Unaccustomed exercise may result in significant damage to skeletal muscle and cause delayed onset muscle soreness (DOMS) in both recreational and elite athletes. Two basic mechanisms-'metabolic' and 'mechanical' stress--have been proposed to explain how exercise initiates damage to skeletal muscle fibres. The extent of damage, particularly after eccentrically-biased exercise, has been assessed by histological and ultrastructural examination, and the measurement of the efflux of cytosolic enzymes into the circulation. The role of reactive oxygen species in the mediation of exercise-induced oxidative damage to muscle and the protection offered by anti-oxidant defence systems have been well studied. Free radical generation is normally estimated by indirect methods such as chemiluminescence, spectrophotometry, flow cytometry, or the measurement of products of lipid peroxidation such as malondialdehyde (MDA) and thiobarbituric acid reactive substances (TBARS). Although several theories have been proposed to account for the DOMS phenomenon, the underlying mechanisms are still to be elucidated. A group of proteins known collectively as cytokines regulate inflammatory and immunological processes involved in the repair of damaged tissue.