Carotid Body Chemosensitivity to Hypoxia in Cold Water Diving
Authors: Hess Hayden W. , Hostler David , Johnson Blair D. 
Published: April 2020

Introduction

Cold stress and hyperoxia reduce carotid body (CB) tonic activity, which might reduce the ventilatory response to hypoxia. Therefore, these diving conditions could be an operational risk to divers experiencing closed‐circuit rebreather failure. We tested the hypotheses that cold water diving would lower CB chemosensitivity to hypoxia, but increase ventilation (V̇E) and mean arterial pressure (MAP) more than thermoneutral diving.

Methods

Thirteen subjects (age: 26±4 y; BMI: 26±2 kg·m2) completed two dives (depth: 6.1 meters of sea water [msw]; bottom time: 202±11 min) in either cold (15°C) or thermoneutral (30°C) water. CB chemosensitivity was assessed using hypoxic ventilatory response (HVR) tests pre‐dive, 80 and 160 min into the dives, immediately post‐dive, and 60 min post‐dive. HVR consisted of inhaling 100% N2 for 2–6 breaths, repeated four times, with 2 min between hypoxic exposures. Baseline end‐tidal carbon dioxide (PETCO2), fraction of expired oxygen (FEO2), V̇E, breath frequency (fB), heart rate (HR), and MAP were measured prior to and during each HVR. HVR was calculated as the slope of the linear regression line of the peak V̇E in three consecutive breaths vs. the nadir FEO2. The slope of the linear regression lines of the peak HR and MAP responses to hypoxia vs. the nadir FEO2 were also calculated as indices of CB chemosensitivity. Data were analyzed as a change from pre‐dive.

Results

PETCO2 increased during the dive (time main effect; p<0.01), but was not different between conditions. FEO2 increased during the dive in both conditions (p<0.01), but was not different between conditions. V̇E increased during the cold condition from pre‐dive (+12±7 and 22±13 L·min−1, for D80 and D160, respectively; p<0.01) and increased from D80 to D160 (+11±11 L·min−1; p=0.02) and was greater than thermoneutral condition at both time points during the dive (both p<0.01). V̇E increased from pre‐dive in the thermoneutral condition (p=0.04). fB was elevated from pre‐dive at D160 in the cold condition (+3±3 breaths·min−1; p=0.01) and was greater than the thermoneutral condition (p=0.04). HR decreased during the dive (time main effect; p<0.01) and was lower at D160 in the thermoneutral condition. MAP was elevated during the dive in both conditions (+14±9 mmHg and +16±9 mmHg for cold and thermoneutral conditions, respectively; p<0.01), and remained elevated postdive in the thermoneutral condition at both time points (both p<0.03). HVR was not changed during the dive (time main effect: p=0.59) and was not different between conditions (condition main effect: p=0.76). Additionally, the HR and MAP responses to hypoxia were not changed during the dive and was not different between conditions.

Conclusion

Despite marked changes in baseline ventilation and hemodynamics, these data indicate that the HVR (i.e., CB chemosensitivity) was not changed during cold or thermoneutral diving at 6.1msw. Therefore, it does not appear that CB activity is attenuated due to combined cold stress and hyperoxia in diving and do not contribute to the changes in ventilation and hemodynamics.

Support or Funding Information

Supported by Office of Naval Research Award N000141612954