ABSTRACT
Muscle loss contributes to the weight loss observed during illness. Therefore, it is important to consider factors that may contribute to changes in muscle accretion. Until recently, the numbers of bers within different muscle groups were thought to be xed prior to birth. Increases in muscle size, for example, arising due to resistance exercise, were ascribed to changes in cross-sectional area (CSA) for existing bers.1 According to this antiquated model, the formation of new bers cannot occur after birth and the postnatal growth of muscle is controlled by events taking place within existing bers. Unfortunately, the old model for muscle growth could not account for the enormous capacity for regeneration and adaptation to exercise observed in adult muscles. There are now alternative explanations for muscle growth that allow for the generation of new bers from stem cells.2,3
The major cellular and molecular processes that contribute to muscle loss and accretion are reviewed in this chapter. The contribution of muscle satellite stem cell (MSSC) to muscle size increase is described in Section 5.1. The negative regulation of muscle cell proliferation by myostatin is discussed in Section 5.2. The contribution of muscle cell death to wasting is considered in Section 5.3. The role of the ubiquitin proteasome (UPS) in the breakdown of muscle protein is considered in Section 5.4. Intracellular signaling pathways involved in the promotion of muscle loss or muscle size increase are discussed in Sections 5.5 and 5.6, respectively.
