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

Abstract

The hypercapnic ventilatory response (HCVR) is augmented and cerebrovascular reactivity to CO2 (CVR) is attenuated during thermoneutral head out water immersion (HOWI). It is currently unknown if central hypervolemia contributes to such changes. To this end, waist water immersion (WWI) induces graded central hypervolemia. Therefore, WWI could be used as an experimental model to help determine if central hypervolemia contributes to changes in the HCVR and CVR during HOWI.PurposeWe tested the hypotheses that changes from baseline for the HCVR are higher and CVR are lower during HOWI vs. WWI.MethodsTwelve subjects (age: 24±3 y, BMI: 25±3 kg/m−2) completed one hour of thermoneutral (35±0°C) WWI and HOWI. The partial pressure of end tidal CO2 (PETCO2; capnograph), minute ventilation (pneumotachometer), and middle cerebral artery blood velocity (MCAv; transcranial doppler) were recorded continuously. To assess the HCVR and CVR, subjects rebreathed 7% CO2 and 93% O2 from a 10 L bag for 3.5 min at baseline, 10 min, 30 min, 60 min, and post water immersion. The HCVR and CVR were calculated as the slope of the linear regression line of minute ventilation vs. PETCO2 and MCAv vs. PETCO2 every 30 s throughout the test. Data are reported as a change from baseline (mean ±SD).ResultsPETCO2 increased from baseline during WWI and HOWI at every time point (p≤0.01) and the change in PETCO2 was lower during WWI vs. HOWI at 10 min, 30 min, and 60 min (p<0.01). Minute ventilation decreased from baseline during WWI at 60 min (−1.36±0.84 L/min, p<0.01) and post (−0.93±0.78 L/min, p=0.03). Meanwhile, minute ventilation did not change from baseline during HOWI at any time point (p≥0.38). The change in minute ventilation was lower during WWI vs. HOWI at 60 min (p=0.03). MCAv did not change during WWI at any time point (p≥0.40) and increased from baseline during HOWI at 10 min (4.6±3.5 cm/s, p<0.01) and 30 min (3.5±5.0 cm/s, p <0.01). The change in MCAv was lower during WWI vs. HOWI at 10 min (p<0.01) and 30 min (p<0.01). The HCVR did not change at any time point during WWI (10 min: 0.07±0.19, 30 min: 0.11±0.32, 60 min: 0.12±0.29, and post: 0.12±0.26 L/min/mmHg; p=0.64) and 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, and post: 0.24±0.43 L/min/mmHg; p≤0.02). The change in the HCVR was lower during WWI vs. HOWI at 10 min, 30 min, and 60 min (p<0.01). CVR decreased from baseline during WWI and HOWI at every time point (p<0.01) and was greater during WWI vs. HOWI at 60 min (−0.34±0.41 vs. −0.63±0.44 L/min/mmHg, p<0.01) and post (−0.40±0.36 vs. −0.85±0.42 L/min/mmHg, p<0.01).ConclusionIt appears that an augmented HCVR during HOWI is due to the combined effects of water immersion (i.e., central hypervolemia, hypercapnia, increased work of breathing, etc.), while a reduced CVR during HOWI is due to central hypervolemia and hypercapnia.Support or Funding InformationSupported by the NASA Space Physiology Research Grant from the ACSM Foundation, the Mark Diamond Research Fund of the Graduate Student Association at the University at Buffalo, and the Office of Naval Research Award N00014‐17‐1‐2665.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.