Hormonal and Growth Factor‐Related Mechanisms Involved in the Adaptation of Skeletal Muscle to Exercise

Kadi, Fawzi

doi:10.1002/9780470757826.ch22

Cited by 1 publication

(1 citation statement)

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“…Existing myonuclei in adult muscle fibres are post mitotic, and muscle satellite cells are the major source for the addition of new myonuclei into the hypertrophying muscle fibre ( Moss and Leblond, 1971 ). A variety of alterations in the surrounding environment of the satellite cell, including mechanical and growth factors and also hormonal signalling might regulate the activation and proliferation of satellite cells ( Kadi, 2005 ; Kadi et al ., 2005 ; Mackey et al ., 2007 ). Satellite cells can proliferate and withdraw from differentiation to return to quiescence to replenish satellite cell pool, or to enter differentiation to provide new myonuclei or to generate new muscle fibres (Figure 1) ( Kadi, 2000 ; Kadi et al ., 2005 ).…”

Section: Testosterone and Satellite Cellsmentioning

confidence: 99%

Cellular and molecular mechanisms responsible for the action of testosterone on human skeletal muscle. A basis for illegal performance enhancement

Kadi

2008

British J Pharmacology

155

125

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The popularity of testosterone among drug users is due to its powerful effects on muscle strength and mass. Important mechanisms behind the myotrophic effects of testosterone were uncovered both in athletes using steroids for several years and in short-term controlled studies. Both long-term and short-term steroid usage accentuates the degree of fibre hypertrophy in human skeletal muscle by enhancing protein synthesis. A mechanism by which testosterone facilitates the hypertrophy of muscle fibres is the activation of satellite cells and the promotion of myonuclear accretion when existing myonuclei become unable to sustain further enhancement of protein synthesis. Interestingly, long-term steroid usage also enhances the frequency of fibres with centrally located myonuclei, which implies the occurrence of a high regenerative activity. Under the action of testosterone, some daughter cells generated by satellite cell proliferation may escape differentiation and return to quiescence, which help to replenish the satellite cell reserve pool. However, whether long-term steroid usage induces adverse effects of satellite cells remains unknown. Testosterone might also favour the commitment of pluripotent precursor cells into myotubes and inhibit adipogenic differentiation. The effects of testosterone on skeletal muscle are thought to be mediated via androgen receptors expressed in myonuclei and satellite cells. Some evidence also suggests the existence of an androgen-receptorindependent pathway. Clearly, testosterone abuse is associated with an intense recruitment of multiple myogenic pathways. This provides an unfair advantage over non-drug users. The long-term consequences on the regenerative capacity of skeletal muscle are unknown.

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