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AJP - Regulatory, Integrative and Comparative Physiology, Vol 265, Issue 6 1333-R1338, Copyright © 1993 by American Physiological Society
ARTICLES |
M. M. Wiersma, J. Vissing, A. B. Steffens and H. Galbo
Department of Medical Physiology, Panum Institute, University of Copenhagen, Hellerup, Denmark.
Blood-borne metabolic feedback vs. neural feedforward regulation of glucose homeostasis during exercise was investigated by infusion glucose and [3H]glucose for glucose appearance determination intravenously in rats running for 20 min at 28 m/min [approximately 85% of maximal O2 consumption (VO2max)]. Infused glucose corresponded to the exercise-induced increase in hepatic glucose production (HGP) found in saline-infused rats. Saline- and glucose-infused resting rats were also studied. Arterial blood was sampled for analyses of hormones and metabolites. Plasma epinephrine, norepinephrine, and insulin were always similar and HGP was initially similar in the two exercising groups, although glucose infusion resulted in higher plasma glucose compared with control (P < 0.05). Late during exercise, high plasma glucose (11.3 +/- 0.4 vs. 9.6 +/- 0.3 mM) and low glucagon (16 +/- 2 vs. 27 +/- 3 pM) in glucose- vs. saline-infused rats caused an inhibition of HGP in glucose-infused rats, although never below preexercise levels. In resting rats, glucose infusion resulted in elevated plasma glucose and insulin and, in turn, inhibition of HGP but had no effect on catecholamines, corticosterone, or glucagon. The findings indicate that during heavy exercise, glucose homeostasis is regulated primarily by neural feedforward mechanisms and that blood-borne metabolic feedback mechanisms play a regulatory role if metabolic error signals are pronounced.
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