High production of reactive oxygen species (ROS) in skeletal muscle tissues has serious destructive effects, which alter the integrity of skeletal muscle resulting into fatigue, muscle wasting, and muscle weakness [90,101]. Sources of intramuscular ROS are numerous including mitochondrial dysfunction (e.g., alteration of mitochondrial enzymes in the respiratory chain as well as enzymes responsible for β-oxidation), neutrophil infiltration, and the activity of cytokines and major muscle degrading molecules such as myostatin [21,36,38,101,102,118]. Oxidative and nitrosative damages in skeletal muscle tissues are mediated by the activity of numerous pro-oxidant enzymes that are associated with inflammatory processes such as cyclooxygenase-2 (COX-2) and iNOS [101]. ROS triggers the activity of corrosive molecules such as poly (ADP-ribose) polymerase (PARP), xanthine oxidase, and adenosine deaminase, which contribute to DNA damage, lipid peroxidation (e.g., increased MDA), and protein nitrotyrosylation as well as ATP catabolism in muscle tissues [101,102].