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Muscle protein synthesis and degradation are dynamic processes, the balance of which has been recently termed proteostasis. At any one time muscle has to balance outputs in synthesis and degradation from “inputs” of both extra- and intramuscular derived signals including those of hormones, autocrine/paracrine factors, metabolites, mechanical loading and attachment to the extracellular matrix. If there is a disturbance in whole-body/muscle homeostasis (i.e. due to illness, altered mechanical activity), the concentration of these inputs is altered. The resultant integration of these signaling inputs stimulates reprogramming of proteostasis. If the balance is tipped toward net synthesis or degradation muscles undergo hypertrophy or atrophy, respectively. The first aim of this chapter is to discuss what is currently known about how input signals, largely in isolation, regulate muscle protein turnover and encapsulates evidence from both animal and human work and both in vivo and in vitro studies. The second aim is to describe what is understood about the regulation of muscle proteostasis by extracellular-intracellular signaling with specific attention paid to the key regulators of proteostasis in healthy humans (i.e. responses to feeding, ambulation). The third aim is to discuss the regulation of muscle atrophy under pathological conditions of trauma, illness, disuse and aging.

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