Non‐selective β‐adrenergic blockade prevents reduction of the cerebral metabolic ratio during exhaustive exercise in humans

Abstract

Intense exercise decreases the cerebral metabolic ratio of oxygen to carbohydrates [O(2)/(glucose + (1/2)lactate)], but whether this ratio is influenced by adrenergic stimulation is not known. In eight males, incremental cycle ergometry increased arterial lactate to 15.3 +/- 4.2 mm (mean +/- s.d.) and the arterial-jugular venous (a-v) difference from -0.02 +/- 0.03 mm at rest to 1.0 +/- 0.5 mm (P < 0.05). The a-v difference for glucose increased from 0.7 +/- 0.3 to 0.9 +/- 0.1 mm (P < 0.05) at exhaustion and the cerebral metabolic ratio decreased from 5.5 +/- 1.4 to 3.0 +/- 0.3 (P < 0.01). Administration of a non-selective beta-adrenergic (beta(1) + beta(2)) receptor antagonist (propranolol) reduced heart rate (69 +/- 8 to 58 +/- 6 beats min(-1)) and exercise capacity (239 +/- 42 to 209 +/- 31 W; P < 0.05) with arterial lactate reaching 9.4 +/- 3.6 mm. During exercise with propranolol, the increase in a-v lactate difference (to 0.5 +/- 0.5 mm; P < 0.05) was attenuated and the a-v glucose difference and the cerebral metabolic ratio remained at levels similar to those at rest. Together with the previous finding that the cerebral metabolic ratio is unaffected during exercise with administration of the beta(1)-receptor antagonist metropolol, the present results suggest that the cerebral metabolic ratio decreases in response to a beta(2)-receptor mechanism.