Affiliation:
1. McGill Nutrition and Food Science Centre, Royal Victoria Hospital, Montreal, Canada
2. Department of Internal Medicine and Institute of Gerontology, University of Michigan and Veterans Affairs Medical Centre, Ann Arbor, Michigan
3. Departments of Physiology and Medicine, University of Toronto, Toronto, Canada
Abstract
Intense exercise (IE) (>80% V̇o2max) causes a seven- to eightfold increase in glucose production (Ra) and a fourfold increase in glucose uptake (Rd), resulting in hyperglycemia, whereas moderate exercise (ME) causes both to double. If norepinephrine (NE) plus epinephrine (Epi) infusion during ME produces the plasma levels and Ra of IE, this would prove them capable of mediating these responses. Male subjects underwent 40 min of 53% V̇o2max exercise, eight each with saline (control [CON]), or with combined NE + Epi (combined catecholamine infusion [CCI]) infusion from min 26–40. In CON and CCI, NE levels reached 7.3 ± 0.7 and 33.1 ± 2.9 nmol/l, Epi 0.94 ± 0.08 and 7.06 ± 0.44 nmol/l, and Ra 3.8 ± 0.4 and 12.9 ± 0.8 mg · kg−1 · min−1 (P < 0.001), respectively, at 40 min. Rd increased to 3.5 ± 0.4 vs. 11.2 ± 0.8 mg · kg−1 · min−1 and glycemia 5.2 ± 0.2 mmol/l in CON vs. 6.5 ± 0.2 mmol/l in CCI (P < 0.001). The glucagon-to-insulin ratio did not differ. Comparing CCI data to those from 14-min IE (n = 16), peak NE (33.6 ± 5.1 nmol/l), Epi (5.32 ± 0.93 nmol/l), and Ra (13.0 ± 1.0 mg · kg−1 · min−1) were comparable. The induced increments in NE, Epi, and Ra, all of the same magnitude as in IE, strongly support that circulating catecholamines can be the prime regulators of Ra in IE.
Publisher
American Diabetes Association
Subject
Endocrinology, Diabetes and Metabolism,Internal Medicine
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