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The effects of training, immobilization and remobilization on musculoskeletal tissue

1992; Wiley; Volume: 2; Issue: 3 Linguagem: Inglês

10.1111/j.1600-0838.1992.tb00330.x

1600-0838

R. Kannus, L Józsa, R. Renström, M. Järvtoen, Martti Kvist, Mzukisi Lento, P. Oja, I. Vuorl,

Exercise and Physiological Responses

The effects of different types of training and immobilization on muscle tissue have been studied intensively and have been well established. At the beginning of strength or power training, the increase in muscular performance can be explained by neural and psychological adaptation; that is, recruitment of more motor units per time unit, learning of more effective and economical usage of the active motor units and reduction of the inhibitory inputs to the active alpha motor neurons. After 6 to 8 weeks, further progress is due to gradual muscular hypertrophy, that is, a true increase in size of pre‐existing fibres. Today, the theory of muscular hyperplasia (new fibre formation by a splitting of existing fibres) is not supported in critical reviews. With endurance training, there is an increased concentration and volume density of muscle mitochondria with corresponding biochemical adaptation, allowing the muscle to produce more mechanical power output aero‐bicalry and to be activated for longer periods of time without being fatigued. Immobilization, in turn, atrophies the muscle very quickly, significantly already after one week. The most striking morphological findings are reduction in fibre size and diameter, reduction in the capillary density and a simultaneous increase in intramuscular connective tissue. At the same time, many harmful functional and biochemical effects also occur. Compared with muscle tissue, the knowledge of the effects of training and immobilization on tendon or ligament tissue is scarce and research has not been systematic. In animal experiments the tensile strength, elastic stiffness and total weight of a tendon or ligament have increased due to training (collagen fibre thickening) and decreased due to immobilization (fibre splitting and disorientation). These changes can be explained by an exercise (immobilization‐induced increase (decrease) in synthesis of collagen and proteogrycan‐water matrix due to increased (decreased) fibroblast activity. The effects of training on the myotendinous junction or proprioceptors (muscle spindles and Golgj tendon organs) are largely unknown. Our recent studies showed that immobilization is very detrimental to these organs morphologically as well as biochemically. Slowly progressing physical exercise causes meaningful adaptive changes in the articular cartilage: the cells and nuclei of chondrocytes enlarge and the proteoglycan content and cartilage thickness increase. However, if training is too strenuous or biomechanically misloading, a degeneration process of the cartilage may begin, which is also the case in an immobilized joint Bone tissue adapts to weight‐bearing and muscular work well by increasing bone mass and density, most probably through osteoblast stimulation. The remodelling cycle of bone tissue is, however, a slow process, taking at least several months to occur. The achieved bone mass is also dependent on genetic, nutritional and hormonal factors. Immobilization, on the other hand, causes exactly the reverse effects on bone tissue and may finally (that is, after 5 to 6 months) lead to irreversible osteoporosis.