位同步指数较运动前半段都有显著性的增加,在60%MVC静态屈肘疲劳负荷实验后半段肱二头肌-肱三头肌在Theta、Alpha和Gamma频段,肱桡肌-肱二头肌、肱桡肌-肱三头肌sEMG在Beta频段内的相位同步指数较运动前半段显著性增加。
     (5)20%MVC静态屈肘疲劳负荷运动的运动后半段,肱桡肌-肱二头肌sEMG相干函数在Beta频段内的值和肱二头肌-肱三头肌、肱桡肌-肱三头肌sEMG相干函数在Beta频段和Gamma频段内的值具有显著性的差异,运动后半段相干函数在Beta频段和Gamma频段内的值明显大于运动前半段。在60%MVC静态屈肘疲劳负荷运动后半段记录肱二头肌-肱三头肌sEMG相干函数在Beta频段内的值显著大于运动前半段。
     (6)以20%MVC静态收缩诱发屈肘肌疲劳后进行的静态伸肘运动,记录肱桡肌、肱二头肌、肱三头肌sEMG相互之间的相干函数值在beta频段的值较屈肘肌疲劳前显著减小,肱三头肌sEMG指标C(n)较屈肘肌疲劳前显著减小。
     研究结论
     (1)运动性肌肉疲劳引起主动肌-主动肌、主动肌-拮抗肌协同收缩时的频率、相位关系和运动皮层与主动肌、拮抗肌的耦合度产生一致性的改变,印证了拮抗肌活动控制的“共驱动”理论。
     (2)运动性肌肉疲劳引起运动皮层细胞活动数量和主动肌、拮抗肌运动单位募集数量增加,并引起运动皮层与主动肌、拮抗肌之间的协同增加。在维持关节稳定性的同时维持既定收缩负荷,疲劳后中枢神经系统控制协同收缩肌肉,特别是控制主动肌与拮抗肌以更加同步的方式活动。
     (3)拮抗肌疲劳引起运动皮层对主动肌-拮抗肌共神经输入(common neuralinputs)支配减小,中枢神经系统控制主动肌与拮抗肌同步活动的程度下降。这可能是由拮抗肌疲劳引起主动肌与拮抗肌外周收缩能力及中枢激活能力改变的不同步性、控制主动肌与拮抗肌皮层脊髓神经元之间的相互作用、中枢神经系统为补偿由拮抗肌疲劳带来的关节稳定性下降而对主动肌与拮抗肌运动单位募集采取不同的调节方式等造成的。
Objective:
     The objective of this study is to explore the function connection and thecharacteristics of common neural inputs to co-contracting antagonistic elbow musclesduring sustained isometric fatiguing contraction, basing on examining fatigued relatedtime, frequency and phase association between agonistic, antagonistic muscle SurfaceElectromyogram Signal and EEG, and observing the influence of antagonistic muscleprefatigue on sEMG and EEG in later muscle contraction.
     Methods:
     Fifteen young male volunteers participated in this study. Each subject sustainedisometric elbow flexion at20%and60%maximal level until exhaustion while theirbrain (EEG) and brachioradialis muscle(BR), biceps brachii muscle(BB), tricepsbrachii muscle muscle(BB)(sEMG) activities were recorded. Besides, EEG andsEMG was recorded during elbow extension before and after prefatigue ofantagonistic muscle. The entire elbow flexion fatigue contraction duration of the EEGand sEMG recordings was divided into the first half (stage1) and second half(stage2).Cross correlation, coherence and phase synchronization index of stage1and stage2were observed. Influence of antagonistic muscle prefatigue on sEMG indices andsEMG coherence were also observed and analyzed.
     Results:
     (1)The average power of both EEG and EMG increased significantly in stage2compared with stage1at theta, alpha and beta frequency band. Average and relativepower of sEMG and EEG all increased at beta frequency band.
     (2) In20%MVC elbow flexion, sEMG-EEG Coherence increased significantly instage2compared with stage1in alpha frequency band.
     (3) In20%MVC elbow flexion, phase synchronization index of BR sEMG-EEG inbeta frequency band, BB sEMG-EEG in theta and alpha frequency bands, TBsEMG-EEG in theta, alpha, gamma frequency bands all increased in stage2comparedwith stage1at alpha. In60%MVC elbow flexion, phase synchronization index of BRsEMG-EEG in gamma frequency band, BB sEMG-EEG in theta frequency band, TBsEMG-EEG in theta, alpha, gamma frequency bands increased in stage2comparedwith stage1.
     (4) Phase synchronization index in alpha, gamma frequency bands betweensynergistic muscles and antagonistic muscles increased in stage2compared withstage1at alpha and beta frequency band in20%MVC elbow flexion. In60%MVCelbow flexion, phase synchronization index of BB-TB in theta, alpha, beta frequencyband and phase synchronization index of BR-BB,BR-TB in beta frequency band were increased in stage2compared with stage1.
     (5) Coherence of BR-BB sEMG in beta frequency band and coherence ofBB-TB,BR-TB in beta and gamma frequency band were increased in stage2compared with stage1during20%MVC elbow flexion. In60%MVC elbow flexion,coherence of BB-TB in beta frequency band increased significantly in stage2compared with stage1.
     (6) sEMG-sEMG coherence in beta frequency band after antagonistic muscle fatiguecaused by20%MVC isometric contraction increased compared with coherence beforeantagonistic muscle prefatigue. C(n) of TB decreased significantly after antagonisticmuscle prefatigue caused by20%MVC isometric contraction increased comparedwith coherence before antagonistic muscle prefatigue. sEMG-sEMG coherence intheta frequency band after antagonistic muscle prefatigue caused by60%MVCisometric contraction was significantly different from coherence before antagonisticmuscle prefatigue.
     Conclusions:
     (1) Coherence and phase synchronization association of synergistic muscles andantagonistic muscles and agonistic muscle, antagonistic muscle and motor cortexcoupling had consistency changes caused by exercise-induced muscle fatigue, whichsupports the notion of a "common drive" in antagonistic muscles control.
     (2) Fatigue cause brain and muscle activities and the coupling of motor cortex andperipheral muscles all increased. In order to maintain the target force and jointstability, antagonistic muscles are coordinated to activate in a more synergisticmanner.
     (3) sEMG-sEMG coherence in beta frequency band of antagonistic muscles decreasedcaused by antagonistic muscle fatigue, indicating that the common neural inputs toantagonistic muscles decreased. It might be related to asynchronism change ofagonistic and antagonistic muscles in peripheral and central region, mutual influencesof antagonistic corticospinal neurons as they are closely grouped or intermingled, anddifferent motor unit recruitment patterns adopted to coordinate agonistic andantagonistic muscle activity in order to maintain joint stability.
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