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Updated: Sep 2, 2025

Adapted Resistance Training Improves Strength in Eight Weeks in Individuals with Multiple Sclerosis
Published on: January 29, 2016
Altered muscle oxidative phenotype impairs exercise tolerance but does not improve after exercise training in
Jan Spaas1,2,3, Richie P Goulding4, Charly Keytsman1,2
1University MS Center (UMSC) Hasselt - Pelt, Hasselt, Belgium.
Multiple sclerosis (MS) patients show reduced exercise capacity due to lower skeletal muscle oxidative function. Exercise training improves capacity, but not muscle mitochondria, suggesting other factors are involved.
Area of Science:
- Exercise Physiology
- Neurology
- Muscle Biology
Background:
- Multiple sclerosis (MS) is associated with significantly reduced exercise tolerance, impacting patients' quality of life.
- The precise physiological mechanisms underlying exercise intolerance in MS remain incompletely understood.
- This study investigates the roles of cardiopulmonary and peripheral muscle systems in MS-related exercise intolerance.
Purpose of the Study:
- To determine the contribution of cardiopulmonary and peripheral muscle systems to exercise intolerance in MS patients.
- To assess changes in exercise capacity and underlying physiological factors before and after a structured exercise training program in MS patients.
Main Methods:
- Cardiopulmonary exercise testing was conducted on 23 MS patients and 20 healthy controls.
- Vastus lateralis muscle biopsies were analyzed for fiber type, size, succinate dehydrogenase (SDH) activity, capillarity, and mitochondrial gene/protein expression.
- Nine MS patients underwent a 12-week high-intensity interval and resistance training program, followed by re-examination.
Main Results:
- MS patients exhibited lower peak oxygen uptake (V̇O2peak), gas exchange threshold, and V̇O2/work rate slope compared to controls, indicating impaired muscle function.
- Lower skeletal muscle SDH activity and mitochondrial OXPHOS complex I and II protein levels were observed in MS patients.
- Muscle SDH activity strongly correlated with exercise capacity in MS patients, while capillary-to-fiber ratio correlated in controls.
- Exercise training significantly increased V̇O2peak in MS patients, but did not alter muscle mitochondrial markers.
Conclusions:
- Reduced skeletal muscle oxidative capacity, evidenced by lower SDH activity and mitochondrial content, contributes to exercise intolerance in MS.
- Skeletal muscle mitochondria in MS patients appear unresponsive to exercise training interventions.
- Improvements in exercise capacity following training in MS likely involve physiological systems beyond skeletal muscle mitochondria.
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