Acute effects of caffeine ingestion at rest in humans with impaired epinephrine responses. Soeren, M. Van, T. Mohr, M. Kjaer, and T. E. Graham. Faculty of Nursing, Health Sciences Centre, University of Western Ontario, London, ONTARIO, Canada, N6A 5C1, Department of Medical Physiology, Panum Institute, Copenhagen Muscle Research Centre and Department H Bispedjerg Hospital, University of Copenhagen, Copenhagen, DENMARK, Human Biology, University of Guelph, Guelph, ONTARIO, Canada, N2G 2W1
APStracts 2:0470A, 1995.
Caffeine ingestion has been demonstrated to increase circulating epinephrine (E) and norepinephrine (NE), elevate free fatty acids (FFA) and alter heart rate, blood pressure (BP) and ventilation in humans. Whether these physiological responses are a result of caffeine acting through direct stimulation of specific tissues via adenosine receptors or secondary to E increases is not known. In the present experiment, six tetraplegics (level of spinal cord lesions C4 - C6) were tested at rest for 3 hours to investigate the effects of 6 mg/kg caffeine in capsule form on subjects with impaired epinephrine responses. Ventilatory, cardiovascular, metabolic and hormonal data were collected every 15 - 20 min following caffeine ingestion. There were no significant (p&GT0.05) increases in plasma E following caffeine ingestion (pre-ingestion, 0.19 +/- 0.04; 80 min post -ingestion, 0.20+/- 0.04 nM) (mean +/- SE) nor in plasma NE (pre -ingestion, 0.53+/- 0.16; 80 min post-ingestion, 0.49+/- 0.09 nM) (p&GT0.05). However, significant increases were found in serum FFA (pre-ingestion, 0.53 +/- 0.08; 40 min post-ingestion, 1.03 +/- 0.20 mM) (p&LT0.05) and in glycerol. These concentrations remained elevated throughout the experiment. BP increased in the first hour post-ingestion. These data demonstrate that caffeine in physiological doses directly stimulates specific tissues, i.e. adipose and peripheral vascular tissue, and these effects are not secondary to increases in E following caffeine ingestion.

Received 21 June 1995; accepted in final form 18 October 1995.
APS Manuscript Number A662-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95