Mitochondria-targeted antioxidant supplementation improves 8 km time trial performance in middle-aged trained male cyclists

Abstract

BackgroundExercise increases skeletal muscle ROS production, which may contribute to the onset of muscular fatigue and impair athletic performance. Mitochondria-targeted antioxidants such as MitoQ 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 randomised, double-blind, placebo-controlled crossover study, 19 middle-aged (age: 44 ± 4 years) recreationally trained (VO2peak: 58.5 ± 6.2 ml·kg·min− 1, distance cycled per week during six 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) 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 rate 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 average power output during the time trial being higher following MitoQ supplementation (280 ± 53 W) compared to placebo (270 ± 51 W, P = 0.04). Plasma F2-isoprostanes were lower on completion of the time trial following MitoQ supplementation (35.89 ± 13.6 pg/ml) compared to placebo (44.7 ± 16.9 pg/ml P = 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.Trial registrationThis study was registered with the Australia New Zealand Clinical Trial Registry (ACTRN12619000451101) on 19th March 2019.

Mitochondria-targeted antioxidant supplementation augments acute exercise-induced increases in muscle PGC1α mRNA and improves training-induced increases in peak power independent of mitochondrial content and function in untrained middle-aged men

“…In the present study, MitoQ improved peak power output during the VO 2peak test, but had no effect on 20 km time trial performance when the participant's power output was much lower. Taken together, these results may indicate that oxidative stress plays a more significant role in impairing performance at exercise intensities that require significant anaerobic component, and would be consistent with trained cyclists being able achieve higher power output and plasma lactate during short-duration (<15 min) all out exercise when supplemented with MitoQ [37]. It is therefore possible that MitoQ is acting as a direct ergogenic aid rather than enhancing exercise-training induced improvements in peak power output.…”

“…We have recently shown that MitoQ supplementation improves 8 km time trial performance in trained cyclists, and this was associated with attenuated exercise-induced increases in plasma F 2 -isoprostanes [37]. Furthermore, infusion of the antioxidant N-acetylcysteine has been shown to improve performance in highly trained cyclists, who can achieve very high workloads during a performance test [10].…”

Effect of mitochondrial‐targeted antioxidants on glycaemic control, cardiovascular health, and oxidative stress in humans: A systematic review and meta‐analysis of randomized controlled trials

“…The most common reasons for study exclusion were duplicate of the same study (same study/data published), wrong outcomes (study outcomes not relevant to the review), and wrong study design (non-RCTs). Of the included studies, 16 were full-text articles, 16,17,19,[23][24][25][26][27][28][30][31][32][33][34][35]37 two were abstracts that were linked to clinical trial registry information, 22,29 and one was an unpublished study identified from a clinical trials registry. 36 Ten studies used Elamipretide as the mitoAOX agent, 16,17,[22][23][24]26,27,32,34,36 eight studies used MitoQ, 19,25,[29][30][31]33,35,37 and one study used MitoTEMPO.…”

“…For these studies, mitoAOX group data were combined into a single group for quantitative analyses, with collective means and SDs determined according to recommended methods 38 . Fourteen studies included participants with specific health conditions 16,17,22‐30,32,34,36 and six studies included healthy participants 19,28,31,33,35,37 . Thirteen studies involved chronic mitoAOX supplementation ranging from five to 84 days, 16,17,19,22,25,27,29,31‐33,35‐37 while seven studies involved acute (<1 day) mitoAOX treatment 23,24,26,28,30,34,37 .…”

“…Some studies, particularly in healthy participants, found improvements in oxidative stress markers with MitoQ supplementation. 19,30,31,33 However, overall, the limited evidence is not suggestive of benefits of mitoAOXs on systemic markers of oxidative stress such as malondialdehyde and F 2 -…”