Exercise has been recognised to cause changes in indicators of oxidative stress for 25 years. More recently, it has become apparent that contracting skeletal muscle is a major source of oxidant generation. The main source of intracellular oxidant generation appears to be mitochondria, but contracting skeletal muscle is recognised to release superoxide anions and nitric oxide to the interstitial fluid where hydroxyl radical activity is also increased. The functions of these extracellular species are unclear; nitric oxide released from skeletal muscle may exert a vasodilatory role, but the effects of other reactive oxygen and nitrogen species have not been characterised. Many investigators have suggested that these species might mediate the tissue damage that can accompany excessive or unaccustomed exercise, but there is little data in support of this. Increasingly, there is evidence that these species act as local signals to influence changes in redox-regulated gene expression leading to some adaptive responses to exercise.