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Muscle weakness in persons with multiple sclerosis.

机译:多发性硬化症患者的肌肉无力。

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摘要

Skeletal muscle weakness is a problem for people living with Multiple Sclerosis (MS). Alterations in the central nervous system may be the primary source of muscle weakness because of the pathophysiology of MS. However, changes in peripheral mediators of force production may also contribute to muscle weakness in persons with MS. The main objective of the dissertation was to systematically identify key neural (motor unit discharge rates, spasticity) and muscular (muscle size, contractile function) mechanisms of force production that may explain lower isometric strength and dynamic power in persons with MS compared with age-matched controls. The knee extensor muscles of the weaker leg were studied, because this muscle group is commonly affected by MS.;We showed that persons with MS had lower peak isometric torque and dynamic power compared with controls. Persons with MS had lower motor unit discharge rates, smaller muscle size, and lower specific power compared with controls. There was no difference in passive torque (spasticity), specific strength, or maximal rate of force development between groups. Because differences in isometric strength between persons with MS and controls were abolished when torque was normalized to muscle size, smaller muscle size may explain a large portion of lower isometric strength in persons with MS. Differences in dynamic power were reduced when peak power was normalized to muscle size, but remained lower in persons with MS compared with controls, suggesting that changes in neural factors (e.g., lower motor unit discharge rates) may explain lower dynamic power in persons with MS. These results suggest that different mechanisms may contribute to muscle weakness in MS, depending on the mode of contraction.;Lower motor unit discharge rates and smaller muscle size were identified as key mechanisms of muscle weakness in persons with MS. Each of these mechanisms has been shown to improve with resistance training in controls. Thus, this dissertation provides an evidence-based rationale for resistance training interventions in persons with MS, to improve isometric strength and power production by increasing motor unit discharge rates and muscle size.
机译:骨骼肌无力是多发性硬化症(MS)患者的一个问题。由于MS的病理生理,中枢神经系统的改变可能是肌肉无力的主要来源。然而,力产生的周围介质的改变也可能导致MS患者的肌肉无力。论文的主要目的是系统地识别力产生的关键神经(运动单位放电率,痉挛)和肌肉(肌肉大小,收缩功能)机制,这些机制可以解释与年龄段相比,MS患者的等轴测强度和动态功率较低。匹配的控件。由于该肌肉群通常受MS影响,因此研究了小腿的膝盖伸肌。我们显示,与对照组相比,MS患者的等距峰值扭矩和动态功率更低。与对照组相比,MS患者的运动单位放电率较低,肌肉较小且比功率较低。组之间的被动扭矩(痉挛),比强度或最大力量发展率没有差异。由于将扭矩归一化为肌肉大小后,MS患者与对照组之间等轴测强度的差异被消除了,因此较小的肌肉尺寸可以解释MS患者等轴测强度的很大一部分。将峰值功率标准化为肌肉大小后,动态功率的差异减小,但与对照组相比,MS患者的动态功率差异仍然较小,这表明神经因素的变化(例如,较低的运动单位放电率)可能解释了MS患者的动态功率较低。这些结果表明,不同的机制可能导致MS的肌肉无力,具体取决于收缩的方式。降低运动单位的放电率和减小肌肉的大小被认为是MS患者肌肉无力的关键机制。这些机制中的每一种都显示出可以通过控制中的阻力训练来改善。因此,本论文为多发性硬化症患者的阻力训练干预提供了循证依据,以通过增加运动单位放电速率和肌肉大小来改善等距强度和功率产生。

著录项

  • 作者

    Chung, Linda H.;

  • 作者单位

    University of Massachusetts Amherst.;

  • 授予单位 University of Massachusetts Amherst.;
  • 学科 Health Sciences Recreation.
  • 学位 Ph.D.
  • 年度 2010
  • 页码 197 p.
  • 总页数 197
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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