Abstract

805 The purpose of this study was to test the hypothesis that the decrease in plasma insulin concentrations during exercise is mediated via α-2 receptors. In eight males (25 ± 1 yr., 73 ± 2 kg) we measured plasma insulin (INS) and glucose (GLU) concentrations before and during 60-min ergometer (60-70% VO2max) bicycle exercise. Subjects were studied with (α-1 (Prazosin 1mg) or α-2 (Yohimbine 15mg)) and without (control experiments (CO)) adrenergic blockade. During CO and α-1 blockade, INS always decreased (from 18 ± 1 and 21 ± 1 to 6 ± 1 and 9 ± 1 pM (at t = 60 min), CO and α-1, respectively). The decrease was similar in CO (−11 ± 1 pM) and α-1 (−12 ± pM) experiments (P>0.05). In contrast, during exercise with α-2 blockade, INS increased from 18 ± 1 to 25 ± 1 pM (P<0.05) in the first 20 min, after which INS decreased (to 13 ± 1 pM (at t = 60 min)). At the end of exercise, INS were higher (P<0.05) and the change from before exercise less (P<0.05) in experiments with α-2 blockade compared with CO and α-1 blockade. At the end of exercise GLU was decreased (P<0.05) during CO and α-2 blockade (−0.36 ± 0.04 mM (pooled data)). During α-1 blockade GLU increased (+0.79 ± 0.08 mM (P<0.05)) in the first 30 min but returned to pre-exercise concentrations at the end of exercise. These data suggest: 1) The exercise induced decrease in plasma insulin concentrations is mediated via α-2, but not α-1, receptors located on the pancreatic β-cells. 2) Plasma insulin concentrations during exercise are not influenced by the prevailing plasma glucose concentration.

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