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1. In three healthy individuals, the first breath of cycle ergometer exercise was characterized by increases of minute ventilation (VE) and pulmonary capillary CO2 output (VCO2), with little change of end-tidal PCO2, suggesting a concomitant increase of pulmonary blood flow (Q) and preservation of V/Q status. Functional residual capacity fell, depleting lung gas stores of O2 and CO2. 2. The following hypothesis purporting to account for the initiation of exercise hyperpnoea was examined (Filley, 1976): (a) assuming pulmonary capillary plasma to remain unexposed to carbonic anhydrase, its slow alkalinization consequent upon CO2 exchange causes a more acid plasma to enter the pulmonary veins if Q increases abruptly, as at exercise onset; (b) the fall of pulmonary venous plasma pH stimulates an intrapulmonary chemoreflux to elicit a proportionate hyperpnoea, so preserving arterial isocapnia; (c) the initial hyperpnoea should therefore be abolished if pulmonary capillary VCO2 is suppressed at exercise onset, as the absence of pulmonary capillary plasma alkalinization should sever the postulated intrapulmonary humoral link between Q and VE. 3. In the present study, while abrupt CO2 inhalation (approximately 6% in air) at exercise onset abolished pulmonary capillary VCO2 during the first breath of exercise, the initial hyperpnoea was unaffected. This observation argues against the hypothesis that exercise hyperpnoea is initiated by an intrapulmonary chemoreflex which detects perfusion-related changes in pulmonary venous plasma pH.