Cerebral pulsatility reflects a balance between the transmission and damping of pulsatility in the cerebrovasculature. Females experience greater cerebral pulsatility with aging which may have implications for sex differences in stroke risk and cognitive decline. This study sought to explore vascular contributors to cerebral pulsatility and pulsatile damping in men and women. 282 adults (53% female) underwent measurements of cerebral (middle cerebral artery) pulsatility, pulsatile damping (ratio of cerebral to carotid pulsatility), large artery stiffening (ratio of aortic to carotid pulse wave velocity), and carotid wave transmission/reflection dynamics using wave-intensity analysis. Multiple regression revealed older age, female sex, greater large artery stiffening, higher carotid pulse pressure, and greater forward wave energy was associated with increased cerebral pulsatility (adjusted R2=0.44, p<0.05). Contributors to decreased cerebral pulsatile damping included older age, female sex, and lower wave reflection index (adjusted R2=0.51, p<0.05). Our data link greater large artery stiffening, carotid pulse pressure, and forward wave energy to greater cerebral pulsatility, while greater carotid wave reflection may enhance cerebral pulsatile damping. Lower cerebral pulsatile damping among females may contribute to greater age-associated cerebral pulsatile burden compared to males.

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Arterial stiffness is associated with cerebral flow pulsatility. Arterial stiffness increases following acute resistance exercise (RE). Whether this acute RE-induced vascular stiffening affects cerebral pulsatility remains unknown. Purpose: To investigate the effects of acute RE on common carotid artery (CCA) stiffness and cerebral blood flow velocity (CBFv) pulsatility. Methods: Eighteen healthy men (22 ± 1 yr; 23.7 ± 0.5 kg·m−2) underwent acute RE (5 sets, 5-RM bench press, 5 sets 10-RM bicep curls with 90 s rest intervals) or a time control condition (seated rest) in a randomized order. CCA stiffness (β-stiffness, Elastic Modulus (Ep)) and hemodynamics (pulsatility index, forward wave intensity, and reflected wave intensity) were assessed using a combination of Doppler ultrasound, wave intensity analysis and applanation tonometry at baseline and 3 times post-RE. CBFv pulsatility index was measured with transcranial Doppler at the middle cerebral artery (MCA). Results: CCA β-stiffness, Ep and CCA pulse pressure significantly increased post-RE and remained elevated throughout post-testing (p < 0.05). No changes in MCA or CCA pulsatility index were observed (p > 0.05). There were significant increases in forward wave intensity post-RE (p < 0.05) but not reflected wave intensity (p > 0.05). Conclusion: Although acute RE increases CCA stiffness and pressure pulsatility, it does not affect CCA or MCA flow pulsatility. Increases in pressure pulsatility may be due to increased forward wave intensity and not pressure from wave reflections.

Acute HIC results in CCA constriction and increases in CCA stiffness along with increases in hemodynamic pulsatility. The increase in pulsatility may be due to a combination of increased forward wave intensity from increased LV contractility into a smaller vessel (i.e. impaired matching of diameter and flow) coupled with reduced LV suction.

Objective To investigate racial differences in central blood pressure and vascular structure/function as subclinical markers of atherosclerotic cardiovascular disease (CVD) in children. Study design This cross-sectional study recruited 54 African-American children (18 female, 36 male; age 10.5 ± 0.9) and 54 white children (27 female, 26 male; age 10.8 ± 0.9) from the Syracuse City community as part of the Environmental Exposures and Child Health Outcomes (EECHO) study. Participants underwent blood lipid and vascular testing on two separate days. Carotid artery intima-media thickness (IMT) and aortic stiffness were measured via ultrasonography and carotid-femoral pulse wave velocity (PWV), respectively. Blood pressure (BP) was assessed at the brachial artery and estimated in the carotid artery using applanation tonometry. Results African American children had significantly higher PWV (4.8 ± 0.8 m/s) compared with white children (4.2 ± 0.7 m/s; p<0.05) which remained significant after adjustment for confounding variables including socioeconomic status. African-American children had significantly higher IMT (African-American 0.41 ± 0.06, white 0.39 ± 0.05 mm), and carotid systolic BP (African-American 106 ± 11, white 102 ± 8 mmHg; p<0.05) compared with white children, although these racial differences were no longer present after covariate adjustments for height. Conclusions Racial differences in aortic stiffness are present in childhood. Our findings suggest that racial differences in subclinical CVD occur earlier than previously recognized.

