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

Abstract

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 y, 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 minutes, and post. PETCO2, minute ventilation, expired gases, blood pressure, heart rate, and middle cerebral artery blood velocity were recorded continuously. PETCO2 increased throughout all visits (p£0.011), was matched during HOWI and WWI+CO2 (p³0.264), and was greater during WWI+CO2 vs. WWI at 10, 30, and 60 minutes (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 minutes (0.63±0.45 vs. 0.16±0.34 L/min/mmHg, p<0.001), while there were no differences between conditions for cerebrovascular reactivity to CO2 (p³0.163). When WWI+CO2 vs. WWI were compared, ventilatory sensitivity to CO2 was not different between conditions (p³0.642), while the change in cerebrovascular reactivity to CO2 was different at 30 minutes (-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, while cerebrovascular reactivity to CO2 decreases due to the combined effects of immersion.