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Skeletal muscle is an inherently plastic tissue. There is evidence to suggest that muscles are constantly adapting both in quantity and quality to the changing functional demands imposed by the types and amounts of physical activity routinely performed. To date, the evidence suggests that, in adults, activity induced adaptations of skeletal muscle are orchestrated by local—that is, tissue level as opposed to systemic—mechanosensitive mechanisms, which appear to include a number of growth factors and hormones. Of particular recent interest is the growth hormone (GH)/insulin-like growth factor-I (IGF-I) system. In the context of skeletal muscle homoeostasis, IGF-I is thought to mediate the majority of the growth promoting effects of circulating GH. In addition, it appears to function in a GH independent autocrine/paracrine mode in this tissue.1
As information on the mechanisms that modulate muscle adaptation has been elucidated in the scientific literature, it is tempting for athletes to apply this knowledge to enhance muscle mass and hence function by artificially manipulating these systems. In some cases, this has led to simplistic notions that exogenous anabolic agents can be used to safely and effectively stimulate or augment muscle. Unfortunately, many of these attempts have been unsuccessful, and, …
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