Share this article on:

Carbohydrate availability affects ammonemia during exercise after β2-adrenergic blockade

MATTHYS, DIRK; DERAVE, WIM; CALDERS, PATRICK; PANNIER, JEAN-LOUIS

Medicine & Science in Sports & Exercise: May 2000 - Volume 32 - Issue 5 - p 940-945
Basic Sciences: Original Investigations

MATTHYS, D., W. DERAVE, P. CALDERS, and J.-L. PANNIER. Carbohydrate availability affects ammonemia during exercise after β2-adrenergic blockade. Med. Sci. Sports Exerc., Vol. 32, No. 5, pp. 940–945, 2000.

Purpose β-Adrenergic blockade increases blood ammonia concentration during exercise. The purpose of this study was to assess the role of decreased carbohydrate availability in this process.

Methods Wistar rats (N = 47) were injected intravenously with a selective β2-adrenoceptor blocker (ICI 118,551), placebo, or β2-blocker + glucose 1 h before a treadmill exercise test. Blood samples were taken to measure the concentration of ammonia, glucose, lactic acid, free fatty acids (FFA), glycerol, branched-chain amino acids (BCAA), and muscle samples for determination of glycogen content.

Results β2-adrenergic blockade shortened running time to exhaustion (23 ± 4.3 min compared to 44 ± 5.2 min with placebo), increased blood ammonia levels (146.7 ± 16.21 μmol·L−1 compared to 47.5 ± 0.92 μmol·L−1 with placebo) and prevented exercise-induced glycogen breakdown in soleus and gastrocnemius muscles. Pre-exercise supplementation of glucose during β2-blockade restored exercise-induced glycogen breakdown and reduced blood ammonia concentration during exercise (66.5 ± 5.65 mmol·L−1) but did not improve exercise capacity (26 ± 3.2 min) when compared with β2-blockade alone.

Conclusion The results suggest that the enhanced rise in blood ammonia concentration during exercise after β-blockade is caused by impaired carbohydrate availability.

Department of Pediatric Cardiology, Institute of Kinesiology and Sport Sciences, and Laboratory of Normal and Pathological Physiology, University of Ghent, B-9000 Ghent, BELGIUM

Submitted for publication October 1998.

Accepted for publication June 1999.

Address for correspondence: D. Matthys, M.D., Department of Pediatric Cardiology, University Hospital, De Pintelaan 186, B-9000 Ghent, Belgium. E-mail: dirk.matthys@rug.ac.be.

© 2000 Lippincott Williams & Wilkins, Inc.