Insulin secretion and glucose kinetics during exercise with and without pharmacological alpha(1)- and alpha(2)-receptor blockade.
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-(3)H]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.
Aarnio
P
P
Department of Medical Physiology, the Panum Institute, University of Copenhagen, Denmark.
Lauritsen
T
T
Dela
F
F
D058668:Adrenergic alpha-1 Receptor Antagonists; D058669:Adrenergic alpha-2 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology*; D000328:Adult; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism*; D001794:Blood Pressure; D002096:C-Peptide / Q000097:blood / Q000378:metabolism; D018592:Cross-Over Studies; D004837:Epinephrine / Q000097:blood; D015444:Exercise / Q000502:physiology*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005934:Glucagon / Q000097:blood; D005990:Glycerol / Q000097:blood; D006339:Heart Rate; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D007328:Insulin / Q000097:blood / Q000378:metabolism*; D000078790:Insulin Secretion; D007700:Kinetics; D007773:Lactates / Q000097:blood; D008297:Male; D005082:Physical Exertion / Q000502:physiology*; D011224:Prazosin / Q000494:pharmacology*; D018340:Receptors, Adrenergic, alpha-1 / Q000502:physiology; D018341:Receptors, Adrenergic, alpha-2 / Q000502:physiology; D013997:Time Factors; D014316:Tritium; D015016:Yohimbine / Q000494:pharmacology*
D058668:Adrenergic alpha-1 Receptor Antagonists; D058669:Adrenergic alpha-2 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists; D001786:Blood Glucose; D002096:C-Peptide; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D007773:Lactates; D018340:Receptors, Adrenergic, alpha-1; D018341:Receptors, Adrenergic, alpha-2; D014316:Tritium; D015016:Yohimbine; D005934:Glucagon; D005990:Glycerol; D011224:Prazosin; D004837:Epinephrine