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 CO tension, or a combination of both. We hypothesized that the hydrostatic pressure and elevated CO tension that occur during HOWI will contribute to an augmented ventilatory sensitivity to CO and an attenuated cerebrovascular reactivity to CO during water immersion. Twelve subjects [age: 24 ± 3 yr, body mass index (BMI): 25 ± 3 kg/m] completed HOWI, waist water immersion with CO (WWI + CO), 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 ( ≤ 0.011), was similar during HOWI and WWI + CO ( ≥ 0.264), and was greater during WWI + CO versus WWI at 10, 30, and 60 min ( < 0.001). When HOWI vs. WWI + CO were compared, the change in ventilatory sensitivity to CO was different at 10 (0.59 ± 0.34 vs. 0.06 ± 0.23 L/min/mmHg; < 0.001), 30 (0.58 ± 0.46 vs. 0.15 ± 0.25 L/min/mmHg; < 0.001), and 60 min (0.63 ± 0.45 vs. 0.16 ± 0.34 L/min/mmHg; < 0.001), whereas there were no differences between conditions for cerebrovascular reactivity to CO ( ≥ 0.163). When WWI + CO versus WWI were compared, ventilatory sensitivity to CO was not different between conditions ( ≥ 0.642), whereas the change in cerebrovascular reactivity to CO was different at 30 min (-0.56 ± 0.38 vs. -0.30 ± 0.25 cm/s/mmHg; = 0.010). These data indicate that during HOWI, ventilatory sensitivity to CO increases due to the hydrostatic pressure, whereas cerebrovascular reactivity to CO decreases due to the combined effects of immersion. 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 CO during immersion may be due to the hydrostatic pressure across the chest wall, whereas an attenuated cerebrovascular reactivity to CO may be due to the combined effects of immersion.