Muscle weakness in persons with multiple sclerosis

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 muscl...

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Bibliographic Details
Main Author: Chung, Linda H
Language:ENG
Published: ScholarWorks@UMass Amherst 2010
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Online Access:https://scholarworks.umass.edu/dissertations/AAI3427511
Description
Summary: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.