Sharma K R, Kent-Braun J, Mynhier M A, Weiner M W, Miller R G
Department of Neurology, California Pacific Medical Center, University of California, San Francisco, USA.
Muscle Nerve. 1995 Dec;18(12):1403-11. doi: 10.1002/mus.880181210.
The goals of this study were to investigate muscle fatigue in patients with multiple sclerosis (MS), and to determine the relationships between muscle fatigue, clinical status, and perceived fatigue. The fatigability of the anterior tibial muscle was quantitated in patients and controls during 9 min of intermittent stimulation (used to eliminate central sources of muscle fatigue). During exercise, the decline in tetanic force, phosphocreatine, and intracellular pH was greater in patients than in controls. The compound muscle action potential amplitude did not decrease during exercise, indicating that there was no failure of neuromuscular transmission during fatigue. Thus, the excessive fatigue in MS developed from sources beyond the muscle membrane. Following exercise, the recovery of tetanic force was delayed in patients (a pattern that suggests abnormal excitation-contraction coupling), whereas the recovery of metabolites was complete in both groups. Muscular fatigue was correlated with clinical disability but not with perceived fatigue. These results suggests that fatigue in MS has both central (perception, upper motor neuron dysfunction) and peripheral (impaired metabolism and excitation-contraction coupling) components.
本研究的目的是调查多发性硬化症（MS）患者的肌肉疲劳情况，并确定肌肉疲劳、临床状态和感知疲劳之间的关系。在间歇性刺激9分钟期间（用于消除肌肉疲劳的中枢来源），对患者和对照组的胫前肌疲劳性进行了定量分析。运动期间，患者的强直收缩力、磷酸肌酸和细胞内pH值的下降幅度大于对照组。复合肌肉动作电位幅度在运动期间没有下降，表明疲劳期间神经肌肉传递没有失败。因此，MS患者的过度疲劳源于肌肉膜以外的来源。运动后，患者的强直收缩力恢复延迟（这种模式表明兴奋-收缩偶联异常），而两组代谢产物的恢复均已完成。肌肉疲劳与临床残疾相关，但与感知疲劳无关。这些结果表明，MS患者的疲劳具有中枢（感知、上运动神经元功能障碍）和外周（代谢受损和兴奋-收缩偶联受损）成分。
