Exercise always stimulates a temporary change in redox balance towards a more oxidized state since active skeletal muscle cells continuously produce reactive oxygen and nitrogen species (ROS, RNS), as part of metabolic processes involving increased oxygen consumption . Free radicals produced during exercise provoke a “hormetic” adaptive response to physical activity that is highly muscle fiber-specific and also positively modulate several physiological functions, such as cell signaling, immune response, and apoptosis [2, 3]. However, duration, intensity, and mode of exercise appear to affect differently the oxidative stress balance, and this may be dependent on age, gender, individual fitness levels, and nutritional status . In particular, while regular exercise induces the upregulation of antioxidant as well as oxidative damage repairing systems [2, 5], acute exercise (“vigorous physical activity”) triggers a massive generation of ROS and RNS, also by anaerobic metabolism, with depletion in antioxidant defenses, and produces oxidative damage to proteins and DNA and secondary inflammation due to the phagocytic activity of immune cells [3, 6, 7]. These events result in varying degrees of mechanical and metabolic stress on the human body, finally leading to an impairment in cell and tissue functions . Indeed, it is well known that oxidative stress is involved in the pathogenesis of hypertension, atherosclerosis, diabetes, and cancer and also accelerates aging process [9, 10].