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The responses to oral propranolol (80 mg) and placebo were compared in normal subjects during three studies on a cycle ergometer (progressive exercise and two 5-min constant work rate studies at 50 and 70% maximum). Heart rate (HR), ventilation (VE), CO2 output (VCO2) and O2 uptake (VO2) were measured in each study and metabolites in venous blood in the 70% study. Propranolol reduced HR in all studies and endurance time during progressive exercise. During constant-work-rate exercise the changes with propranolol depended on time and work rate. At 50% max, VO2, VCO2, and VE were reduced in early exercise but were similar by min 5. At 70% max, VO2 and VCO2 were again lower initially with propranolol but then rose more rapidly. By min 5 VE was greater with propranolol, coinciding with a rapidly rising venous lactate. We interpret the initial reduction in VO2 and VCO2 to reduced cardiac output and muscle perfusion with propranolol. The resulting increase in anaerobic metabolism during heavy exercise would explain the increased VE at min 5. The metabolic data are compatible with glycogen being the predominant muscle fuel.

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Pulmonary and airway mechanics were assessed in seven asthmatic patients in remission, when asthma was induced by exercise and again after spontaneous recovery or bronchodilator treatment. After exercise there was a sustained fall in forced expiratory volume in 1 s (FEV 1.0) in all patients, varying from 30 to 80 percent of the initial value. Total lung capacity (TLC) increased significantly in four of the seven patients. In one of the four patients the increase in TLC was associated with an increase in static transpulmonary pressure at full inflation but in the remaining three patients it was associated with a parallel shift of the pressure-volume curve of the lung without change in its slope. In all patients residual volume increased, regardless of change in TLC; both pressure-volume and maximum expiratory flow-volume curves suggested that widespread airway closure (or virtual closure) occurred at positive transpulmonary pressures when asthma was induced. Loss of lung recoli pressure sometimes contributed to the reduction in maximum expiratory flow but diffuse airway narrowing was probably the dominant abnormality. When air-flow obstruction became more severe the ratio of expiratory to inspiratory time was increased and although expiratory flow limitation was present excessive expiratory pressures were not generated.

No abstract