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Journal of Applied Physiology, Vol 79, Issue 6 1977-1985, Copyright © 1995 by American Physiological Society
ARTICLES |
J. H. Engdahl, J. D. Veldhuis and P. A. Farrell
Department of Exercise and Sport Science, Pennsylvania State University, University Park 16802, USA.
Endurance exercise training reduces glucose-stimulated insulin secretion while elevating insulin action on target tissues. Under some conditions, hormone action is enhanced by pulsatile delivery to tissues. We tested the hypothesis that different insulin secretory pulse profiles would be observed in endurance-trained vs. sedentary men. Seven endurance-trained [T; maximal O2 consumption 62.5 +/- 4.3 (SD) ml.kg-1.min-1)] and seven untrained (UT; maximal O2 consumption 40.3 +/- 3.3 ml.kg-1.min-1) age- and weight-matched men were studied. All subjects had normal oral glucose-tolerance tests; however, the insulin responses for the T subjects were significantly lower than for the UT subjects (P < 0.05). After 2 days of no exercise and an overnight fast, arterialized venous blood was sampled at 1-min intervals for 120 min and assayed for insulin. Characteristics of the insulin pulse profile were quantified with deconvolution analysis. The mass of insulin secreted per burst was significantly lower for the T than for the UT subjects (50.1 +/- 14 vs. 107.4 +/- 35 pM; P < 0.05), as was the peak height per burst (14.3 +/- 5 vs. 37.5 +/- 3.2 pM), rate of insulin production (429.6 +/- 161 vs. 1,002.4 +/- 393 pmol/90 min), and mean plasma insulin concentration (32.2 +/- 17 vs. 53.7 +/- 35 pM). The interpulse interval between bursts and the half-duration of insulin secretory bursts were not significantly different between the groups. Nonpulsatile basal insulin secretion was similar for the T and UT subjects (3.58 +/- 1.6 vs. 5.55 +/- 2.3 pM/min). These data show that regular endurance exercise in young men is associated with an insulin pulse profile in the resting fasted state characterized by less insulin secreted per burst but a similar number of bursts over a 90-min period. As a working hypothesis, we suggest that training-induced elevations in target-tissue sensitivity to insulin reduce the requirement for pulsatile insulin secretion.
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