Hypoxia following voluntary hyperventilation during exercise in man.

The importance of carbon dioxide in the control of ventilation during exercise was tested by emptying CO2 stores by voluntary hyperventilation. Healthy subjects were studied after 3 min hyperventilation down to an end-tidal PCO2 of about 20 mmHg on a background of steady exercise at 75 W. Control runs were performed when the hyperventilation was made isocapnic by the addition of CO2. Following hypocapnic hyperventilation, there was a period when ventilation fell below control and this was accompanied by a fall in end-tidal PO2 (minimum 48 mmHg) and oximeter reading (minimum 73%). Ventilation rapidly returned to baseline following isocapnic hyperventilation and hypoxia was not seen. A mathematical simulation suggested that brain PCO2 recovered more slowly than arterial PCO2 and that at the times that ventilation was depressed central chemoreceptor PCO2 would have been low. We conclude that CO2 provides a crucial drive for maintaining adequate ventilation during steady exercise and that the central chemoreceptor may be involved.