Prevention of Overt Hypoglycemia During Exercise
Stimulation of Endogenous Glucose Production Independent of Hepatic Catecholamine Action and Changes in Pancreatic Hormone Concentration
- Robert H. Coker1,
- Yoshiharu Koyama1,
- Joshua C. Denny1,
- Raul C. Camacho1,
- D. Brooks Lacy2 and
- David H. Wasserman1
- 1Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee
- 2Diabetes Research and Training Center, Vanderbilt University School of Medicine, Nashville, Tennessee
Abstract
These studies were conducted to determine the magnitude and mechanism of compensation for impaired glucagon and insulin responses to exercise. For this purpose, dogs underwent surgery >16 days before experiments, at which time flow probes were implanted and silastic catheters were inserted. During experiments, glucagon and insulin were fixed at basal levels during rest and exercise using a pancreatic clamp with glucose clamped (PC/GC; n = 5), a pancreatic clamp with glucose unclamped (PC; n = 7), or a pancreatic clamp with glucose unclamped + intraportal propranolol and phentolamine hepatic α- and β-adrenergic receptor blockade (PC/HAB; n = 6). Glucose production (Ra) was measured isotopically. Plasma glucose was constant in PC/GC, but fell from basal to exercise in PC and PC/HAB. Ra was unchanged with exercise in PC/GC, but was slightly increased during exercise in PC and PC/HAB. Despite minimal increases in epinephrine in PC/GC, epinephrine increased approximately sixfold in PC and PC/HAB during exercise. In summary, during moderate exercise, 1) the increase in Ra is absent in PC/GC; 2) only a moderate fall in arterial glucose occurs in PC, due to a compensatory increase in Ra; and 3) the increase in Ra is preserved in PC/HAB. In conclusion, stimulation of Ra by a mechanism independent of pancreatic hormones and hepatic adrenergic stimulation is a primary defense against overt hypoglycemia.
Footnotes
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R.H.C. is currently affiliated with the Nutrition, Metabolism, and Exercise Laboratory, Donald W. Reynolds Center on Aging, University of Arkansas for Medical Sciences, Little Rock, Arkansas.
Address correspondence and reprint requests to Robert H. Coker, Nutrition, Metabolism, and Exercise Laboratory, Donald W. Reynolds Center on Aging, University of Arkansas for Medical Sciences, 4301 W. Markham, Slot 806, Little Rock, AR 72205. E-mail: cokerrobert{at}uams.edu.
Received for publication 2 July 2001 and accepted in revised form 24 January 2002.
CV, coefficient of variation; FFA, free fatty acids; NHAU, net hepatic alanine uptake; NHGlyU, net hepatic glycerol uptake; NHGO, net hepatic glucose output; NHLU, net hepatic lactate uptake; PC, pancreatic clamp with glucose unclamped; PC/GC, pancreatic clamp with glucose clamped; PC/HAB, pancreatic clamp with hepatic α- and β-adrenergic receptor blockade.
- DIABETES
