Abstract
In intense exercise (>80% maximal oxygen consumption [V̇O2 max]), the 7- to 8-fold increase in glucose production (Ra) is tightly correlated with the greater than 14-fold increase in plasma norepinephrine (NE) and epinephrine (EPI). To distinguish the relative roles of α- and β-adrenergic receptors, the responses of 12 control (C) lean, healthy, fit young male subjects to 87% V̇O2 max cycle ergometer exercise were compared with those of 7 subjects (at 83% V̇O2max) receiving intravenous phentolamine (Ph). The Ph group received a 70-μg/kg bolus and then 7 μg/kg/min from -30 minutes, during exercise and for 60 minutes of recovery. The data were analyzed by comparing exercise responses to exhaustion in Ph subjects (11.4 ± 0.6 min) with those at both 12 minutes and at exhaustion in C subjects (14.6 ± 0.3 min) and during recovery. There were no significant differences between groups in the plasma glucose response during exercise, but values were higher in C versus Ph subjects during the first 40 minutes of postexercise 'recovery.' The Ra response during the first 12 minutes of exercise was not different by repeated-measures ANOVA, reaching 10.6 ± 1.3 mg/kg/min in C and 9.6 ± 1.5 in Ph subjects at 12 minutes. However, in C subjects, Ra increased significantly to 14.1 ± 1.2 mg/kg/min by exhaustion, and remained higher versus Ph subjects until 15 minutes of recovery. The Rd during recovery was not different between groups; thus, the higher Ra in C subjects in early recovery was responsible for the greater hyperglycemia observed in C subjects. Ph subjects showed a more rapid, marked increment (P = .002) in both plasma NE (to 64 v 38 nmol/L) and EPI at exhaustion, and catecholamine concentrations remained higher in Ph versus C subjects during recovery. Whereas plasma insulin (IRI) declined in the C group, it increased 3-fold (P = .001) in the Ph group during exercise and until 15 minutes of recovery, Ph had no effect on glucagon (IRG). Thus, the glucagon to insulin ratio decreased in Ph subjects from baseline levels during exercise and early recovery, but increased in C subjects. The increase in Ra among Ph subjects despite the decrease in the glucagon to insulin ratio supports our earlier evidence that these hormones are not principal regulators of the Ra in intense exercise. The shorter time to exhaustion and markedly higher catecholamine levels in Ph subjects limited our ability to isolate the effects of α-adrenergic receptors on the Ra. α-Adrenergic receptors appear to have little influence on the Rd. (C) 2000 by W.B. Saunders Company.
Original language | English |
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Pages (from-to) | 386-394 |
Number of pages | 9 |
Journal | Metabolism: Clinical and Experimental |
Volume | 49 |
Issue number | 3 |
DOIs | |
State | Published - 2000 |
Bibliographical note
Funding Information:From the McGill Nutrition and Food Science Centre, Royal Wctoria Hospital. Montreal, Quebec; Departments of Physiology and Medicine, University of Toronto, Toronto, Ontario; Department of Medicine, University of Ottawa, Ottawa, Ontario, Canada; and Department Internal Medicine and Institute of Gerontology, University of Michigan and Veterans Affairs Medical Centec Ann Arbol; MI. Submitted May 26,1999; accepted August 13,1999. Supported by Grants No. MT9581 (E.B.M.) and MT2197 (M.V) from the Medical Research Council of Canada, the Medical Reseach Service of the US Department of Veterans Affairs (J.B.H.), and in part by postdoctoral fellowships ftvm the Canadian Diabetes Association and the Juvenile Diabetes Foundation International (R.J.S.). Present address: A.M., Berkshire Medical Centec 725 North St, Pittsjeld MA 01201. Address reprint requests to Errol B. Marliss, MD, McGill Nutrition and Food Science Centre, Royal Victoria Hospital, 687 Pine Ave U! Montreal, Quebec, Canada H3A IAl. Copyright 0 2000 by U!B. Saunders 0026~0495/00/4903-0019$10.00/0
Funding
From the McGill Nutrition and Food Science Centre, Royal Wctoria Hospital. Montreal, Quebec; Departments of Physiology and Medicine, University of Toronto, Toronto, Ontario; Department of Medicine, University of Ottawa, Ottawa, Ontario, Canada; and Department Internal Medicine and Institute of Gerontology, University of Michigan and Veterans Affairs Medical Centec Ann Arbol; MI. Submitted May 26,1999; accepted August 13,1999. Supported by Grants No. MT9581 (E.B.M.) and MT2197 (M.V) from the Medical Research Council of Canada, the Medical Reseach Service of the US Department of Veterans Affairs (J.B.H.), and in part by postdoctoral fellowships ftvm the Canadian Diabetes Association and the Juvenile Diabetes Foundation International (R.J.S.). Present address: A.M., Berkshire Medical Centec 725 North St, Pittsjeld MA 01201. Address reprint requests to Errol B. Marliss, MD, McGill Nutrition and Food Science Centre, Royal Victoria Hospital, 687 Pine Ave U! Montreal, Quebec, Canada H3A IAl. Copyright 0 2000 by U!B. Saunders 0026~0495/00/4903-0019$10.00/0
Funders | Funder number |
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Medical Reseach Service | |
U.S. Department of Veterans Affairs | |
Juvenile Diabetes Research Foundation International | |
Canadian Diabetes Association | |
Medical Research Council Canada |
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Endocrinology