Exercise hyperpnea in the duck without intrapulmonary chemoreceptor involvement.

To determine the involvement of intrapulmonary chemoreceptors (IPC) in the control of breathing during exercise, it is necessary to hold the PCO2 in the microenvironment of these receptors constant at the resting value. We accomplished this in unanesthetized Pekin ducks by ligating the left pulmonary artery and diverting all of the cardiac output to the right lung, which was denervated. The ducks were then unidirectionally ventilated with a constant gas stream (5% CO2, 19% O2, balance N2) at a flow rate of 12 L X min-1. This procedure provided a constant microenvironment for the receptors in the left lung despite any changes in the chemical composition or flow rate of the blood going to the right lung during exercise. Ventilatory effort increased during running exercise (1.44 km X h-1 at a 3 degrees incline) by an average of 145% over resting values because of an increase in both respiratory frequency and tidal volume. Because no altered stimuli were presented to the IPC using this procedure, the increased ventilation with exercise could not have resulted from changes in their discharge frequency. We conclude that ventilation can increase during exercise in the duck in the absence of IPC involvement and that other neural input, possibly from muscle, is responsible for the hyperpnea.