Ageing of the musculoskeletal system is characterised by a loss of muscle mass and strength (sarcopenia). This process has a multiple aetiology, involving neuropathic changes, inflammation and oxidative stress, hormonal, nutritional, metabolic and lifestyle factors (Narici and Maffulli 2010). Amongst the lifestyle factors, inactivity is a main cause of sarcopenia. Tendons are also affected by ageing and inactivity, as both conditions lead to a decline in stiffness, mostly due to a deterioration in material properties rather than to tendon atrophy (De Boer et al. 2007, Onanbele et al 2006). On the other hand, regular training, and in particular resistive exercise, has been found to be highly effective for recovering muscle mass, strength and tendon stiffness in older people (Reeves et al 2003). Probably, the best example of the efficacy of regular exercise in combating musculoskeletal frailty in old age, is the case of master athletes. These athletes, normally ranging from the age of 40 to 100+ years, not only achieve remarkable sporting records for their age but also display a smaller reduction in many physiological parameters linked to performance than their sedentary age-peers. In terms of musculoskeletal characteristics, from 20 to 55 years of age, muscle volume of master sprinters (MS) is greater than those of master endurance (ME) runners and of untrained controls (UC) but beyond 55 years of age the difference tapers off progressively, becoming non significant at the age of 75 years (Grassi et al. 1999). In line with these observations, Type I and II fibre cross-sectional area (CSA) of ME runners is not different from that of UC, whereas type II fibre CSA of MS is consistently larger than that of ME and, particularly for the Type IIx fibres, larger than of UC (Aagaard et al. 2007). Fibre type proportion, shows a prevalence if type I fibres in the ME runners and a lower proportion of type IIX fibres in ME than in MS, while UC show the highest proportion of the fastest fibres. This high proportion of type IIX fibres in UC is consistent with the suggestion that physical activity level modulates myosin heavy chain composition in old age (D’Antona et al. 2003). Instead, type IIA fibre proportion is similar in all groups. Single fibre contractile properties of master runners are also different from those of controls. Widrick et al. (1996) found that gastrocnemius muscle type I and IIa fibres of the runners produced 15% and 22% less force than of controls while maximal shortening velocity (Vmax) was not different between the two groups. Muscle power of type I and type IIa fibres was 13% and 27% lower than in the master runnners than in the sedentary controls. Comparing single fibres of young and old sprint runners, Korhonen et al. (2006) reported no difference in specific tension between the two age groups. However, maximum unloaded shortening velocity (Vo) of fibres expressing type I MHC was lower in the older runners while no difference in Vo of type IIa MHC fibres was found. Hence these data suggest that the decrease in Vo of slow fibres with old age is not due to a reduction in physical activity, as master athletes are highly active, but are mostly the result of ageing per se. Whole muscle strength and power of power-trained athletes has also been found to be higher than those of endurance athletes and of untrained controls, with some studies reporting greater values also for endurance athletes. Also, the rate of force development of MS and ME is faster than that of UC. This preservation of muscle strength and power in master athletes seems also related to a protection from the age-related loss of motor units, probably due to a decrease in oxidative stress afforded by regular physical activity. Scanty data exist on tendon mechanical properties of master athletes but it has been shown that resistive training in older men reverses the age-related decline in tendon stiffness. Reeves et al (2003) have indeed shown a 73% increase in tendon stiffness after 14 week resistive training in septuagenarian men. While no data exists on tendon stiffness in master athletes, recent measurements performed by our group show tendon strain values of master runners similar to those of young untrained controls; these seem due to a greater tendon CSA in the master runners. However, tendon hypertrophy in master runners seems a pathophysiological compensation to tendon injury and is correlated to the hours of training.