Cerebral hemodynamic and ventilatory responses to hypoxia, hypercapnia, and hypocapnia during 5 days at 4,350 m

Abstract

This study investigated the changes in cerebral near-infrared spectroscopy (NIRS) signals, cerebrovascular and ventilatory responses to hypoxia and CO2 during altitude exposure. At sea level (SL), after 24 hours and 5 days at 4,350 m, 11 healthy subjects were exposed to normoxia, isocapnic hypoxia, hypercapnia, and hypocapnia. The following parameters were measured: prefrontal tissue oxygenation index (TOI), oxy- (HbO2), deoxy- and total hemoglobin (HbTot) concentrations with NIRS, blood velocity in the middle cerebral artery (MCAv) with transcranial Doppler and ventilation. Smaller prefrontal deoxygenation and larger ΔHbTot in response to hypoxia were observed at altitude compared with SL (day 5: ΔHbO2-0.6±1.1 versus -1.8±1.3 μmol/cmper mm Hg and ΔHbTot 1.4±1.3 versus 0.7±1.1 μmol/cm per mm Hg). The hypoxic MCAv and ventilatory responses were enhanced at altitude. Prefrontal oxygenation increased less in response to hypercapnia at altitude compared with SL (day 5: ΔTOI 0.3±0.2 versus 0.5±0.3% mm Hg). The hypercapnic MCAv and ventilatory responses were decreased and increased, respectively, at altitude. Hemodynamic responses to hypocapnia did not change at altitude. Short-term altitude exposure improves cerebral oxygenation in response to hypoxia but decreases it during hypercapnia. Although these changes may be relevant for conditions such as exercise or sleep at altitude, they were not associated with symptoms of acute mountain sickness.

Figure 1

Description of the main phases of the protocol to measure ventilatory and cerebral hemodynamic responses with simultaneous changes in end-tidal O₂ (PetO₂) and CO₂ (PetCO₂) partial pressures at SL and at high altitude. End-tidal CO2 partial pressure values illustrate typical SL measurements. During poikilocapnic conditions (phases 1, 3, 5, 7), PetCO₂ was uncontrolled; during the isocapnic condition (phase 2), PetCO₂ was maintained at the same level as the end of phase 1, whereas during hypercapnic conditions (phases 4 and 6), PetCO₂ was increased by +5 and +12 mm Hg above the value at the end of phase 1. See Materials and Methods for more details.

Figure 2

Typical changes in prefrontal oxy-(HbO₂), deoxy-(HHb) and total hemoglobin (HbTot) concentrations in response to hypoxic isocapnia (A), hypoxic hypercapnia +5 (B), and +12 mm Hg (C), and normoxic hypocapnia (D), from a baseline in poikilocapnic normoxia. Oxyhemoglobin is black, HHb is dark gray and HbTot is light gray. Raw data are presented for a representative subject at SL.

Figure 3

Hypoxic responses: Ventilatory (V_E, panel A), transcranial Doppler (TCD) (TCD cerebrovascular responses (CVR), panel B) and near-infrared spectroscopy (NIRS) (oxyhemoglobin (HbO₂), panel C; tissue oxygenation index (TOI), panel D; deoxyhemoglobin (HHb), panel E; total hemoglobin (HbTot), panel F) responses to isocapnic hypoxia at sea level (SL), at day 1 (D1) and 5 (D5) at altitude. Changes in V_E, TCD CVR and NIRS variables are expressed per mm Hg of change in end-tidal O₂ partial pressure. *significantly different from SL;⁺significantly different from D1.

Figure 4

Hypercapnic responses: Ventilatory (V_E, panel A), TCD (TCD CVR, panel B) and NIRS (oxyhemoglobin (HbO₂), panel C; tissue oxygenation index (TOI), panel D; deoxyhemoglobin (HHb), panel E; total hemoglobin (HbTot), panel F) responses to hypercapnia (expressed per mm Hg of change in end-tidal CO₂ partial pressure) at sea level (SL), at day 1 (D1) and 5 (D5) at altitude. *significantly different from SL;⁺significantly different from D1.

Figure 5

Hypocapnic responses: TCD (TCD CVR, panel A) and NIRS (oxyhemoglobin (HbO₂), panel B; tissue oxygenation index (TOI), panel C; deoxyhemoglobin (HHb), panel D; total hemoglobin (HbTot), panel E) responses to hypocapnia (expressed in mm Hg of change in end-tidal CO₂ partial pressure) at sea level (SL), at day 1 (D1) and 5 (D5) at altitude.