Ventilatory responses to hypercapnia and hypoxia after 6 h passive hyperventilation in humans

1. Acute exposure to hypoxia, stimulates ventilation and induces hypocapnia . Long-term exposure to hypoxia generates changes in respiratory control kn own as ventilatory acclimatization to hypoxia. The object of this study was to investigate the degree to which the hyperventilation and hypocapnia can induce the changes known as ventilatory acclimatization to hypoxia, in the absence of the primary hypoxic stimulus itself. 2. Three 6 h protocols were each performed on twelve healthy volunteers: (1 ) passive hypocapnic hyperventilation, with end-tidal CO2 pressure (P-ET,P- CO2) held 10 Torr below the eupnoeic value; (2) passive eucapnic hyperventi lation, with P-ET,P-CO2 maintained eucapnic; (3) control. 3. Ventilatory responses to acute hypercapnia, and hypoxia were assessed be fore and half an hour after each protocol. 4. The presence of prior hypocapnia, but not prior hyperventilation, caused a reduction in air-breathing P-ET,P-CO2 (P < 0.05, ANOVA), and a leftwards shift of the ventilatory response to hypercapnia (P < 0.05). The presence of prior hyperventilation, but not prior hypocapnia, caused an increase in the ventilatory sensitivity to CO2 (P < 0.05). No significant effects of an y protocol were detected on the ventilatory sensitivity to hypoxia. 5. We conclude that following 6 h of passive hyperventilation: (i) the left shift of the (V) over dot (E)-P-ET,P-CO2 relationship is due to alkalosis and not to hyperventilation; (ii) the increase in dope of the (V) over dot( E)-P-ET,P-CO2 relationship is due to the hyperventilation and not the alkal osis; and (iii) ventilatory sensitivity to hypoxia is unaltered.