It is well established that the increase in reactive oxygen species (ROS) and free radicals production during exercise has both positive and negative physiological effects. Among them, the present review focuses on oxidative stress caused by acute exercise, mainly on evidence in healthy individuals. This review also summarizes findings on the determinants of exercise-induced oxidative stress and sources of free radical production. Moreover, we outline the effects of antioxidant supplementation on exercise-induced oxidative stress, which have been studied extensively. Finally, the following review briefly summarizes future tasks in the field of redox biology of exercise. In principle, this review covers findings for the whole body, and describes human trials and animal experiments separately.

Molecular hydrogen (H₂) is a colorless, tasteless, odorless, and minimal molecule with high flammability. Although H₂ has been thought to be an inert gas in living bodies for many years, an animal study reported that inhalation of H₂ gas decreased oxidative stress and suppressed brain injury caused by ischemia and reperfusion injury due to its antioxidant action. Since then, the antioxidant action of H₂ has attracted considerable attention and many studies have reported on its benefits. Most studies have reported the effects of H₂ on diseases such as cancer, diabetes, cerebral infarction, and Alzheimer’s disease. However, little is known regarding its effects on healthy subjects and exercise. Thus far, including our study, only 6 studies have explored the effect of H₂ on exercise. H₂ is the smallest molecule and therefore can easily penetrate the cellular membrane and rapidly diffuse into organelles. H₂ is thought to be able to selectively reduce hydroxyl radicals and peroxynitrite and does not affect physiologically reactive species. H₂ can be supplied to the body through multiple routes of administration, such as oral intake of H₂ water and H₂ bathing. Therefore, H₂ may be a potential alternative strategy for conventional exogenous antioxidant interventions in sports science. The purpose of this review is to provide evidence regarding the effects of H₂ intake on changes in physiological and biochemical parameters, centering on exercise-induced oxidative stress, for each intake method. Furthermore, this review highlights possible future directions in this area of research.

Extensive research has confirmed numerous advantages of exercise for promoting brain health. More recent studies have proposed the potential benefits of lactate, the by-product of exercise, in various aspects of brain function and disorders. However, there remains a gap in understanding the effects of lactate dosage and its impact on aged rodents. The present study first examined the long-term effects of three different doses of lactate intervention (2000 mg/kg, 1000 mg/kg, and 500 mg/kg) and high-intensity interval training (HIIT) on aging mice (20–22 months) as the 1st experiment. Subsequently, in the 2nd experiment, we investigated the long-term effects of 500 mg/kg lactate intervention and HIIT on brain neuroplasticity in aged mice (25–27 months).

DNA methylation‐based age estimators (DNAm ageing clocks) are currently one of the most promising biomarkers for predicting biological age. However, the relationships between cardiorespiratory fitness (CRF), measured directly by expiratory gas analysis, and DNAm ageing clocks are largely unknown. We investigated the relationships between CRF and the age‐adjusted value from the residuals of the regression of DNAm ageing clock to chronological age (DNAmAgeAcceleration: DNAmAgeAccel) and attempted to determine the relative contribution of CRF to DNAmAgeAccel in the presence of other lifestyle factors. DNA samples from 144 Japanese men aged 65–72 years were used to appraise first‐ (i.e., DNAmHorvath and DNAmHannum) and second‐ (i.e., DNAmPhenoAge, DNAmGrimAge, and DNAmFitAge) generation DNAm ageing clocks. Various surveys and measurements were conducted, including physical fitness, body composition, blood biochemical parameters, nutrient intake, smoking, alcohol consumption, disease status, sleep status, and chronotype. Both oxygen uptake at ventilatory threshold (VO₂/kg at VT) and peak oxygen uptake (VO₂/kg at Peak) showed a significant negative correlation with GrimAgeAccel, even after adjustments for chronological age and smoking and drinking status. Notably, VO₂/kg at VT and VO₂/kg at Peak above the reference value were also associated with delayed GrimAgeAccel. Multiple regression analysis showed that calf circumference, serum triglyceride, carbohydrate intake, and smoking status, rather than CRF, contributed more to GrimAgeAccel and FitAgeAccel. In conclusion, although the contribution of CRF to GrimAgeAccel and FitAgeAccel is relatively low compared to lifestyle‐related factors such as smoking, the results suggest that the maintenance of CRF is associated with delayed biological ageing in older men.

The purpose of this study was to investigate the involvement of neutrophil dynamics and function in exercise-induced muscle damage (EIMD) and delayed-onset muscle soreness (DOMS), and the effect of molecular hydrogen (H₂) intake on these parameters. Nine healthy and active young men performed H₂ and placebo bath trial in a crossover design. They carried out downhill running (−8% slope) for 30 min at a speed corresponding to 75~85% of peak oxygen uptake (VO₂peak). Subsequently, they repeated bathing for 20 min per day for one week. Degree of muscle soreness (visual analogue scale: VAS), peripheral leukocyte counts, neutrophil dynamics and function, muscle damage, and inflammation markers were measured. Plasma interleukin (IL)-6 concentration was significantly correlated with peripheral neutrophil count, VAS, and serum creatine kinase activity, respectively, after downhill running. Peripheral neutrophil count and serum myoglobin concentration were also significantly correlated. Conversely, there were no effects of H₂ bath. These results suggest that IL-6 may be involved in the mobilization of neutrophils into the peripheral blood and subsequent EIMD and DOMS after downhill running; however, it is not likely that H₂ bath is effective for the inflammatory process that is centered on neutrophils after downhill running.

Long-term high-fat diet increases muscle mitochondrial enzyme activity and endurance performance. However, excessive calorie intake causes intra-abdominal fat accumulation and metabolic syndrome. The purpose of this study was to investigate the effect of an alternating day high-fat diet on muscle mitochondrial enzyme activities, protein content, and intra-abdominal fat mass in rats. Male Wistar rats were given a standard chow diet (CON), high-fat diet (HFD), or alternate-day high-fat diet (ALT) for 4 weeks. Rats in the ALT group were fed a high-fat diet and standard chow every other day for 4 weeks. After the dietary intervention, mitochondrial enzyme activities and protein content in skeletal muscle were measured. Although body weight did not differ among groups, the epididymal fat mass in the HFD group was higher than those of the CON and ALT groups. Citrate synthase and beta-hydroxyacyl CoA dehydrogenase activities in the plantaris muscle of rats in HFD and ALT were significantly higher than that in CON rats, whereas there was no difference between HFD and ALT groups. No significant difference was observed in muscle glycogen concentration or glucose transporter-4 protein content among the three groups. These results suggest that an alternate-day high-fat diet induces increases in mitochondrial enzyme activities and protein content in rat skeletal muscle without intra-abdominal fat accumulation.