Aging reduces cerebral blood flow regulation following an acute hypertensive stimulus

Rosenberg, Alexander J.; Schroeder, Elizabeth; Grigoriadis, Georgios; Wee, Sang Ouk; Bunsawat, Kanokwan; Heffernan, Kevin S.; Fernhall, Bo; Baynard, Tracy

doi:10.1152/japplphysiol.00137.2019

Cited by 19 publications

(14 citation statements)

References 58 publications

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“…This is in line with the findings of De Heus et al ( 2018 ), who reported a lower (better) %MCAv response for a given change in blood pressure in MCI compared to control, which is suggestive of maintained cerebral autoregulation in MCI. Our group (Klein et al 2020 ) and others (Rosenberg et al 2020 ) have recently suggested that higher arterial stiffness leads to the greater transmission of pulsatile blood velocity in healthy older adults. We observed that higher pressure-responsiveness in the control group was positively associated with systemic pressure augmentation (AIx) in this study.…”

Section: Discussionmentioning

confidence: 78%

Cerebrovascular function and its association with systemic artery function and stiffness in older adults with and without mild cognitive impairment

et al. 2022

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Purpose Our aim was to compare cerebrovascular and systemic vascular function between older adults with and without mild cognitive impairment (MCI), and to determine which measures of vascular function best predict the presence of MCI. Methods In 41 adults with MCI and 33 adults without MCI (control) we compared middle cerebral artery velocity (MCAv) and cerebrovascular pulsatility index (PI) at rest, cerebrovascular reactivity to CO2, and responsiveness to changes in blood pressure (%∆MCAv/%∆MAP). Systemic vascular function was assessed by flow-mediated dilation (FMD) and stiffness by pulse wave velocity (PWV). Results Cerebrovascular PI was higher in MCI compared with control (mean ± SD: 1.17 ± 0.27 vs. 1.04 ± 0.21), and MCI exhibited a lower %∆MCAv/%∆MAP (1.26 ± 0.44 vs. 1.50 ± 0.55%). Absolute (p = 0.76) and relative cerebrovascular reactivity to CO2 (p = 0.34) was similar between MCI and control. When age was included as a covariate the significant difference in cerebral PI between groups was lost. PWV was higher (13.2 ± 2.2 vs. 11.3 ± 2.5 m s−1) and FMD% (4.41 ± 1.70 vs. 5.43 ± 2.15%) was lower in MCI compared with control. FMD% was positively associated with PI across the cohort. Logistic regression analysis indicated that FMD and PWV significantly discriminated between MCI and controls, independent of age, whereas the inclusion of cerebrovascular measures did not improve the predictive accuracy of the model. Conclusion These findings raise the possibility that early changes in systemic vascular stiffness and endothelial function may contribute to altered cerebrovascular haemodynamics and impaired cognitive function, and present potential targets for prevention and treatment strategies in people with MCI.

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Section: Discussionmentioning

confidence: 78%

Cerebrovascular function and its association with systemic artery function and stiffness in older adults with and without mild cognitive impairment

et al. 2022

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“…Vessel reactivity, assessed by CO 2 ‐challenge in MRI and positron emission tomography (PET), shows widespread age‐related reduction (Ito et al., 2001; Lu et al., 2011). These in vivo findings are supported by histological observations that aging is associated with vascular stiffness, necrosis of vascular smooth muscle, thickening of basement membrane, venous collagenosis, increased tortuosity and “blind‐ends” in vessel morphometry, providing microscopic evidence that vessel reactivity declines with aging (Fabiani, Low, et al., 2014; Fang, 1976; Rosenberg et al, 2020; see Abdelkarim et al., 2019; D'Esposito et al., 2003; Tsvetanov et al., 2021; for reviews).…”

Section: Current Neurocognitive Aging Theories and Their Predictionsmentioning

confidence: 72%

The neural–vascular basis of age‐related processing speed decline

et al. 2021

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Most studies examining neurocognitive aging are based on the blood‐oxygen level‐dependent signal obtained during functional magnetic resonance imaging (fMRI). The physiological basis of this signal is neural–vascular coupling, the process by which neurons signal cerebrovasculature to dilate in response to an increase in active neural metabolism due to stimulation. These fMRI studies of aging rely on the hemodynamic equivalence assumption that this process is not disrupted by physiologic deterioration associated with aging. Studies of neural–vascular coupling challenge this assumption and show that neural–vascular coupling is closely related to cognition. In this review, we put forward a theory of processing speed decline in aging and how it is related to age‐related neural–vascular coupling changes based on the results of studies elucidating the relationships between cognition, cerebrovascular dynamics, and aging.

