Blood Pressure Responses to Acute Peripheral Chemoreceptor Activation are Augmented during Head Out Water Immersion
Authors: Sackett James R. , Schlader Zachary J. , Sarker Suman , Chapman Christopher L. , Johnson Blair D. 
Published: November 2023

Water immersion causes carbon dioxide (CO2) retention which may contribute to changes in hemodynamic control. Tonic afferent activity originating from the peripheral chemoreceptors modulates hemodynamics. Activation of the peripheral chemoreceptors increases heart rate and blood pressure. However, it is not known if water immersion alters heart rate and blood pressure during activation of the peripheral chemoreceptors.

PURPOSE

We tested the hypothesis that heart rate (HRR) and blood pressure (BPR) responses to acute hypercapnia and acute hypoxia are augmented during head out water immersion (HOWI).

METHODS

We assessed the HRR and BPR to hypercapnia and hypoxia in 8 participants (age: 23 ± 2 y, BMI: 26 ± 3 kg/m2, 3 women) during two randomized trials: a thermoneutral (35 ± 0°C) HOWI trial and a time‐control dry trial (DRY). HRR and BPR to hypercapnia and hypoxia were assessed at baseline, at 10, 60, and 120 min of HOWI or DRY, and 10 min post HOWI or DRY. Heart rate (ECG), blood pressure (Nexfin), the partial pressure of end tidal CO2 (PETCO2), and arterial oxygen saturation (%SaO2) were recorded continuously. For the hypercapnic test, participants inhaled 1 breath of 13% CO2, 21% O2, and 66% N2, followed by 3 min of room air breathing, 4 separate times. For the hypoxic test, participants inhaled 2–6 breaths of 100% N2, followed by 3 min of room air breathing, 4 separate times. We determined peak heart rate, peak mean arterial pressure, the peak PETCO2, and the lowest %SaO2 within 2 min following each hypercapnic or hypoxic administration. The HRR and BPR data are reported as the slope of the linear regression line of heart rate and mean arterial pressure vs. PETCO2 or %SaO2, respectively.

RESULTS

Resting PETCO2 was higher during HOWI vs. DRY at 10 min (46 ± 2 vs. 44 ± 2 mmHg, p ≤ 0.001), 60 min (47 ± 2 vs. 44 ± 2 mmHg, p ≤ 0.001), and 120 min (46 ± 2 vs. 44 ± 2 mmHg, p ≤ 0.001) of HOWI. Resting heart rate was not different between baseline, 10, 60, and 120 min of HOWI or DRY, and 10 min post HOWI or DRY, but was higher during HOWI vs. DRY at 10 min post (70 ± 12 bpm vs. 62 ± 10 bpm, p ≤ 0.001) HOWI. The HRR to hypercapnia was not different between HOWI and DRY (time: p = 0.66, condition: p = 0.84, interaction: p = 0.35). The HRR to hypoxia was not different between HOWI and DRY (time: p = 0.44, condition: p = 0.17, interaction: p = 0.88). Resting mean arterial pressure was lower during HOWI vs. DRY at 60 min (85 ± 9 vs. 94 ± 9 mmHg, p ≤ 0.001) and 120 min (88 ± 9 vs. 94 ± 8 mmHg, p ≤ 0.001) of HOWI, and 10 min post (91 ± 7 vs. 96 ± 9 mmHg, p = 0.002) HOWI. The mean arterial BPR to hypercapnia was higher during HOWI vs. DRY at 10 min (0.30 ± 0.15 vs. 0.51 ± 0.44 mmHg/mmHg; p = 0.07) of HOWI. The mean arterial BPR to hypoxia was higher during HOWI vs. DRY at 60 min (1.92 ± 2.36 vs. 0.82 ± 0.34 mmHg/%SaO2; p = 0.04) of HOWI.

CONCLUSION

These data indicate that the HRR to hypercapnia and hypoxia are not augmented during thermoneutral HOWI. However, the BPR to hypercapnia and hypoxia are augmented at 10 min and 60 min of HOWI, respectively. This suggests that water immersion increases blood pressure responses to peripheral chemoreceptor activation.