Handbook of Vitamin C Research

8Kelsey H. Fisher-Wellman and Richard J. Bloomeroxidative damage to various mitochondrial enzymes involved in energy (i.e., ATP)production would also be expected to impair performance [52].The information in the preceding section is particularly relevant to RONS-mediateddamage within the exercise bout itself and represents a potential primary role for RONS ineffecting performance. Additionally, secondary production of RONS during the recoveryperiod has been suggested to result in further oxidative stress and tissue injury following theperformance of muscle damaging exercise (i.e., protocols involving long duration and oreccentric exercise) [53]. In this respect, initial mechanical trauma/injury imposed upon themusculature during exercise results in the initiation of an inflammatory response,subsequently leading to an increase in inflammatory cytokines and influx of phagocytic cellsand neutrophils to the affected area [47]. These phagocytic cells promote secondary RONSgeneration via respiratory burst activity [53]. Moreover, this increased circulation ofinflammatory cytokines and production of RONS may further promote oxidative stress andcontribute to delayed muscle injury [54,55], as invading neutrophils have been shown to playa role in both the muscle injury [56] and oxidative damage [57] induced following eccentriccontractions.It should be understood that while the above discussion certainly makes sound scientificsense, direct evidence for RONS actually ―causing‖ decrements is performance is somewhatlacking in humans. None the less, because numerous investigators have reported increases invarious oxidative stress biomarkers following acute exercise, coupled with their associationwith reduced performance, exercise-induced RONS have historically been viewed asdetrimental by-products of muscle contraction that should be prevented and/or attenuated inan effort to enhance performance and/or recovery from demanding exercise. For this reason,several researchers have attempted to elucidate methods designed to attenuate such a stresswith the use various antioxidant supplements, pharmacological, or nutritional interventions.In opposition to this notion, an ever-increasing body of literature in now available inwhich it is suggested that RONS produced during exercise actually exist as a necessary―signal‖ for the initiation and/or propogation of several beneficial adaptations to exercise[29,47,58]. Moreover, with respect to muscle damaging exercise, the secondary productionof RONS as a component of the inflammatory response may actually assist in degradingdamaged tissue, thereby accelerating muscle regeneration and recovery following exercise[59]. Clearly, more research is needed within the area, incorporating both oxidative stressand performance measures within the same study design, in order to provide a more clearunderstanding of the role of RONS in skeletal muscle function and adaptations to exercise.Formation of RONS: Non-Exercise ConditionsFree radicals are produced by a variety of mechanisms in biological systems, however allreactions involve either the initial reduction (addition) or oxidation (removal) of an electronvia enzymatic or nonenzymatic action [12]. In short, radical species are simply aconsequence of chemical reactions occurring within the body. Moreover, RONS areproduced as a result of normal cellular metabolism and consist of a variety of both radical(e.g., superoxide, hydroxyl radical, nitrogen monoxide) and nonradical (e.g., hydrogen