The independent effects of hydrostatic pressure and hypercapnic breathing during water immersion on ventilatory sensitivity and cerebrovascular reactivity.

Head-out water immersion (HOWI) induces ventilatory and hemodynamic changes, which may be a result of hydrostatic pressure, augmented arterial CO₂ tension, or a combination of both. We hypothesized that the hydrostatic pressure and elevated CO₂ tension that occur during HOWI will contribute to an augmented ventilatory sensitivity to CO₂ and an attenuated cerebrovascular reactivity to CO₂ during water immersion. Twelve subjects [age: 24 ± 3 yr, body mass index (BMI): 25 ± 3 kg/m²] completed HOWI, waist water immersion with CO₂ (WWI + CO₂), and WWI, where a rebreathing test was conducted at baseline, 10, 30, and 60 min, and postimmersion. End-tidal pressure of carbon dioxide ([Formula: see text]), minute ventilation, expired gases, blood pressure, heart rate, and middle cerebral artery blood velocity were recorded continuously. [Formula: see text] increased throughout all visits (P ≤ 0.011), was similar during HOWI and WWI + CO₂ (P ≥ 0.264), and was greater during WWI + CO₂ versus WWI at 10, 30, and 60 min (P < 0.001). When HOWI vs. WWI + CO₂ were compared, the change in ventilatory sensitivity to CO₂ was different at 10 (0.59 ± 0.34 vs. 0.06 ± 0.23 L/min/mmHg; P < 0.001), 30 (0.58 ± 0.46 vs. 0.15 ± 0.25 L/min/mmHg; P < 0.001), and 60 min (0.63 ± 0.45 vs. 0.16 ± 0.34 L/min/mmHg; P < 0.001), whereas there were no differences between conditions for cerebrovascular reactivity to CO₂ (P ≥ 0.163). When WWI + CO₂ versus WWI were compared, ventilatory sensitivity to CO₂ was not different between conditions (P ≥ 0.642), whereas the change in cerebrovascular reactivity to CO₂ was different at 30 min (-0.56 ± 0.38 vs. -0.30 ± 0.25 cm/s/mmHg; P = 0.010). These data indicate that during HOWI, ventilatory sensitivity to CO₂ increases due to the hydrostatic pressure, whereas cerebrovascular reactivity to CO₂ decreases due to the combined effects of immersion.NEW & NOTEWORTHY Although not fully elucidated, the ventilatory and hemodynamic alterations during water immersion appear to be a result of the combined effects of immersion (i.e., elevated [Formula: see text], central hypervolemia, increased cerebral perfusion, increased work of breathing, etc.). Our findings demonstrate that an augmented ventilatory sensitivity to CO₂ during immersion may be due to the hydrostatic pressure across the chest wall, whereas an attenuated cerebrovascular reactivity to CO₂ may be due to the combined effects of immersion.