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discharged from an intensive care unit return to normal function, including work, within 2 years (Bams and Miranda, 1985). The persistent disability following severe burn injury is also well documented (Chang and Herzog, 1976). Although many factors may contribute to these statistics, loss of muscle strength and function is central to the problem of rehabilitation. This chapter interprets the goal of nutritional and metabolic support during acute hospitalization following severe injury and the period immediately following discharge to be a rapid return to normal physiological function. Therefore, the focus here will be on the response of muscle.

The net synthesis or catabolism of muscle protein depends on the balance between the rate of protein synthesis and breakdown. The precursors for protein synthesis are derived from either protein breakdown or from transmembrane transport from the plasma. The amine acids resulting from protein breakdown can either be re-incorporated into protein or released into plasma. Exogenous amine acids given in nutrition can only be incorporated into protein after being transported into the muscle cells from the blood. Thus, the processes of protein synthesis, breakdown, and transmembrane amine acid transport are linked, and it is necessary to evaluate the response to stress by quantifying these three related processes. Consequently, results will be presented from a technique involving the infusion of tracer amounts of amine acids labeled with heavy stable isotopes of carbon (13C) or hydrogen (2H) and sampling from the femoral artery and vein and from the intramuscular pool of the vastus lateralis (obtained by biopsy) (Biolo et al., 1995a). This approach allows quantification of transmembrane transport rate of various amine acids, as well as the rates of muscle protein synthesis and breakdown.

The negative protein balance caused by severe injury results from a large increase in the rate of protein breakdown. Although synthesis is also increased, the increase is insufficient to offset the increased rate of breakdown. The increase in muscle protein breakdown is coupled with an increase in the outward transport of amine acids, which is consistent with the role of the muscle to provide amine acid precursors for synthesis elsewhere in the body. The negative amine acid balance persists across the muscle even for a person in the fed state. Furthermore, increasing the amount of protein intake has no effect on the rate of muscle protein synthesis.

The alteration in transport kinetics across the muscle cell membrane may be central in the altered muscle protein kinetics. The inward transport of phenylalanine and leucine in severely burned patients is less than half the normal rate. This explains the inefficiency of amine acid or protein intake in stimulating synthesis, because the exogenous amine acids must enter the cells before they can be incorporated into protein. This point can be seen clearly in the case of glutamine. The intramuscular glutamine concentration is decreased in severely burned patients to about one-third its normal value. This is in large part due to an accelerated rate of outward transport, as the intracellular appearance from protein breakdown is double the normal rate and de novo

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