Advances in Redox Research (Aug 2024)

Oral administration of glutathione modulates exercise-related metabolic and oxidative factors in skeletal muscles of mice

  • Wataru Aoi,
  • Kenji Sato

Journal volume & issue
Vol. 12
p. 100104

Abstract

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Exercise activates the metabolic system in skeletal muscles, which is modulated by antioxidant supplementation. Some antioxidants such as glutathione accelerate metabolic adaptation induced by exercise training, whereas other antioxidants such as vitamin C suppress it. Thus, the present study aimed to elucidate the effects of oral administration of glutathione and vitamin C on metabolic and redox responses after acute exercise in mice. ICR mice were randomly divided into sedentary, exercise, exercise with glutathione, and exercise with vitamin C groups. In the exercise groups, mice were subjected to treadmill running at 30 m/min for 30 min. Immediately after exercise, glutathione (2% w/v, 5uL/g body weight) or vitamin C (10% w/v, 5uL/g body weight) were administered. Gastrocnemius muscle and plasma samples were collected at 3 h post-exercise. We found that plasma creatine kinase levels were only elevated in the exercise group. Malondialdehyde levels in skeletal muscle were elevated after exercise, but this elevation was suppressed by glutathione administration. PGC-1α expression was increased in both the exercise and glutathione groups compared with the sedentary group; however, the expressions of its downstream proteins were only increased in the glutathione group. Reduced glutathione form was notably increased in the mitochondria, whereas oxidized glutathione was significantly increased in the cytosol of the glutathione administration group compared with the exercise group. Thioredoxin reductase activity was also higher in the glutathione group than in the sedentary and exercise groups. Thus, this study demonstrates that post-exercise glutathione administration accelerates the exercise-induced responses of mitochondrial factors in skeletal muscle, which may be mediated by the modulation of the redox system.

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