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Effect of adrenaline on glucose kinetics during exercise in adrenalectomised humans

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posted on 1999-09-01, 00:00 authored by Kirsten HowlettKirsten Howlett, H Galbo, J Lorentsen, R Bergeron, T Zimmerman-Belsing, J Bulow, U Feldt-Rasmussen, M Kjaer
1. The role of adrenaline in regulating hepatic glucose production and muscle glucose uptake during exercise was examined in six adrenaline deficient, bilaterally adrenalectomised humans. Six sex and age matched healthy individuals served as controls (CON).

2. Adrenalectomised subjects cycled for 45 min at 68 ± 1% maximum pulmonary Oμ uptake (VOμ,max), followed by 15 min at 84 ± 2% VOμ,max without (−ADR) or with (+ADR) adrenaline infusion, which elevated plasma adrenaline levels (45 min, 4·49 ± 0·69 nmol l¢; 60 min, 12·41 ± 1·80 nmol l¢; means ± s.e.m.). Glucose kinetics were measured using [3_ÅH]glucose.

3. Euglycaemia was maintained during exercise in CON and −ADR, whilst in +ADR plasma glucose was elevated. The exercise induced increase in hepatic glucose production was similar in +ADR and −ADR; however, adrenaline infusion augmented the rise in hepatic glucose production early in exercise. Glucose uptake increased during exercise in +ADR and −ADR, but was lower and metabolic clearance rate was reduced in +ADR.

4. During exercise noradrenaline and glucagon concentrations increased, and insulin and cortisol concentrations decreased, but plasma levels were similar between trials. Adrenaline infusion suppressed growth hormone and elevated plasma free fatty acids, glycerol and lactate. Alanine and â_hydroxybutyrate levels were similar between trials.

5. The results demonstrate that glucose homeostasis was maintained during exercise in adrenalectomised subjects. Adrenaline does not appear to play a major role in matching hepatic glucose production to the increase in glucose clearance. In contrast, adrenaline infusion results in a mismatch by simultaneously enhancing hepatic glucose production and inhibiting glucose clearance.

History

Journal

Journal of physiology

Volume

519

Issue

3

Pagination

911 - 921

Publisher

Wiley-Blackwell Publishing

Location

Oxford, England

ISSN

0022-3751

eISSN

1469-7793

Language

eng

Publication classification

C1.1 Refereed article in a scholarly journal