This study clearly shows that vitamin E plays a role in modulating skeletal muscle mass. In this case, the muscle studied was the predominantly slow-twitch (>90%) soleus muscle.
Vitamin C, vitamin E (tocopherols), and some precursors to vitamin A (the carotenoids) exhibit antioxidant activity. Each of these vitamins has independently been shown to alter immunity. The antioxidant function of these vitamins is of interest to some athletes primarily because exercise increases the production of reactive oxygen species (ROS) which have been associated with muscular fatigue and muscular damage. In addition, neutrophils and macro phages produce ROS. The ROS produced by the immune system may have a role in modulating postexercise muscle damage. The other reason that vitamins A, C, and E may be of interest to athletes relates to their potential immunostimulatory properties. The antioxidant properties of the vitamins may differ from the immunomodulatory effects.Reactive oxygen species (ROS) are produced during strenuous exercise, result in oxidative stress, and are associated with a depletion of antioxidants, muscle damage, and fatigue. High concentrations of antioxidants may protect against the damaging effects of ROS. An assumption has been made that a high intake of vitamins A, C, E, or betacarotene may protect against the exercise-induced oxidative stress and several studies have examined this possibility. Vitamin E (alpha-tocopherol) is considered the most important scavenger of ROS at the level of membranes and is probably the most well studied with respect to exercise. Several studies have established that exercise training is associated with a decrease in the accumulation of the products used to assess oxidative stress or an enhancement of antioxidant enzymes. The findings from some studies suggest that vitamin E supplementation may protect against the oxidative damage induced by exercise. However, the results from both human and animal studies show that vitamin E supplementation does not improve performance and may not attenuate muscular damage following a marathon. An understanding of interactions between the immune system, ROS production, and muscle damage may provide some insight regarding antioxidants and exercise-induced muscle damage. Although these interactions are not completely understood at this time, it appears that the production of ROS by cells of the immune system may be an important part of the postexercise muscle repair process. Neutrophils and macrophages appear to infiltrate sites of postexercise muscle damage and both of these cell types produce ROS. The release of ROS can enhance the release of cytokines and cytokines can induce the production of ROS The release of both cytokines and ROS are important in removing damaged muscle tissue and may assist in the repair process. The findings from a recent study suggest that the generation of ROS postexercise may be beneficial in the repair process. In this study, normal mice demonstrated greater oxidative stress postexercise than mice with inhibited neutrophil function; however, 4 days later normal mice showed evidence of less muscle damage Based on this evidence and findings from other studies mentioned previously, it should be noted that the production of free radicals or ROS during exercise may be an important part of the muscle tissue repair process and the consumption of high levels of antioxidants may not necessarily be beneficial. Some researchers have examined life span and whether it can be extended by increased antioxidant intake. The evidence from two recent studies suggests that supplementing diets with high levels of antioxidants does not increase maximum life span and exercised rodents fed a diet containing additional antioxidants did not have a greater life span than exercised rodents on a normal diet. It appears that although exercise may be associated with a greater production of ROS, this does not result in a shortened life span and the consumption of additional antioxidants confers no additional increase in longevity. Taken together, the findings from the studies above suggest that additional antioxidants do not improve performance, do not appear to improve muscle tissue repair postexercise, and are not beneficial in terms of increasing life span in exercised rodents. Although the interactions between the immune system and ROS produced during exercise need further research, at this time it does not appear that additional antioxidants will enhance immune responses such as postexercise muscle tissue repair.