Intense exercise (IE) (>80% (V) over dot O-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 Ra of IE, this would prove them capable of mediating these responses. Male subjects underwent 40 min of 53% (V) over dot(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.
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