Abstract

BackgroundExercise increases skeletal muscle reactive oxygen species (ROS) production, which may contribute to the onset of muscular fatigue and impair athletic performance. Mitochondria-targeted antioxidants such as MitoQ, which contains a ubiquinone moiety and is targeted to mitochondria through the addition of a lipophilic triphenylphosphonium cation, are becoming popular amongst active individuals as they are designed to accumulate within mitochondria and may provide targeted protection against exercise-induced oxidative stress. However, the effect of MitoQ supplementation on cycling performance is currently unknown. Here, we investigate whether MitoQ supplementation can improve cycling performance measured as time to complete an 8 km time trial.MethodIn a randomized, double-blind, placebo-controlled crossover study, 19 middle-aged (age: 44 ± 4 years) recreationally trained (VO2peak: 58.5 ± 6.2 ml·kg− 1·min− 1, distance cycled per week during 6 months prior to study enrollment: 158.3 ± 58.4 km) male cyclists completed 45 min cycling at 70% VO2peak followed by an 8 km time trial after 28 days of supplementation with MitoQ (20 mg·day− 1) and a placebo. Free F2-isoprostanes were measured in plasma samples collected at rest, after 45 min cycling at 70% VO2peak and after completion of the time trial. Respiratory gases and measures of rating of perceived exertion (RPE) were also collected.ResultsMean completion time for the time trial was 1.3% faster with MitoQ (12.91 ± 0.94 min) compared to placebo (13.09 ± 0.95 min, p = 0.04, 95% CI [0.05, 2.64], d = 0.2). There was no difference in RPE during the time trial between conditions (p = 0.82) despite there being a 4.4% increase in average power output during the time trial following MitoQ supplementation compared to placebo (placebo; 270 ± 51 W, MitoQ; 280 ± 53 W, p = 0.04, 95% CI [0.49, 8.22], d = 0.2). Plasma F2-isoprostanes were lower on completion of the time trial following MitoQ supplementation (35.89 ± 13.6 pg·ml− 1) compared to placebo (44.7 ± 16.9 pg·ml− 1p = 0.03).ConclusionThese data suggest that MitoQ supplementation may be an effective nutritional strategy to attenuate exercise-induced increases in oxidative damage to lipids and improve cycling performance.

Highlights

  • Oxygen-derived radical and non-radical species, collectively referred to as reactive oxygen species (ROS), are continuously produced by skeletal muscle [1]

  • While exercise-induced ROS play an important role in adaptation, acute exposure to O2·− and H2O2 can impair sarcoplasmic reticulum calcium release and myofibrillar calcium sensitivity resulting in the development of muscular fatigue [13,14,15,16]

  • Increasing the capacity of skeletal muscle to neutralise ROS by using exogenous antioxidant supplements has received much attention as a potential strategy to delay the onset of muscular fatigue and improve athletic performance

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Summary

Introduction

Oxygen-derived radical and non-radical species, collectively referred to as reactive oxygen species (ROS), are continuously produced by skeletal muscle [1]. Increasing the capacity of skeletal muscle to neutralise ROS by using exogenous antioxidant supplements has received much attention as a potential strategy to delay the onset of muscular fatigue and improve athletic performance. Several general antioxidants such as N-acetylcysteine and vitamin C and E have been studied for their effectiveness as ergogenic aids. Exercise increases skeletal muscle reactive oxygen species (ROS) production, which may contribute to the onset of muscular fatigue and impair athletic performance. We investigate whether MitoQ supplementation can improve cycling performance measured as time to complete an 8 km time trial

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