The Hypercapnic Ventilatory Response and Cerebrovascular Reactivity to CO2 during Waist Water Immersion with Acute Hypercapnia and Head Out Water Immersion

Abstract

During head out water immersion (HOWI), the hypercapnic ventilatory response (HCVR) is augmented and cerebrovascular reactivity to CO2 (CVR) is attenuated; possibly due to water pressure exerted on the chest wall, central hypervolemia, and/or hypercapnia. Waist water immersion with acute hypercapnia (WWI+CO2) causes central hypervolemia and hypercapnia without exerting water pressure on the chest wall. However, it is unknown if HCVR and CVR are different during WWI+CO2 vs. HOWI. PURPOSE: We tested the hypotheses that the HCVR is augmented and CVR is attenuated during WWI+CO2 and HOWI. METHODS: Twelve subjects (age: 24±3 y, BMI: 25±3 kg/m2, 6 women) completed one hour of thermoneutral (35±0°C) WWI+CO2 and HOWI. The partial pressure of end tidal CO2 (PETCO2; capnograph), minute ventilation (MV; pneumotachometer), and middle cerebral artery blood velocity (MCAv; transcranial doppler) were recorded. CO2 was added to the inspirate during WWI+CO2 to match the increase in PETCO2 during HOWI. Subjects rebreathed 7% CO2 and 93% O2 from a 10 L bag for 3.5 min at baseline, 10 min, 30 min, and 60 min of water immersion. The HCVR and CVR were calculated as the slope of the linear regression line of MV vs. PETCO2 and MCAv vs. PETCO2 every 30 s throughout the test. Data are reported as a change from baseline (mean±SD). RESULTS: PETCO2 increased from baseline during WWI+CO2 and HOWI at every time point (p<0.01) and was matched between conditions (p≥0.26). MV increased from baseline during WWI+CO2 at 60 min (p=0.03) but did not change during HOWI at any time point (p≥0.38). MCAv increased from baseline during WWI+CO2 at every time point and during HOWI at 10 min and 30 min (all p<0.01). The HCVR did not change from baseline during WWI+CO2 at any time point (all p≥0.35) but increased from baseline during HOWI at every time point (10 min: 0.59±0.34, 30 min: 0.58±0.46, 60 min: 0.63±0.45 L/min/mmHg; p<0.01). The HCVR was lower during WWI+CO2 vs. HOWI at 10 min, 30 min, and 60 min (p<0.01). CVR decreased from baseline during WWI+CO2 and HOWI at every time point (p<0.01) but was not different between conditions at any time point (p≥0.16). CONCLUSIONS: The elevated HCVR during HOWI is likely caused by water pressure exerted on the chest wall. However, reductions in CVR during HOWI are likely caused by central hypervolemia and/or hypercapnia.