Ventilatory and cerebral hemodynamic responses to hypoxia, hypercapnia and hypocapnia during 5 days at 4350 m

This study investigated changes in cerebral near-infrared spectroscopy (NIRS), cerebrovascular and ventilatory responses to hypoxia and CO 2 during prolonged high altitude exposure. At sea level and at day 1 and 5 at 4350 m, 11 healthy subjects were exposed during 10-min periods to i) normoxia (end-tidal O 2 partial pressure (PetO 2 ) = 100 mmHg), ii) isocapnic hypoxia (PetO 2 =55 mmHg), iii) hypercapnia (PetCO 2 +5 and +12 mmHg) and iv) hypocapnia (PetCO 2 -15 mmHg). The following parameters were measured during each period: pre-frontal oxygenation index (TOI), oxy- (HbO 2 ), deoxy- and total hemoglobin (HbTot) changes with NIRS, blood velocity in the middle cerebral artery (MCAv) with transcranial Doppler and ventilation. Smaller pre-frontal deoxygenation (HbO 2 and TOI) and larger HbTot in response to isocapnic hypoxia were observed at altitude compared to sea level (at day 5: HbO 2 0.6±1.1 vs. 1.8±1.3 µmol• mmHg -1 , HbTot 1.4±1.3 vs. 0.7±1.1 µmol• mmHg -1 ). The hypoxic MCAv and ventilatory responses were enhanced at altitude. Pre-frontal oxygenation increased less in response to hypercapnia at altitude compared to sea level (at day 5: TOI 0.3±0.2 vs. 0.5±0.3 %• mmHg -1 ). The hypercapnic MCAv and ventilatory responses were increased and decreased, respectively, at altitude. Hemodynamic responses to hypocapnia did not change at altitude. These data show that altitude exposure induces a better preservation of cerebral oxygenation in response to hypoxia but reduced cerebral oxygenation during hypercapnia. Changes in hypoxic and hypercapnic NIRS responses provide complementary insights to MCAv and ventilatory adaptations. Their relevance for altitude acclimatization remains to be clarified.