Attenuated responses to redox stress are a common feature of aged organisms and these appear to present in skeletal muscle as a reduced ability to respond to contractile activity. Contracting skeletal muscle generates superoxide from membrane-localised NADPH oxidases and this is rapidly converted to hydrogen peroxide (H₂O₂) which acts to stimulate specific adaptive responses. The nature of these responses is extensive and includes increased generation of stress proteins and upregulation of mitochondrial biogenesis. Recent data indicate that the concentrations of H₂O₂ generated within muscle fibres are insufficient to directly oxidise redox-sensitive proteins in key response pathways and indicate that effector proteins, such as peroxiredoxins, play a key role in mediating adaptations. Understanding the specific mechanisms involved and how these are modified in ageing and other conditions of skeletal muscle loss provides a potential route for interventions to maintain muscle mass and function.