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Exercise and Hypercapnia Differentially Modify Ratios of Extracranial and Intracranial Pulsatility
Author(s) -
DuBose Noah,
Ainslie Philip N.,
Sherman Sara R.,
Baynard Tracy,
Hoiland Ryan,
Smith Kurt J.,
Green Daniel J.
Publication year - 2022
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2022.36.s1.r5027
Subject(s) - pulsatile flow , cardiology , middle cerebral artery , medicine , hypercapnia , hemodynamics , cerebral arteries , cerebral autoregulation , internal carotid artery , cerebral blood flow , anterior cerebral artery , anesthesia , blood pressure , ischemia , autoregulation , respiratory system
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 (CO 2 ; F I CO 2 :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 CO 2 (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.