Cerebrovascular Regulation in Breath‐Hold Divers with Chronic Exposure to Long‐Duration Apneas
Authors: Moir M. Erin , Woehrle Emilie , Smith Sydney O. , Klassen Stephen A. , Matushewski Brad J. , Kozic Dusko , Dujic Zeljko , Barak Otto F. , Shoemaker J. Kevin 
Published: June 2021

Breath‐hold divers (BHD) are exposed to repeated long‐duration apneas during training and competition. With long‐duration apneas divers experience severe hypoxia and hypercapnia with large increases in blood pressure. This blood pressure response is critical to elevate brain perfusion and oxygen delivery above that enabled by cerebral vasodilation alone. Despite studies regarding cerebral perfusion in BHD during prolonged apneas, no studies have evaluated cerebrovascular regulatory mechanisms in this population. The current investigation tested the hypothesis that BHD would demonstrate impaired dynamic cerebral autoregulation. Seventeen BHD (3 females; 33 ± 9 years; 11 ± 9 years diving) and seventeen healthy controls (4 females; 26 ± 9 years) completed two or three repeated sit‐to‐stand trials during spontaneous breathing and poikilocapnic conditions. Heart rate (HR), finger arterial blood pressure (BP), and cerebral blood flow velocity (CBFV) from the right middle cerebral artery were measured continuously with three‐lead electrocardiography, finger photoplethysmography, and transcranial Doppler ultrasonography, respectively. End‐tidal carbon dioxide partial pressure (PETCO2) was measured with a gas analyzer. Offline, an index of cerebrovascular resistance (CVRi) was calculated as the quotient of mean BP and mean CBFV. The rate of the drop in CVRi relative to the change in BP provided the rate of regulation (RoR; [ΔCVRi/ΔT]/ΔBP). The sit‐to‐stand protocol elicited a similar reduction in BP between the BHD and controls (−29 ± 8 vs. −25 ± 8 mmHg; P = 0.23, d = 0.5). Despite a similar pressure stimulus between groups, BHD demonstrated slower RoR than controls (0.10 ± 0.05 vs. 0.20 ± 0.09 %·sec−1; P ≤ 0.001, d = 1.4). Underlying the reduced RoR in the BHD was a longer time to reach nadir CVRi or peak dilation, as estimated from CBFV, compared with the controls (7.1 ± 1.5 vs. 5.2 ± 1.3 sec; P ≤ 0.001, d = 1.4). In concert with the longer CVRi response, the time to reach peak CBFV following standing was longer in the BHD than the controls (13.1 ± 1.2 vs. 12.4 ± 1.8 sec; P = 0.04, d = 0.5). Further, the BHD demonstrated a greater increase in HR with standing than the controls (34 ± 7 vs. 28 ± 7 bpm; P = 0.02, d = 1.3). We observed lower PETCO2 levels in the BHD than the controls during sitting (32 ± 4 vs. 37 ± 5 mmHg); standing elicited reductions in PETCO2 in both groups (posture: P ≤ 0.001, group: P = 0.002, posture x group interaction: P = 0.57). The lower PETCO2 (known to enhance RoR) in the BHD may have minimized between‐group differences in RoR. The data suggest impaired dynamic cerebrovascular autoregulatory mechanisms in BHD.

Support or Funding Information

This research was supported by the National Sciences and Engineering Research Council of Canada.

This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.