Vigorous exercise generates large amounts of reactive oxygen species (ROS) as a result of the consumption of large volumes of O₂ in athletes, causing some athletes to consume antioxidants in the erroneous belief that this will counteract the damaging effects of ROS. There is currently no convincing evidence to support the benefits of antioxidant supplementation in acute physical exercise and exercise training. On the contrary, exogenous antioxidants prevent some physiological functions of free radicals that are needed for cell signaling, causing higher dosages of antioxidants to hamper or prevent performance-enhancing and health-promoting training adaptation such as mitochondrial biogenesis, skeletal and cardiac muscle hypertrophy, and improved insulin sensitivity. However, there remains the perception that antioxidants can counterbalance oxidative stress and benefit exercise adaptation and performance in athletes. It is likely that the negative effects of high doses of antioxidant supplementation exceed their potential benefits. We discuss some proposed pathways of potential side effects of exogenous antioxidant supplementation in athletes.

Physical inactivity remains a pressing global public health concern. Prolonged periods of sedentary behavior have been linked to heightened risks of non-communicable diseases such as cardiovascular diseases and type 2 diabetes, while engaging in any form of physical activity can elicit favorable effects on health. Nevertheless, epidemiological research indicates that people often struggle to meet recommended physical activity guidelines, citing time constraints, lack of exercise equipment, and environmental limitations as common barriers. Exercise snacks represents a time-efficient approach with the potential to improve physical activity levels in sedentary populations, cultivate exercise routines, and enhance the perception of the health benefits associated with physical activity. We review the existing literature on exercise snacks, and examine the effects of exercise snacks on physical function and exercise capacity, while also delving into the potential underlying mechanisms. The objective is to establish a solid theoretical foundation for the application of exercise snacks as a viable strategy for promoting physical activity and enhancing overall health, particularly in vulnerable populations who are unable to exercise routinely.

Object: The aim of our study was to evaluate and compare the effects of physical exercise interventions on physical fitness and executive functions in children. Methods: Six-year-old children participated in the study and were randomly divided into physical exercise group (PE group, n = 43) and control group (C group, n = 46). The children in the PE group participated in a physical exercise program for 45 min daily, four days a week for 11 weeks. The children in the C group continued with their usual routines. Then, all the children were tested before and after the experiment for body composition (height, weight, BMI), physical fitness (20-m shuttle run test, standing long jump test, grip strength test, 4 × 10 m shuttle run test and sit and reach tests), and executive functions test (animal go/no-go task, working memory span task, simple reaction test and flexible item selection task) before and after the 11-week period. Results: The 11 weeks of physical exercise did not significantly affect the body composition of the children (p > 0.05). The physical fitness and executive functions test results showed that 11 weeks of physical exercise interventions improves physical fitness (cardiopulmonary fitness, muscle strength, speed sensitivity and flexibility quality) and executive functions parameters (inhibitory control, working memory, the reaction time, and cognitive flexibility) in children (p < 0.05, p < 0.01). Conclusion: 11 weeks of physical exercise can improve the physical fitness and executive functions of six-year-old children.

Cardiac remodeling is a physiological adaptation to aerobic exercise and which is characterized by increases in ventricular volume and the number of cardiomyocytes. The mitochondrial derived peptide MOTS-c functions as an important regulator in physical capacity and performance. Exercise elevates levels of endogenous MOTS-c in circulation and in myocardium, while MOTS-c can significantly enhance exercise capacity. However, the effects of aerobic exercise combined with MOTS-c on cardiac structure and function are unclear. We used pressure–volume conductance catheter technique to examine cardiac function in exercised rats with and without treatment with MOTS-c. Surprisingly, MOTS-c improved myocardial mechanical efficiency, enhanced cardiac systolic function, and had a tendency to improve the diastolic function. The findings suggest that using exercise supplements could be used to modulate the cardiovascular benefits of athletic training.

Myocardial remodeling and dysfunction are commonly observed in type 2 diabetes mellitus (T2DM). Aerobic exercise can partly alleviate diabetes-induced myocardial dysfunction through its antioxidant actions. MOTS-c is a potential exercise mimic. This study aimed to investigate the effects of MOTS-c on improving diabetic heart function and its mechanism and to identify whether MOTS-c improved antioxidant defenses due to aerobic exercise. Herein, we established a rat model of T2DM induced by high-fat diet combined with a low-dose streptozotocin injection. Interventions were performed using intraperitoneal injections of MOTS-c (i.p. 0.5 mg/kg/day, 7 days/week) or aerobic exercise training (treadmill, 20 m/min, 60 min/day, 5 days/week) for 8 weeks. Myocardial ultrastructure was assessed using transmission electron microscopy (TEM), myocardial lipid peroxidation levels (MDA), superoxide dismutase (SOD), glutathione (GSH), and catalase (CAT) levels were assessed using colorimetric methods, and molecular analyses including MOTS-c, Kelch-like ECH-associated protein 1 (Keap1), Nuclear factor E2-related factor 2 (Nrf2), adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK)and phospho-AMPK (p-AMPK) were examined using Western blot. The results showed that MOTS-c, with or without exercise, reduced myocardial ultrastructural damage and improved glucolipid metabolism and cardiac function in T2DM. Furthermore, MOTS-c increased antioxidant markers such as SOD, CAT, and the protein expression of myocardial MOTS-c, Keap1, Nrf2, and p-AMPK. MOTS-c with exercise treatment reduced myocardial MDA and increased p-AMPK significantly comparing to only exercise or MOTS-c alone. Our findings suggest that MOTS-c may be a helpful supplement for overcoming exercise insufficiency and improving myocardial structure and function in diabetes.

Cardiac structure remodeling and dysfunction are common complications of diabetes, often leading to serious cardiovascular events. MOTS-c, a mitochondria-derived peptide, regulates metabolic homeostasis by accelerating glucose uptake and improving insulin sensitivity. Plasma levels of MOTS-c are decreased in patients with diabetes. MOTS-c can improve vascular endothelial function, making it a novel therapeutic target for the cardiovascular complications of diabetes. We investigated the effects of MOTS-c on cardiac structure and function and analyzed transcriptomic characteristics in diabetic rats. Our results indicate that treatment with MOTS-c for 8-week repaired myocardial mitochondrial damage and preserved cardiac systolic and diastolic function. Transcriptomic analysis revealed that MOTS-c altered 47 disease causing genes. Functional enrichment analysis indicated MOTS-c attenuated diabetic heart disease involved apoptosis, immunoregulation, angiogenesis and fatty acid metabolism. Moreover, MOTS-c reduced myocardial apoptosis by downregulating CCN1 genes and thereby inhibiting the activation of ERK1/2 and the expression of its downstream EGR1 gene. Our findings identify potential therapeutic targets for the treatment of T2D and diabetic cardiomyopathy.