(555.24) Exercise and Hypercapnia Differentially Modify Ratios of Extracranial and Intracranial Pulsatility
Sunday, April 3, 2022
10:15 AM – 12:15 PM
Location: Exhibit/Poster Hall A-B - Pennsylvania Convention Center
Poster Board Number: E84
Noah DuBose (University of Illinois at Chicago), Philip Ainslie (University of British Columbia), Sara Sherman (University of Illinois at Chicago), Tracy Baynard (University of Illinois at Chicago), Ryan Hoiland (University of British Columbia), Kurt Smith (University of Victoria), Daniel Green (University of Western Australia)
Presenting Author University of Illinois at Chicago
Introduction: Damping of pulsatile flow between extracranial and intracranial cerebral arteries is an essential allostatic mechanism protecting cerebral microvessels from recalcitrant hemodynamics. The ratio of pulsatility between proximal and distal cerebral arteries may provide a measure of cerebrovascular hemodynamic damping. This might prove useful as an evaluation of cerebrovascular regulation in response to pulsatile perturbations.
Purpose: To characterize cerebral pulsatile damping between extracranial and intracranial environments in response to perturbations eliciting matched shear stress, such as exercise and hypercapnia.
Methods: Participants (n=10) completed two 30-min experimental conditions aimed at matching cerebral artery shear stress, each separated by 48 hrs: (1) mild hypercapnia (CO2; FICO2:0.045) and (2) submaximal cycling (EX; 60%HRreserve). Cerebral pulsatility index (PI: (systolic velocity-diastolic velocity)/mean velocity)) was assessed at baseline, during, and following each condition in the internal carotid artery (ICA) and middle cerebral artery (MCA) using Doppler ultrasound. Heart rate (HR) and blood pressure (BP) were assessed continuously using ECG and photoplethysmography, respectively. Cerebral pulsatile damping was calculated: (ICA PI / MCA PI) to investigate ratios of cerebral pulsatile hemodynamics between extracranial and intracranial arteries.
Results: Cerebral pulsatile damping was greater during CO2 (1.66 ± 0.31) than EX (1.22 ± 0.35) (time*condition effect, p=0.002). The change in cerebral pulsatile damping was related to the change in heart rate (r = -0.70, p = 0.04), but not BP between baseline and the experimental conditions.
Conclusions: As evidenced by the response in cerebral pulsatile damping, exercise and hypercapnia result in different ratios of extracranial to intracranial pulsatility despite inducing similar vasodilation when shear stress was matched. This might in part be explained by differences in HR between conditions. Further research is important to elucidate the mechanisms behind the deviance in hemodynamic responses.
