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1 Department of Surgery, The University of Texas Medical Branch and Metabolism Unit, Shriners Burns Hospital, Galveston, Texas, USA
* To whom correspondence should be addressed. E-mail: djpaddon{at}utmb.edu.
Debilitating injury is accompanied by hypercortisolemia, muscle wasting and disruption of the normal anabolic response to food. We sought to determine if acute hypercortisolemia alters muscle protein metabolism following ingestion of a potent anabolic stimulus: essential amino acids (EAA). A 27hr infusion (80µg.kg-1.hr-1) of hydrocortisone sodium succinate mimicked cortisol levels accompanying severe injury (>30 µg.dl-1), (C+AA; n=6). The control group received IV saline (AA; n=6). Femoral arterio-venous blood samples and muscle biopsies were obtained during a primed (2.0µmol.kg-1) constant infusion (0.05µmol.kg-1.min-1) of L-[ring-2H5] phenylalanine, before and after ingestion of 15g EAA. Hypercortisolemia (36.5±2.1 (C+AA) vs. 9.0±1.0µg.dl-1 (AA)) increased post-absorptive arterial, venous and muscle intracellular phenylalanine concentrations. Hypercortisolemia also increased post-absorptive and post EAA insulin concentrations. Net protein balance was blunted (40% lower) following EAA ingestion, but remained positive for a greater period of time (60 vs. 180 min) in the C+AA group. Thus, while differences in protein metabolism were evident, EAA ingestion improved muscle protein anabolism during acute hypercortisolemia and may help minimize muscle loss following debilitating injury.
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