The role of metabolites of arachidonic acid in the physiology and pathophysiology of muscle protein metabolism.

In young mammals protein deposition in muscle may account for up to 60% of the daily deposition of protein. Merely by virtue of the fact that the skeletal musculature may account for 50% of total body protein, this tissue is likely to play a major role in the changes in the protein economy of the body that accompany trauma and infection. Protein synthesis in skeletal muscle is particularly sensitive to nutritional and hormonal changes. For example, a short (IOh) fast is sufficient to reduce muscle protein synthesis by 30% in young rats (Garlick et ul., 1983) and refeeding for as little as 1 h or the infusion of insulin for 40 min is sufficient to restore the rate of protein synthesis virtually to that characteristic of the fully fed animal (Garlick et al., 1983; Reeds e t al., 1985). Although similar evidence regarding protein degradation is lacking in vivo, in vitro this process can be altered as rapidly as protein synthesis (Palmer et a/., 1985). The fact that extrinsic factors, such as insulin (Garlick et al., 1983), the imposition of mechanical changes (Vandenburgh & Kaufman, 1979; Reeds e t al., 1980; Palmer et al., 1981~) and lymphokines (Baracos r t ul., 1983) are able to produce rapid changes in protein turnover suggests that there exists a system, probably related to components of the plasma membrane, that transduces changes in the external environment into changes in both ribosomal and proteolytic activity (Rodemann et al., 1982; Palmer et al., 1985).