Objectives:This study was conducted to evaluate the effect of the different intensity levels of single-session aerobic exercise on serum levels of lipid peroxidation and muscle damage markers in sedentary males.Method:Fifty one sedentary healthy males aged 21.76±1.89 years were randomly divided into four groups, with one control (n=10) and three treatment groups that attended single-session aerobic exercise with low (n=14), moderate (n=14), and high (n=13) intensities. The serum levels of malondialdehyde (MDA) and creatine kinase (CK) were measured.Results:Data analysis revealed a significant effect by the intensity levels of aerobic exercise on MDA (P=0.001) and CK (P=0.003) post-test when the participants in the treatment groups were compared with the control. When the intensity of aerobic exercise was increased, the amount of MDA and CK was also found to be increased.Conclusion:Single-session aerobic exercise can increase the amount of MDA and CK, suggesting that low intensity level of aerobic exercise should be utilized for more adaptation, and to prevent lipid peroxidation and muscle damage in sedentary males.

The role of autophagy and lysosomal degradation pathway in the regulation of skeletal muscle metabolism was previously studied. However, underlying molecular mechanisms are poorly understood. L‐lactate which is utilized as an energetic substrate by skeletal muscle can also augment genes expression related to metabolism and up‐regulate those being responsive to reactive oxygen species (ROS). Since ROS is the most important regulator of autophagy in skeletal muscle, we tested if there is a link between cellular lactate metabolism and autophagy in differentiated C2C12 myotubes and the gastrocnemius muscle of male wistar rats. C2C12 mouse skeletal muscle was exposed to 2, 6, 10, and 20 mM lactate and evaluated for lactate autophagic effects. Lactate dose‐dependently increased autophagy and augmented ROS generation in differentiated C2C12 myotubes. The autophagic effect of lactate deterred in N‐acetylcysteine presence (NAC, a ROS scavenger) indicated lactate regulates autophagy with ROS participation. Lactate‐induced up‐regulation of extracellular signal‐regulated kinase 1/2 (ERK1/2) through ROS was required to regulate the autophagy by lactate. Further analysis about ERK1/2 up‐ and downstream indicated that lactate regulates autophagy through ROS‐mediated the activation of ERK1/2/mTOR/p70S6K pathway in skeletal muscle. The in vitro effects of lactate on autophagy also occurred in the gastrocnemius muscle of male Wistar rats. In conclusion, we provided the lactate‐associated regulation evidence of autophagy in skeletal muscle by activating ROS‐mediated ERK1/2/mTOR/p70S6K pathway. Since the increase in cellular lactate concentration is a hallmark of energy deficiency, the results provide insight into a skeletal muscle mechanism to fulfill its enhanced energy requirement.

Objectives. Hypertension (HTN) is one of the most important risk factors for cardiovascular diseases. Despite advances in treatment and control of HTN, the prevalence of HTN is still increasing. MitoQ is a supplement that acts on mitochondria and attenuates reactive oxygen species (ROS), which plays an important role in cardiovascular health. miRNAs play an important role in the pathophysiology of HTN. We evaluated the effects of MitoQ supplementation and endurance training (ET), alone and in combination, on functional indices of the heart and serum levels of miR-126, miR-27a, antioxidants, and NO, in patients with HTN. Methods. In a double-blind randomized clinical trial, 52 male participants (age 40-55 years) were randomly divided into four groups ( n = 13 ) of placebo, MitoQ (20 mg/day, oral), ET (cycle ergometer, moderate intensity, 40-60% VO2 peak, heart rate 120-140 b/min, 45 min a day, three days/week for six weeks), and MitoQ+ET. Cardiac function indices were assessed by echocardiography before and after interventions. Results. Systolic blood pressure (SBP) significantly decreased in all intervention groups ( P < 0.001 ) while DBP ( P < 0.01 ) and LV hypertrophy ( P < 0.05 ) were significantly decreased only in the MitoQ+ET group. Serum levels of SOD, GPx, and NO and the level of miR-126 significantly increased in all treatment groups, while miR-27a reduced in the ET ( P < 0.05 ) and MitoQ+ET ( P < 0.01 ) groups. Conclusions. Compared to MitoQ and ET alone, their combination has more prominent improving effects on cardiac health and amelioration of BP in the patients with HTN. These effects are through miR-126 and miR-27a modulation and ameliorating mitochondrial ROS production.

Background Mitochondrial 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. Methods 32 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. Results EX+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. Conclusions A 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.