Abstract

Intense exercise (IE) (>80% V̇o_2max) causes a seven- to eightfold increase in glucose production (R_a) and a fourfold increase in glucose uptake (R_d), 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 R_a of IE, this would prove them capable of mediating these responses. Male subjects underwent 40 min of 53% V̇o_2max 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 R_a 3.8 ± 0.4 and 12.9 ± 0.8 mg · kg⁻¹ · min⁻¹ (P < 0.001), respectively, at 40 min. R_d 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 R_a (13.0 ± 1.0 mg · kg⁻¹ · min⁻¹) were comparable. The induced increments in NE, Epi, and R_a, all of the same magnitude as in IE, strongly support that circulating catecholamines can be the prime regulators of R_a in IE.