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 concentra tions was examined in eight healthy young men. In addition, the influence o f specific alpha (1)- and alpha (2)-adrenoceptor blockade on glucose kineti cs during exercise was studied. To test the hypothesis that exercise-induce d decreases in insulin secretion are mediated via alpha (2)-adrenoceptors, all subjects exercised for 60 min on separate occasions under four conditio ns: with and without alpha (1)-receptor blockade (1 mg prazosin) and with a nd without or alpha (2)-receptor blockade (15 mg yohimbine). Glucose kineti cs were measured using [3-H-3]glucose. During exercise with alpha (2)-recep tor blockade, the insulin concentration initially increased (first 20 min) then decreased, whereas it continually decreased in the corresponding contr ol experiment. The C-peptide concentration did not change during exercise w ith alpha (2)-receptor blockade but decreased in the control experiment. Du ring exercise with alpha (1)-receptor blockade and corresponding control ex periments, insulin and C-peptide levels always decreased. With alpha (1)-re ceptor blockade, the glucose concentration increased (first 30 min) and the n decreased, whereas it slightly decreased in all other experiments. In add ition, with alpha (2)-receptor blockade, the glucose rate of appearance (Ra ) increased rapidly (because of higher catecholamine concentrations in alph a (1)-receptor blockade versus control) and the glucose rate of disappearan ce (Rd) was higher compared with control. During exercise with alpha (2)-re ceptor blockade, the Ra and Rd were always lower compared with control. The refore, we conclude that exercise-induced decreases in insulin secretion ar e mediated via alpha (2)-adrenoceptors and that blockade of alpha (1)- and alpha (2)-adrenoceptors during exercise elicits opposite responses in gluco se Ra and Rd.