Forearm muscle mitochondrial capacity and resting oxygen uptake: Relationship to symptomatic fatigue in persons with multiple sclerosis

Abstract

Background Mitochondrial dysfunction has been implicated in the pathogenesis of multiple sclerosis (MS). Whether mitochondrial alterations are a function of ambulatory dysfunction or are of a non-ambulatory systemic nature is unclear. Objective To compare oxidative capacity, and rest muscle oxygen consumption (mVO2) in the upper limb of persons with multiple sclerosis (PwMS) to a control group (CON), whereby an upper limb would be comparatively independent of ambulation or deconditioning. Methods Near infra-red spectroscopy was used to measure oxidative capacity of the wrist flexors in PwMS (n = 16) and CON (n = 13). Oxidative capacity was indicated by the time constant (TC) of mVO2 recovery following brief wrist flexion contractions. Measurements included well-being, depression, symptomatic fatigue, disability, handgrip strength, cognition, and functional endurance. Analysis was by T-tests and Pearson correlations with p ≤ 0.05. Data are mean (SD). Results TC of mVO2 recovery was slower in PwMS (MS = 47(14) sec, CON = 36(11) sec; p = 0.03). No significant correlations were found between oxidative capacity and any other measures. Rest mVO2 was not different between groups, but correlated with symptomatic fatigue (r = 0.694, p = 0.003) and strength (0.585, p = 0.017) in PwMS. Conclusion Oxidative capacity was lower in the wrist flexors of PwMS, possibly indicating a systemic component of the disease. Within PwMS, rest mVO2 was associated with symptomatic fatigue.

The pathophysiology of motor fatigue and fatigability in multiple sclerosis

“…Whereas, deconditioning can be expected to be prominent in the leg muscles of MS patients with impaired ambulation, one would not expect it to occur in non-affected upper extremity muscles. Thus, the results of two recent studies that demonstrated reduced oxidative capacity in both leg (gastrocnemius) and wrist flexor muscles of MS patients compared to controls raise a challenge to the deconditioning hypothesis ( 99 , 100 ).…”