Skeletal muscle represents the major repository of body protein. In addition to its functional role, skeletal muscle provides amino acids for processing by visceral organs during times of stress and nutrient deprivation. Caloric or protein deficiency may result in less than optimal skeletal muscle energy metabolism thereby affecting muscle function before changes in structure or composition can be detected. We hypothesize that variation in muscle high energy metabolism at rest, during mild to moderate exercise and during recovery from exercise may be used to characterize the various nutritional and metabolic states associated with nutritional depletion and injury. These changes may be used to understand the effects of nutritional support in surgical patients and to determine the optimal nutrient requirements for skeletal muscle. Phosphorus nuclear magnetic resonance spectroscopy (31P NMR) will be used to study the effects of malnutrition on high energy phosphate metabolism in skeletal muscle. The relative quantities of ATP, phosphocreatine, and inorganic phosphate will be measured and the rate of reconstitution of the high energy pool will be monitored before, during and after standard work loads. NMR techniques will also be used to measure creatine kinase activity in vivo, pH changes, free ADP concentrations, and the phosphorylation potential. The effects of caloric protein deprivation, refeeding, operative stress and an anabolic hormone will be studied.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
First Independent Research Support & Transition (FIRST) Awards (R29)
Project #
5R29GM042224-04
Application #
3467659
Study Section
Surgery, Anesthesiology and Trauma Study Section (SAT)
Project Start
1989-04-01
Project End
1994-03-31
Budget Start
1992-04-01
Budget End
1993-03-31
Support Year
4
Fiscal Year
1992
Total Cost
Indirect Cost
Name
Brigham and Women's Hospital
Department
Type
DUNS #
071723621
City
Boston
State
MA
Country
United States
Zip Code
02115
Santos, A A; Rodrick, M L; Jacobs, D O et al. (1994) Does the route of feeding modify the inflammatory response? Ann Surg 220:155-63
Santos, A A; Browning, J L; Scheltinga, M R et al. (1994) Are events after endotoxemia related to circulating phospholipase A2? Ann Surg 219:183-92
Kobayashi, T; Robinson, M K; Robinson, V et al. (1993) Glutathione depletion alters hepatocellular high-energy phosphate metabolism. J Surg Res 54:189-95
Robinson, M K; Rodrick, M L; Jacobs, D O et al. (1993) Glutathione depletion in rats impairs T-cell and macrophage immune function. Arch Surg 128:29-34;discussion 34-5
Holtzman, D; Offutt, M; Tsuji, M et al. (1993) Creatine kinase-catalyzed reaction rate in the cyanide-poisoned mouse brain. J Cereb Blood Flow Metab 13:153-61
Robinson, M K; Ahn, M S; Rounds, J D et al. (1992) Parenteral glutathione monoester enhances tissue antioxidant stores. JPEN J Parenter Enteral Nutr 16:413-8
Robinson, M K; Rounds, J D; Hong, R W et al. (1992) Glutathione deficiency increases organ dysfunction after hemorrhagic shock. Surgery 112:140-7;discussion 148-9
Gatzen, C; Scheltinga, M R; Kimbrough, T D et al. (1992) Growth hormone attenuates the abnormal distribution of body water in critically ill surgical patients. Surgery 112:181-7
Scheltinga, M R; Jacobs, D O; Kimbrough, T D et al. (1992) Identifying body fluid distribution by measuring electrical impedance. J Trauma 33:665-70
Scheltinga, M R; Helton, W S; Rounds, J et al. (1991) Impedance electrodes positioned on proximal portions of limbs quantify fluid compartments in dogs. J Appl Physiol 70:2039-44

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