Skeletal muscle generates superoxide, nitric oxide and a number of secondary reactive oxygen and nitrogen species (ROS) at rest and the production of these species is increased by contractile activity. These substances are potentially generated by a number of sites including mitochondria, membrane-localised oxidases etc. Whether the ROS generated during contractions have predominantly deleterious or beneficial effects on muscle and other tissues has become the subject of substantial discussion. Although all initial studies assumed these species had negative effects on tissue function and viability, recent data indicate that contraction-induced ROS modulate at least some of the adaptive responses that occur in skeletal muscle following contractile activity. This process involves activation of redox-regulated transcription factors, such as AP-1, NFkB and HSF-1 and leads to increased expression of cytoprotective proteins that protect muscle cells against potential damage following subsequent rises in ROS activity. During ageing of skeletal muscle there is evidence that this ability to adapt to contraction-induced ROS fails with consequent increase in oxidative damage to skeletal muscle associated with the age-related loss of muscle mass and function. Supported by the Wellcome Trust and United States National Institutes of Health.