The Effects of Mitochondria-targeted Antioxidant Supplementation on the Adaptive Response to Exercise, Athletic Performance, and Recovery

Abstract

Exercise promotes reactive oxygen species (ROS) production from multiple sources in skeletal muscle. It is common for athletes to consume antioxidant supplements to attenuate exercise-induced increases in skeletal muscle ROS levels, with the intention of improving performance and recovery. However, ROS play an important role as signalling molecules that mediate exercise adaptations in skeletal muscle. Therefore, supplementation with general antioxidants, which have unknown tissue distribution and act by non-specifically neutralizing ROS from multiple cellular sources, may be detrimental for adaptation. Mitochondria-targeted antioxidants such as MitoQ are designed to accumulate in mitochondria and provide targeted protection against oxidative stress. However, the effects of mitochondria-targeted antioxidant supplementation on the adaptive response to exercise in skeletal muscle, athletic performance, and recovery have not been investigated. Chapter 3 investigated the effect of MitoQ supplementation on 1) the acute exerciseinduced cell signalling response in skeletal muscle and 2) exercise-training induced adaptations in middle-aged untrained men. MitoQ supplementation augmented acuteexercise induced increases in skeletal muscle mRNA expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1-α) and vascular endothelial growth factor (VEGF) compared to placebo. However, exercise traininginduced increases in skeletal muscle citrate synthase activity were similar between groups, indicating that MitoQ had no effect on training-induced increases in skeletal muscle mitochondrial content. While training-induced improvements in peak rate of oxygen uptake (V̇ O2peak) and 20 km cycling time trial performance were also similar between groups, MitoQ augmented training-induced improvements in peak power output achieved during the V̇ O2peak test. Chapter 4 investigated the effect of MitoQ supplementation on cycling performance in middle-aged recreationally trained cyclists. Mean 8 km time trial completion time was 1.3% faster with MitoQ compared to placebo. There was no difference in rating of perceived exertion (RPE) during the time trial between conditions despite there being a 4.4% increase in average power output during the time trial following MitoQ supplementation compared to placebo. The improvement in time trial performance following MitoQ supplementation was associated with an attenuation of exercise-induced increases in plasma F2-isoprostanes, which are a systemic marker of lipid peroxidation. Chapter 5 investigated the effect of MitoQ supplementation on recovery of muscle function following a bout of eccentric exercise involving the knee extensors in young, untrained men. While the loss of peak isometric and concentric torque following exercise was similar between groups, MitoQ delayed recovery of peak eccentric torque compared to placebo. Exercise also resulted in delayed onset muscle soreness (DOMS) and this effect was similar between groups. Exercise-induced increases in F2-isoprostanes measured in urine samples collected during the 24 hours before exercise and 24 and 48 hours after exercise were unaffected by MitoQ. The findings in this thesis provide evidence that mitochondria-targeted antioxidant supplementation augments acute exercise-induced increases in skeletal muscle mRNA expression of signalling intermediates involved in mitochondrial biogenesis and angiogenesis and improves high-intensity cycling performance when taken during exercise training. However, while mitochondria-targeted antioxidant supplementation may be beneficial for performance, it does not affect DOMS and may delay recovery of muscle function following muscle-damaging exercise.