Abstract
We investigated the relationship between markers of mitochondrial biogenesis, cell signaling, and antioxidant enzymes by depleting skeletal muscle glutathione with diethyl maleate (DEM) which resulted in a demonstrable increase in oxidative stress during exercise. Animals were divided into six groups: (1) sedentary control rats; (2) sedentary rats + DEM; (3) exercise control rats euthanized immediately after exercise; (4) exercise rats + DEM; (5) exercise control rats euthanized 4 h after exercise; and (6) exercise rats + DEM euthanized 4 h after exercise. Exercising animals ran on the treadmill at a 10% gradient at 20 m/min for the first 30 min. The speed was then increased every 10 min by 1.6 m/min until exhaustion. There was a reduction in total glutathione in the skeletal muscle of DEM treated animals compared to the control animals (P < 0.05). Within the control group, total glutathione was higher in the sedentary group compared to after exercise (P < 0.05). DEM treatment also significantly increased oxidative stress, as measured by increased plasma F2–isoprostanes (P < 0.05). Exercising animals given DEM showed a significantly greater increase in peroxisome proliferator activated receptor γ coactivator‐1α (PGC–1α) mRNA compared to the control animals that were exercised (P < 0.05). This study provides novel evidence that by lowering the endogenous antioxidant glutathione in skeletal muscle and inducing oxidative stress through exercise, PGC‐1α gene expression was augmented. These findings further highlight the important role of exercise induced oxidative stress in the regulation of mitochondrial biogenesis.
Highlights
It is well-documented that exhaustive exercise increases the production of reactive oxygen species (ROS) within skeletal muscle leading to oxidative stress (Bailey et al 2003, 2004)
Animals were divided into six groups: (1) sedentary control rats (n = 8); (2) sedentary rats treated with diethyl maleate (DEM) (n = 8); (3) exercise control rats euthanized immediately after exercise (n = 8); (4) exercise rats + DEM (n = 8); (5) exercise control rats euthanized 4 h after exercise (n = 8); and (6) exercise rats + DEM euthanized 4 h after exercise (n = 6)
Time to fatigue was significantly decreased as a result of DEM treatment (P < 0.05; 68 Æ 5 min exercise control [n = 16] vs. 51 Æ 5 min exercise DEM [n = 14])
Summary
It is well-documented that exhaustive exercise increases the production of reactive oxygen species (ROS) within skeletal muscle leading to oxidative stress (Bailey et al 2003, 2004). It has been previously speculated that the increase in exercise-induced oxidative stress can reduce muscle performance (Bailey et al 2003). Antioxidants have been proposed to reduce exercise-induced oxidative stress and increase performance (Williams et al 2006). Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.
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