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Diabetes 50:1834-1843, 2001
© 2001 by the American Diabetes Association, Inc.

Insulin Secretion and Glucose Kinetics During Exercise With and Without Pharmacological {alpha}1- and {alpha}2-Receptor Blockade

Pauliina Aarnio1,2, Torsten Lauritsen3, and Flemming Dela1,2,4

1 Department of Medical Physiology, the Panum Institute, University of Copenhagen, Copenhagen
2 Copenhagen Muscle Research Centre, Rigshospitalet, Copenhagen
3 Department of Anesthesia, Rigshospitalet, Copenhagen
4 Department of Clinical Physiology and Nuclear Medicine, Herlev Hospital, Herlev, Denmark

The mechanism behind exercise-induced decreases in plasma insulin concentrations was examined in eight healthy young men. In addition, the influence of specific {alpha}1- and {alpha}2-adrenoceptor blockade on glucose kinetics during exercise was studied. To test the hypothesis that exercise-induced decreases in insulin secretion are mediated via {alpha}2-adrenoceptors, all subjects exercised for 60 min on separate occasions under four conditions: with and without {alpha}1-receptor blockade (1 mg prazosin) and with and without or {alpha}2-receptor blockade (15 mg yohimbine). Glucose kinetics were measured using [3-3H]glucose. During exercise with {alpha}2-receptor blockade, the insulin concentration initially increased (first 20 min) then decreased, whereas it continually decreased in the corresponding control experiment. The C-peptide concentration did not change during exercise with {alpha}2-receptor blockade but decreased in the control experiment. During exercise with {alpha}1-receptor blockade and corresponding control experiments, insulin and C-peptide levels always decreased. With {alpha}1-receptor blockade, the glucose concentration increased (first 30 min) and then decreased, whereas it slightly decreased in all other experiments. In addition, with {alpha}1-receptor blockade, the glucose rate of appearance (Ra) increased rapidly (because of higher catecholamine concentrations in {alpha}1-receptor blockade versus control) and the glucose rate of disappearance (Rd) was higher compared with control. During exercise with {alpha}2-receptor blockade, the Ra and Rd were always lower compared with control. Therefore, we conclude that exercise-induced decreases in insulin secretion are mediated via {alpha}2-adrenoceptors and that blockade of {alpha}1- and {alpha}2-adrenoceptors during exercise elicits opposite responses in glucose Ra and Rd.


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Copyright © 2001 by the American Diabetes Association.