Endurance exercise training suppresses myostatin upregulation and nuclear factor-kappa B activation in a mouse model of Parkinson's disease

Muscle atrophy is common in Parkinson's disease (PD). Although myostatin has been implicated in muscle atrophy, its expression in PD skeletal muscle has not been investigated. Therefore, this study aimed to elucidate the influence of PD induction and exercise training on myostatin expression in the gastrocnemius skeletal muscle. Materials and

The present data are the first to indicate a correlation between PD induction and myostatin overexpression and NF-kB activation in the gastrocnemius muscle, potentially promoting the muscle atrophy commonly seen in PD. Additionally, the current data are the first to indicate the beneficial effects of exercise training on PD-associated myostatin overexpression, NF-κB activation, and muscle atrophy. Thus, our data are the first to suggest that myostatin and NF-κB might be regarded as potential therapeutic targets in an attempt to ameliorate skeletal muscle abnormalities commonly observed in PD.

Thirty albino mice were randomly selected and separated into three groups of 10 mice each: Sedentary control, sedentary PD (SPD), and exercised PD (EPD). 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine and probenecid were used to induce chronic parkinsonism in the PD groups. Immunohistochemistry was used to investigate the expression of myostatin and nuclear factor kappa B (NF-kB) in gastrocnemius muscles of all three groups.

Myostatin expression and NF-kB nuclear localization, indicative of its activation, were significantly (p<0.01) higher in gastrocnemius skeletal muscle in the SPD group than in the control and EPD groups. Concomitantly, the average cross-sectional area of gastrocnemius muscle fibers in the SPD albino mice was significantly smaller (p<0.01) than in the control and EPD groups, indicating muscle atrophy.