During ageing there is a gradual loss of muscle mass, and strength, known as sarcopenia which results in which leads to reduced functional capacity, an increased risk of developing chronic metabolic disease and morbidity. Several mechanisms have been proposed to underlay sarcopenia, including higher evels of oxidative stress, muscle fiber denervation and reduced regenerative potential. Skeletal muscle is composed of heterogeneous muscle fibers that differ in their physiological, biochemical and metabolic parameters. The slow-twitch myofibers express the type I myosin heavy chain isoform and exhibit oxidative metabolism, which support sustained aerobic activity and contraction endurance. The fast-twitch myofibers contain type II MHC isoforms, rely mostly on anaerobic glycolysis for energy production, and display considerable strength and contraction speed, but only for short bursts of activity. Fiber type distribution is determined during embryonal development, however changes in the fiber type profile take place during the early stages of postnatal development under hormonal and neural influence. In adult muscle, myofibers can switch their fiber type in response to environmental demands, a property that is defined muscle plasticity. Muscle wasting during ageing is mostly observed in smaller type II, fast type myofibers, whereas slow-twitch type I myofibers are more resistant to age-dependent muscle loss.