| Popis: |
Abstract Vigorous training increases the production of reactive oxygen species (ROS) from skeletal muscle, which can contribute to impairing athletic performance and health. Mitochondrial antioxidant such as MitoQ may contribute to protecting against training-induced oxidative stress such as mitochondrial ROS, but the effects on athletic performance are unknown. The purpose of this study was to determine the effects of MitoQ to exercise training (EX) on VO2max, miRNA expression involved in inflammation and oxidative stress. In this double-blind clinical trial, 32 professional cyclists (25.6±3.8yr) were randomly divided into 4 groups (n=8); 1) Placebo, 2) EX (cycle ergometer, 75% of VO2max, 90 minutes, 3 sessions/week, and 4 weeks), 3) MitoQ (20 mg.day-1 for 4 weeks), and 4) EX+MitoQ (combined EX with MitoQ for 4 weeks). V˙O2max and gene expression of MicroRNAs (miRNAs)-19b, -181b, -155, and -146a and Serum levels of ROS (peroxides, superoxide, hydroxyl radical, singlet oxygen, and alpha oxygen), glutathione peroxidase (GPx), and superoxide dismutase (SOD) were measured by the gas analyzer, real-time polymerase chain reaction (2-ΔΔCt) and ELISA, respectively. Both EX+MitoQ and MitoQ reduced serum levels of ROS (P < 0.05), but there was no change in EX group. Serum GPx levels were increased in EX, MitoQ, and EX+MitoQ (P < 0.05), but there was no difference between groups. Serum SOD remained unchanged in all groups. miRNA-155 and miRNA-19b expressions were decreased in EX+MitoQ compared to EX, whereas miRNA-146a was increased in EX+MitoQ compared to EX (P < 0.05). Placebo-controlled intervention (tapioca powder) had no effects on all outcomes (P < 0.05). MitoQ supplementation and EX reduced ROS levels and altered expression of key miRNAs mediating ROS generation and vascular endothelial inflammation could contribute to improving vascular function. |
