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The ageing process is associated with a number of physiological changes. One of the most marked of them is the loss of muscle mass or sarcopenia. Beginning in midlife, ageing is associated with a time-dependent loss of muscle mass. It is a major cause of disability, frailty, and loss of independence in the mainly due to the associated loss of muscle strength and to a lesser extent stamina. Decrease in muscle strength is associated with a decrease in the cross-sectional area of the muscle fibres and in capillary bed density as well as in a reduction in the number of muscle fibres. These morphological and metabolic modifications in the skeletal muscle can be explained in part by reduced physical activity, altered nutritional status, and disease factors, which accompany the ageing process. In addition, some recent results indicate that functional/structural properties of contractile proteins and in particular the slow MyHC isoform is altered upon ageing leading to a slowdown of the contractile speed. The reasons why muscle fibres are lost and fast-twitch fibres atrophy, and protein synthesis rate decreases in old age remain important questions in the aethiology of sarcopenia. At an anatomical level it seems the aged muscle comprises fewer muscle fibres. Electrophysiological evidence suggests that motor unitsare lost as a result of the ageing process and that those remaining motor units are larger having apparently reinnervated some of the abandoned or dying muscle fibres through on process of collateral sprouting. The aim of the present project is to investigate the mechanism of development of sarcopenia in dependence of age, skeletal muscle unloading and effect of different types of mechanical loading on sarcopenia. We hypothesised that in the mechanism of development of sarcopenia in dependence of age and skeletal muscle unloading there are similarities in the turnover rate of contractile proteins synthesis and degradation and in distribution of myosin heavy and light chain isoforms relative content and synthesis rate in different types of skeletal muscles. We also hypothesised that there are relations between changes in contractile proteins and extracellular matrix components during muscle unloading and mechanical loading which may help to explain the mechanism of sarcopenia. |