Effect of six weeks ubiquinol supplementation on mitochondrial respiratory function and exercise capacity in healthy...

Coenzyme Q10 (CoQ₁₀) is an integral component of the mitochondrial electron transfer system. Most studies have administered the oxidised form of CoQ₁₀ (ubiquinone) and observed no effects on mitochondrial respiratory function or endurance exercise performance. The reduced form of CoQ₁₀, ubiquinol (UQH₂), has greater bioavailability than ubiquinone, but the effects of UQH₂ supplementation on mitochondrial respiratory function and exercise capacity are unclear. Fifty-four healthy, recreationally active males were randomised to receive either 300 mg·day^- 1 UQH₂ or placebo (PLA) for 6 weeks in a double-blind independent-group design. Before and after the supplementation period, skeletal muscle mitochondrial respiration variables and protein content of the mitochondrial leak proteins, adenine nucleotide translocase1 + 2 (ANT1 + 2) and uncoupling protein-3 (UCP-3), were assessed. In addition, participants completed a severe-intensity cycle test to exhaustion to assess time to the limit of tolerance (T_Lim) and oxygen uptake (V̇O₂) kinetics. Compared to pre-supplementation and PLA, UQH₂ supplementation increased plasma [CoQ₁₀] (P < 0.05), and lowered inverse respiratory control ratio (Pre-PLA: 0.064 ± 0.034 vs. Post-PLA: 0.072 ± 0.026; Pre- UQH₂: 0.073 ± 0.039 vs. Post-UQH₂: 0.044 ± 0.019; P < 0.05), suggestive of improved oxidative phosphorylation coupling efficiency. There were no differences in ANT1 + 2 or UCP-3 protein content post-supplementation compared to pre-supplementation between groups (P > 0.05). End-exercise V̇O₂, change in V̇O₂ between 2 min and end-exercise, and T_Lim were not different between groups post-supplementation (P > 0.05). Six-weeks UQH₂ supplementation increased plasma [CoQ₁₀] and oxidative phosphorylation coupling efficiency, but did not alter mitochondrial leak proteins, T_Lim or V̇O₂ kinetics during severe-intensity exercise in healthy, active males.