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“…For instance, long-term, 1 m/s increase in cfPWV is associated with a 14-15% increase in cardiovascular events (Vlachopoulos et al, 2010). Acutely, among older adults with and without hypertension, transiently increased cfPWV is associated with cerebrovascular pulsatility (Lefferts et al, 2018;Rosenberg et al, 2020) and end-organ damage (Keith et al, 2013) following an acute bout of aerobic exercise. Prolonged exposure to elevated cfPWV may transmit pulsatile flow to the cerebrovasculature and increase the risk of cerebrovascular events in aging populations (Rosenberg et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

“…Acutely, among older adults with and without hypertension, transiently increased cfPWV is associated with cerebrovascular pulsatility (Lefferts et al, 2018;Rosenberg et al, 2020) and end-organ damage (Keith et al, 2013) following an acute bout of aerobic exercise. Prolonged exposure to elevated cfPWV may transmit pulsatile flow to the cerebrovasculature and increase the risk of cerebrovascular events in aging populations (Rosenberg et al, 2020). It is possible that individuals with preexisting cardiovascular risk factors may be sensitive to sustained elevations in pulsatility through arterial stiffness acutely after exercise.…”

Section: Discussionmentioning

confidence: 99%

Prolonged Elevation of Arterial Stiffness Following Peak Aerobic Exercise in Individuals With Chronic Stroke

et al. 2021

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BackgroundStroke is a highly disabling condition and is the second leading cause of death globally. Engaging in aerobic exercise is important for the prevention of a recurrent stroke through improving markers of cardiovascular health such as blood pressure and arterial stiffness. While higher intensities of aerobic exercise generally elicit greater cardioprotective effects, little is known about the acute cardiovascular effects of a single session of high intensity aerobic exercise in people with stroke. The objective of this study was to model the recovery of arterial stiffness (carotid-femoral pulse wave velocity, cfPWV), heart rate and blood pressure following peak intensity aerobic exercise in individuals with chronic stroke.MethodsTen participants with chronic stroke (mean ± SD age = 56.9 ± 11.8 years, median [IQR] years post-stroke = 2.9 [1.9]) performed a symptom-limited cardiopulmonary exercise test (CPET) on a recumbent stepper. Before the CPET, resting cfPWV, heart rate and blood pressure were measured. Immediately following the CPET, all outcomes were measured again continuously for 20 min to use all available observations (n = 245 observations) and capture any potential non-linear changes. Mixed model analyses were then applied to model post-exercise changes of cfPWV, heart rate and blood pressure.ResultsCarotid-femoral pulse wave velocity was increased from rest following the CPET (9.0 ± 0.53 to 9.9 ± 0.52 m/s, p < 0.001) and remained elevated for 20 min into post-exercise recovery, independent of heart rate (p = 0.001). Heart rate also increased from baseline (71.2 ± 3.2 to 77.4 ± 3.1 bpm, p < 0.001) and remained elevated for 10 min post-exercise (p < 0.001). Finger systolic blood pressure was reduced from rest (117.3 ± 4.7 to 111.8 ± 4.6 mmHg, p < 0.001) and remained reduced for 15 min after exercise (p < 0.001). There were no significant differences in finger diastolic or mean arterial pressures from rest.ConclusionThis was the first study to capture continuous changes in cfPWV following peak aerobic exercise in any clinical population. The present study revealed that cfPWV is elevated for 20 min after peak aerobic exercise in individuals with stroke, which was independent of heart rate. These findings suggest there may be autonomic imbalances in large arteries following peak intensity aerobic exercise in individuals with stroke.

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Aging reduces cerebral blood flow regulation following an acute hypertensive stimulus

Cited by 19 publications

References 58 publications

Cerebrovascular function and its association with systemic artery function and stiffness in older adults with and without mild cognitive impairment

Cerebrovascular function and its association with systemic artery function and stiffness in older adults with and without mild cognitive impairment

The neural–vascular basis of age‐related processing speed decline

Prolonged Elevation of Arterial Stiffness Following Peak Aerobic Exercise in Individuals With Chronic Stroke

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