Moreover, some data indicate that excessive antioxidant administration might paradoxically enhance oxidative stress, an idea supported by a study investigating the intake of vitamin C in the course of three-week training program. Therefore, the awareness of the mechanisms underlying the transition from beneficial effects to an increase in muscle fatigue and delayed recovery stands as a critical point in ROS/RNS research. However, the use of antioxidants may lead to diminutions in prominent physiological cellular signals that depend on the presence of ROS/RNS and are essential in the development of skeletal muscle adaptations to exercise. Other evidence indicates that antioxidants enhance muscle recovery following intense muscle-damaging exercise. For example, NAC supplementation in well-trained athletes, preceding strenuous physical training, improved redox balance and promoted adaptive processes. Indeed, pretreatment with ROS scavengers was found to reduce the extent of fatigue in isolated muscle fibers and in humans. Years of extensive studies have provided data to support both the beneficial health-effects of antioxidant treatment and the potentially deleterious consequences of antioxidant supplementation that override potential benefits. Experimental observations of ROS/RNS-driven deterioration in muscle performance encourage the use of exogenous antioxidants to counteract oxidative stress and enhance force generation. One of the challenges faced by contracting muscle is a rise in reactive oxygen/nitrogen species (ROS/RNS) content, which is a necessary prerequisite for the control of the signaling pathways associated with fatigue delay. Skeletal muscle’s ability to regenerate and remodel in response to metabolic changes brought on by exercise is crucial to contractile function. The mechanisms underlying the two faces of ROS/RNS in exercise, as well as the role of antioxidants in muscle fatigue, are presented in detail in this review. Ultimately, both high (exercise-induced) and low (antioxidant intervention) ROS concentrations can trigger beneficial responses as long as they do not override the threshold range for redox balance. Consequently, growing evidence suggests that exogenous antioxidant supplementation might hamper exercise-engendering upregulation in the signaling pathways of mitogen-activated protein kinases (MAPKs), peroxisome-proliferator activated co-activator 1α (PGC-1α), or mammalian target of rapamycin (mTOR). On the other hand, low ROS/RNS concentrations can likely upregulate an array of cellular adaptative responses related to mitochondrial biogenesis, glucose transport and muscle hypertrophy. Exposure to ROS/RNS can affect Na +/K +-ATPase activity, intramyofibrillar calcium turnover and sensitivity, and actin–myosin kinetics to reduce muscle force production. One of the many stressors imposed on skeletal muscle through exercise is the increased production of reactive oxygen species (ROS) and reactive nitrogen species (RNS), which intensifies as a function of exercise intensity and duration. Muscle fatigue is defined as a decrease in maximal force or power generated in response to contractile activity, and it is a risk factor for the development of musculoskeletal injuries.
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