MitoQ supplementation improves oxygen uptake kinetic by reduced reactive oxygen species levels and altered expression of miR‐155 and miR‐181b

Abstract

BackgroundMitochondrial antioxidant (MitoQ) has been developed as a pharmaceutical for diseases. Few studies have investigated the role of MitoQ in enhancing athletic performance. Thus, the purpose of the study was to determine the effects of MitoQ supplementation to exercise training (EX) on the oxygen uptake kinetic, oxidative stress, and MicroRNAs (miRNAs) regulating vascular inflammation and reactive oxygen species (ROS) generation.Methods32 healthy young cyclists (25.6±3.8yr) were randomly divided into 4 groups (n=8); 1) Placebo, 2) EX (Cycle ergometer, moderate intensity), 3) MitoQ (20 mg/day, oral), and 4) EX+MitoQ. Oxygen uptake kinetics during low, moderate, and severe intensity cycling were measured before and after two weeks of interventions. Serum levels of ROS, glutathione peroxidase (GPx), and superoxide dismutases (SOD) were measured. miR‐19b, miR‐155, miR‐181b, and miRNA‐146a were measured by RT‐qPCR.ResultsEX+MitoQ accelerated the phase Ⅱ of oxygen uptake kinetic (moderate intensity) compared to EX (P<0.05). Both EX+MitoQ and MitoQ reduced ROS levels but there was no change in EX (P<0.05). GPx was increased in EX, MitoQ, and EX+MitoQ (P<0.05) whereas SOD levels in all groups were not different. miR‐155 and miR‐19b expressions were decreased in EX+MitoQ compared to EX (P<0.05). miR‐146a was increased in EX+MitoQ compared to EX only (P<0.05). There was no difference of miR‐181b between EX and Mito+Q. Placebo effects were not found.ConclusionsA short‐term MitoQ supplementation to aerobic training enhanced oxygen utilization during a moderate performance in cyclists compared to training alone by reduced ROS levels and altered expression of miR‐155 and miR‐181b mediating vascular endothelial inflammation and ROS generation.