Stressed pathophysiological conditions, for example, burn, result in a hypermetabolic and catabolic state leading to muscle wasting. In burns, the most common determinants for muscle catabolism are subject weight, burn size, time from injury to surgical treatment, resting energy expenditure, and sepsis.1 However, long lasting hospitalization with prolonged bed rest and major surgeries are contributors to loss of lean body mass. Furthermore, muscle catabolism is correlated with morbidity during acute burn treatment.2–4 It is well-established that pediatric burn patients are hypermetabolic and catabolic for more than 12 months postinjury.5 They also demonstrate delayed linear growth up to 2 years postinjury.6 Recent studies have shown that in a pediatric burn patient population, muscle catabolism persists up to 9 months beyond the injury.5 In this patient population, persistent muscle catabolism has multiple negative effects. First, children are in the physiological process of growing and for normal growth to occur, the catabolic condition must be reversed, that is, the rates of protein synthesis are greater than the rates of proteolysis leading to a higher net protein deposition. Second, burn victims spend days and/or months in intensive care unit during the acute phase after injury. This results in loss of mobility, loss of lean body mass, and delayed start of rehabilitation. Third, burn patients undergo numerous reconstructive surgeries in years after wound healing has occurred. Major surgeries are known stressors for the catabolic state. The combination of the acute burn injury, prolonged intensive care unit stays, and years of reconstruction surgery render the skeletal muscle persistently catabolic, making amelioration of muscle wasting an important consideration during the treatment of pediatric burn patients. Studies have shown that the tissue response to nutritional signaling (eg, amino acids) plays a critical role in protein net deposition via coordination of protein synthesis and breakdown mechanisms. In normal conditions, amino acid abundance increases muscle protein synthesis with no change or decrease in the breakdown rate, resulting in an increased net protein deposition.7–10 In critical or catabolic conditions, this depends on the severity of the condition. In less severe critical illness, there are milder changes in both protein synthesis and breakdown rates.11–13 Whereas in severe cases, namely acute phase after burn injury, amino acid availability increases protein synthesis but this increase is not sufficient to match the increase in breakdown and prevent the protein loss.14 It is not known, however, how the skeletal muscle of pediatric burn patients responds to amino acid supplementation at later periods after burn injury, for example, 6 month postinjury. Therefore, in this study we examined the effect of a steady state amino acid (AA) infusion (Travasol) on leg muscle protein turnover in pediatric burn patients at 6 month postinjury compared with that of healthy subjects. We also examined whole-body and whole-body nonmuscle basal and AA affected protein breakdown rates. Nonmuscle protein turnover represents protein turnover from tissues other than muscle, such as liver. We hypothesize that in burn victims, protein turnover is unresponsive to the anabolic signaling of AAs.