The matching of oxygen supply to neural demand (i.e., neurovascular coupling (NVC)) is an important determinant of cognitive performance. The impact of hypoxia on NVC remains poorly characterized. NVC is partially modulated by nitric oxide (NO), which may initially decrease in hypoxia. This study investigated the effect of acute NO-donor (nitrate) supplementation on NVC and cognitive function in hypoxia. Twenty healthy men participated in this randomized, double-blind, crossover design study. Following normoxic cognitive/NVC testing, participants consumed either nitrate (NIT) or a NIT-depleted placebo (PLA). Participants then underwent 120 min of hypoxia (11.6% ± 0.1% O2) and all cognitive/NVC testing was repeated. NVC was assessed as change in middle cerebral artery (MCA) blood flow during a cognitive task (incongruent Stroop) using transcranial Doppler. Additional computerized cognitive testing was conducted separately to assess memory, executive function, attention, sensorimotor, and social cognition domains. Salivary nitrite significantly increased following supplementation in hypoxia for NIT (+2.6 ± 1.0 arbitrary units (AU)) compared with PLA (+0.2 ± 0.3 AU; p < 0.05). Memory performance (-6 ± 13 correct) significantly decreased (p < 0.05) in hypoxia while all other cognitive domains were unchanged in hypoxia for both PLA and NIT conditions (p > 0.05). MCA flow increased during Stroop similarly in normoxia (PLA +5 ± 6 cm·s(-1), NIT +7 ± 7 cm·s(-1)) and hypoxia (PLA +5 ± 9 cm·s(-1), NIT +6 ± 7 cm·s(-1)) (p < 0.05) and this increase was not altered by PLA or NIT (p > 0.05). In conclusion, acute hypoxia resulted in significant reductions in memory concomitant with preservation of executive function, attention, and sensorimotor function. Hypoxia had no effect on NVC. Acute NIT supplementation had no effect on NVC or cognitive performance in hypoxia.

These data suggest adults with treated HTN experience similar increases in aortic stiffness and cerebrovascular hemodynamic pulsatility during early recovery from acute aerobic exercise as their counterparts without HTN.

Hypertension accelerates brain aging, resulting in cognitive dysfunction with advancing age. Exercise is widely recommended for adults with hypertension to attenuate cognitive dysfunction. Whether acute exercise benefits cognitive function in this at-risk population is unknown. The purpose of this study was to compare the effects of acute aerobic exercise on cognitive function in 30 middle-aged hypertensive (HTN) and 30 age, sex, and body mass index (BMI)-matched non-HTN adults (56 ± 6 years, BMI 28.2 ± 2.9 kg/m2; 32 men). Subjects underwent cognitive testing pre/post 30-min cycling (≈55% peak oxygen consumption). Cognition was assessed using standard metrics of accuracy and reaction time (RT) across memory recognition, 2-back, and Flanker tasks. Behavioral data was further analyzed using drift-diffusion modeling to examine underlying components of decision-making (strength of evidence, caution, bias) and RT (non-decision time). Exercise elicited similar changes in cognitive function in both HTN and non-HTN groups (p > 0.05). Accuracy was unaltered for Flanker and 2-back tasks, while hits and false alarms increased for memory recognition post-exercise (p < 0.05). Modeling results indicated changes in memory hits/false alarms were due to significant changes in stimulus bias post-exercise. RT decreased for Flanker and memory recognition tasks and was driven by reductions in post-exercise non-decision time (p < 0.05). Our data indicate acute exercise resulted in similar, beneficial cognitive responses in both middle-age HTN and non-HTN adults, marked by unaltered task accuracy, and accelerated RT post-exercise. Additionally, drift-diffusion modeling revealed that beneficial acceleration of cognitive processing post-exercise (RT) is driven by changes in non-decision components (encoding/motor response) rather than the decision-making process itself.