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Altered plasma amino acid and acylcarnitine concentrations with protein-leucine feeding might partly explain the acute post-exercise reduction in neutrophil function and increased exercise-stimulated neutrophil oxidative burst on day 6, which could impact neutrophil-dependent processes during recovery from intense training.
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Reactive oxygen species can be important in the initiation of exercise-induced muscle damage and in the initiation and propagation of the subsequent acute muscle inflammatory response. Oxygen radicals generated via the neutrophil respiratory burst are vital in clearing away muscle tissue that has been damaged by exercise and they may also be responsible for propagation of further damage. Intervention by antioxidants to limit the postexercise inflammatory response and its potential to impair optimal muscle function are of interest to serious and recreational sports participants. Although antioxidants have the potential to limit muscle oxidative stress during the postexercise period, direct evidence for their role in this is limited. It is likely that short-term training can protect muscle from subsequent exercise-induced damage and inflammation without necessarily improving muscle antioxidant status. Although muscle antioxidant status may be enhanced by longer term training, diet, or antioxidant administration, the significance of antioxidants in limiting muscle damage during the acute inflammatory response needs to be more clearly defined. It may even be counterproductive to limit neutrophil function during the inflammatory response, since this may inhibit subsequent muscle repair