Beta-adrenergic blockers have been reported to depress central ventilatory drive. The authors investigated this possibility in a double-blind, randomized fashion in 12 healthy volunteers who received 0.1 mg.kg-1 of propranolol and normal saline intravenously at two separate study sessions. A modified Read rebreathing technique was used. Both ventilatory and occlusion pressure responses to CO2 were measured to help separate peripheral (airway) from central mechanisms. Significant beta blockade was demonstrated by statistically lower heart rate responses to CO2 rebreathing after propranolol, but not normal saline. Nevertheless, propranolol exerted no significant effect on resting end-tidal CO2 or the ventilatory and occlusion pressure responses to CO2. Although health subjects appear to have minimal alterations in their ventilatory response to CO2 after beta-adrenergic blockade, patients with airway disease may still experience significant changes in ventilation. In addition, drug interaction studies may give further insight into the presence or absence of any respiratory effects of propranolol.