Mitochondrial Biogenesis in Response to Exercise or Hydrogen Peroxide Treatment is Not Blunted by Upregulation of Endogenous Antioxidants

Abstract

Although prolonged exposure to reactive oxygen species (ROS) may cause cellular damage, beneficial adaptations to exercise including mitochondrial biogenesis may occur, in part, through ROS signaling. Evidence suggests that treatment with an exogenous antioxidant (vitamin C (VitC)) may prevent beneficial redox signaling. A possible alternative strategy to prevent damage while allowing ROS induced signaling is to increase endogenous antioxidants using a Nrf2 activator. We hypothesized that, compared to VitC, treatment with the Nrf2 activator Protandim® (Pro, LifeVantage) would not blunt mitochondrial adaptations to exercise in vivo, or H2O2 treatment in vitro. Deuterium oxide labeling was used to measure mitochondrial protein synthesis (mPS) in vivo, and mPS and breakdown (mPB) in vitro. In vivo, skeletal muscle mPS was significantly greater in high volume runners compared to sedentary controls. This increase in mPS was blunted by VitC but not by Pro. When mPS and mPB were assessed in vitro during H2O2 treatment, Pro did not inhibit mitochondrial responses. From these data, it appears that although treatment with exogenous antioxidants may blunt the positive ROS‐induced mitochondrial responses, treatment with a Nrf2 activator that upregulates endogenous antioxidants does not blunt mitochondrial adaptations.