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Decreased protein catabolism after exercise in subjects with IDDM

Decreased protein catabolism after exercise in subjects with IDDM 125 37 37 4 4 Dr. J. T. Devlin A. Scrimgeour I. Brodsky S. Fuller Division of Endocrinology Maine Medical Center 22 Bramhall St. 04102 Portland ME USA Metabolic Unit University of Vermont College of Medicine Burlington Vermont USA Summary We examined whether the increased rates of protein catabolism (proteolysis and leucine oxidation) associated with moderate insulinopenia in subjects with IDDM would be accentuated by prior bicycle exercise (53% VO 2max for 82 min). Insulin infusions maintained plasma glucose concentrations on one study day in “tight” control (TC: 6 mmol/l) and on a separate day in “loose” control (LC: 12 mmol/l). Elevations in serum ketone body, plasma NEFA, and whole-blood branched-chain amino acid concentrations on the loose control day during the basal period persisted throughout the post-exercise recovery period. Amino acid kinetics were estimated during a primed, constant infusion of l -(1- 13 C)leucine from plasma dilution of α -(1- 13 C)KIC and expired air 13 CO 2 enrichments. Loose control was associated with increased rates of whole-body leucine oxidation (LC 25±7 vs TC 21±8 μmol · kg −1 · h −1 ) and protein degradation (LC 127±12 vs TC 118±18 μmol · kg −1 · h −1 ) (both p<0.05). During the 2-h post exercise recovery period, there were significant decreases in rates of leucine oxidation (LC 21±7, TC 16±7) and protein degradation (LC 112±13, TC 107±11), compared to the basal period (both p<0.05, basal vs recovery). Rates of wholebody protein synthesis were unchanged by prior exercise. In conclusion, moderate insulinopenia is associated with significantly higher rates of protein degradation and leucine oxidation in the basal state. Following exercise, net protein catabolism is diminished due to reduced rates of protein degradation in the presence of maintained rates of protein synthesis. The significantly increased concentrations of fat-derived substrates (ketone bodies, NEFA) may have prevented the predicted increases in protein catabolism which we anticipated would follow acute exercise during periods of relative insulin deficiency. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Diabetologia Springer Journals

Decreased protein catabolism after exercise in subjects with IDDM

Devlin, J.; Scrimgeour, A.; Brodsky, I.; Fuller, S.
Diabetologia , Volume 37 (4) – Apr 1, 1994
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References (35)

Publisher
Springer Journals
Copyright
Copyright © 1994 by Springer-Verlag
Subject
Medicine & Public Health; Human Physiology; Internal Medicine; Metabolic Diseases
ISSN
0012-186X
eISSN
1432-0428
DOI
10.1007/BF00408471
Publisher site
See Article on Publisher Site

Abstract

125 37 37 4 4 Dr. J. T. Devlin A. Scrimgeour I. Brodsky S. Fuller Division of Endocrinology Maine Medical Center 22 Bramhall St. 04102 Portland ME USA Metabolic Unit University of Vermont College of Medicine Burlington Vermont USA Summary We examined whether the increased rates of protein catabolism (proteolysis and leucine oxidation) associated with moderate insulinopenia in subjects with IDDM would be accentuated by prior bicycle exercise (53% VO 2max for 82 min). Insulin infusions maintained plasma glucose concentrations on one study day in “tight” control (TC: 6 mmol/l) and on a separate day in “loose” control (LC: 12 mmol/l). Elevations in serum ketone body, plasma NEFA, and whole-blood branched-chain amino acid concentrations on the loose control day during the basal period persisted throughout the post-exercise recovery period. Amino acid kinetics were estimated during a primed, constant infusion of l -(1- 13 C)leucine from plasma dilution of α -(1- 13 C)KIC and expired air 13 CO 2 enrichments. Loose control was associated with increased rates of whole-body leucine oxidation (LC 25±7 vs TC 21±8 μmol · kg −1 · h −1 ) and protein degradation (LC 127±12 vs TC 118±18 μmol · kg −1 · h −1 ) (both p<0.05). During the 2-h post exercise recovery period, there were significant decreases in rates of leucine oxidation (LC 21±7, TC 16±7) and protein degradation (LC 112±13, TC 107±11), compared to the basal period (both p<0.05, basal vs recovery). Rates of wholebody protein synthesis were unchanged by prior exercise. In conclusion, moderate insulinopenia is associated with significantly higher rates of protein degradation and leucine oxidation in the basal state. Following exercise, net protein catabolism is diminished due to reduced rates of protein degradation in the presence of maintained rates of protein synthesis. The significantly increased concentrations of fat-derived substrates (ketone bodies, NEFA) may have prevented the predicted increases in protein catabolism which we anticipated would follow acute exercise during periods of relative insulin deficiency.

Journal

Diabetologia – Springer Journals

Published: Apr 1, 1994

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