Chronic loss of skeletal muscle mass and function is a major contributor to frailty and weakness in the elderly. The major cause of age-related loss of muscle mass is a decrease in the number of skeletal muscle fibres associated with atrophy and weakness of the remaining fibres. The fundamental causes of loss of tissue function with increasing age are the subject of considerable research activity, but remain unclear. A large number of studies have reported a dysregulation of reactive oxygen species (ROS) homeostasis during ageing that may potentially lead to increased oxidative damage to tissues and/or to defective redox signalling. Skeletal muscle tissue from aged organisms contains increased amounts of oxidative damage, but whether this is the cause of age-related deficits in muscle or a consequence of ageing has been the subject of controversy. Studies from our group have examined the changes in ROS generation that occur with ageing in man and experimental models and have also utilised a transgenic approach to modify ROS generation in model organisms. Data from these experiments support the hypothesis that aberrant ROS regulation plays a role in the deficits in skeletal muscle and motor neurons that occur during ageing, but also indicate this does not simply occur through increased oxidative damage to tissues. A number of studies have focussed on the role played by mitochondria in aberrant generation of ROS during ageing. There is little evidence that ageing is associated with gross changes in mitochondrial function in skeletal muscle, but most studies have reported increased generation of ROS by mitochondria isolated from muscle tissue of old animals and man although interpretation of such data is complicated by the potential presence of a small number of denervated fibres in biopsy samples since these fibres may have gross elevations in mitochondrial ROS generation.