Interrelationships Between Cerebrovascular Hemodynamics And Arterial Stiffness Across Sitting Interruption Conditions

Andrew M Koessler¹, Alexander Pomeroy¹, Jeb F Struder¹, Kristen M Paternoster¹, Christopher E Grice¹, Taylor Shorter¹, Craig Paterson¹,², Gaurav Dave¹, Bethany B Gibbs³, Feng-Chang Lin¹, Michelle L Meyer¹, Maihan B Vu¹, and Erik D Hanson, FACSM¹ 1 University of North Carolina at Chapel Hill, Chapel Hill, NC, USA 27599 2 University of Bristol, Bristol, UK, BS8 2PS 3 West Virginia University, Morgantown, WV, USA 260506  Prolonged sitting acutely increases central arterial stiffness and may impair cerebrovascular hemodynamics, yet direct systemic-cerebrovascular relationships remain unclear. Interrupting sitting may mitigate these effects, but whether changes in arterial stiffness directly translate to cerebrovascular responses is not established. PURPOSE: This study examined the relationships among middle cerebral artery velocity (MCAv), cerebrovascular conductance index (CVCi), carotid-femoral pulse wave velocity (cfPWV), and mean arterial pressure (MAP) across sitting interruption strategies, using partial correlation analyses to isolate associations independent of blood pressure. METHODS: 33 healthy adults (82% female, 46.6 ± 5.9 years, 88% white) completed 4 visits under different conditions: (1) 4h of uninterrupted sitting (control) and hourly (2) standing, (3) walking, and (4) combined standing/walking interruptions. After semi-recumbent rest, cfPWV was assessed and MAP was derived via pulse wave analysis. MCAv was measured using transcranial doppler ultrasound and CVCi was calculated by dividing MCAv by MAP. Measures were collected pre- and post- condition. Results were analyzed using partial correlations controlling for MAP where appropriate, with a secondary correlation between MCAv and MAP conducted based on prior evidence of an association. RESULTS: CVCi declined with prolonged sitting independent of condition (MD = -0.045, 95%CI [-0.079 - -0.011], p = 0.10), though it did not reach statistical significance, whereas MCAv and cfPWV did not change across time or condition (p > 0.05). No significant correlations were found between cfPWV and MCAv (r = -0.019, p = .802) or CVCi (r = -0.019, p = .795), when controlling for MAP. Additionally, MCAv was not associated with MAP (r = 0.097, p = .192). CONCLUSIONS: Acute changes in central arterial stiffness may not directly influence cerebrovascular hemodynamics in healthy adults. Additionally, MCAv showed no association with MAP, which may reflect the limited statistical power inherent to a feasibility study. Ongoing analyses will investigate this relationship in a larger sample size with additional vascular assessments.  FUNDING SOURCE: National Heart, Lung, and Blood Institute of the National Institutes of Health under Award Number R01HL157187.