Cerebrovascular adaptations to habitual resistance exercise with aging.

Resistance training (RT) is associated with improved metabolism, bone density, muscular strength, and lower risk of osteoporosis, sarcopenia, and cardiovascular disease. Although RT imparts many physiological benefits, cerebrovascular adaptations to chronic RT are not well defined. Participation in RT is associated with greater resting peripheral arterial diameters, improved endothelial function, and general cardiovascular health, whereas simultaneously linked to reductions in central arterial compliance. Rapid blood pressure fluctuations during resistance exercise, combined with reduced arterial compliance, could lead to cerebral microvasculature damage and subsequent cerebral hypoperfusion. Reductions in cerebral blood flow (CBF) accompany normal aging, where chronic reductions in CBF are associated with changes in brain structure and function, and increased risk of neurodegeneration. It remains unclear whether reductions in arterial compliance with RT relate to subclinical cerebrovascular pathology, or if such adaptations require interpretation in the context of RT specifically. The purpose of this narrative review is to synthesize literature pertaining to cerebrovascular adaptations to RT at different stages of the life span. This review also aims to identify gaps in the current understanding of the long-term impacts of RT on cerebral hemodynamics and provide a mechanistic rationale for these adaptations as they relate to aging, cerebral vasculature, and overall brain health.

Cerebral haemodynamics during arrhythmia in health, ischaemic heart disease and heart failure with reduced ejection fraction, and in a preclinical swine model.

Ventricular arrhythmias are associated with neurological impairment and could represent a source of cerebral hypoperfusion. In the present study, data from healthy individuals (n = 11), patients with ischaemic heart disease (IHD; ejection fraction >40%; n = 9) and patients with heart failure with reduced ejection fraction (HFrEF; EF = 31 (5)%, n = 11), as well as data from swine surgeries, where spontaneous ventricular arrhythmias were observed during cerebrovascular examination (transcranial Doppler ultrasound in humans and laser Doppler in swine) were analysed retrospectively to investigate the effect of arrhythmia on cerebral microvascular haemodynamics. A subset of participants also completed the Montreal Cognitive Assessment (MoCA). Middle cerebral artery mean blood velocity (MCAVmean ) decreased during premature ventricular contraction (PVC) in all groups, and data from swine indicate PVCs reduced cerebral microvascular perfusion. Overall MCAVmean was decreased in the HFrEF vs. control group. Further, %∆MCAVmean /%∆mean arterial pressure during the PVC was greater in the HFrEF vs. control group and was correlated with decreased MoCA scores. Subanalysis of HFrEF data revealed that during bigeminy MCAVmean decreased owing to reductions during irregular beats only. During non-sustained ventricular tachycardia, MCAVmean decreased but recovered above baseline upon return to sinus rhythm. Also, haemodynamic perturbations during and following the PVC were greater in the brachial artery vs. the MCA. Therefore, ventricular arrhythmias decreased indices of cerebral perfusion irrespective of IHD or HFrEF. The relative magnitude of arrhythmia-induced haemodynamic perturbations appears to be population specific and arrhythmia type and organ dependent. The cumulative burden of arrhythmia-induced deficits may exacerbate existing cerebral hypoperfusion in HFrEF and contribute to neurological abnormalities in this population. KEY POINTS: Irregular heartbeats are often considered benign in isolation, but individuals who experience them frequently have a higher prevalence of cerebrovascular and/or cognitive associated disorders. How irregular heartbeats affect blood pressure and cerebral haemodynamics in healthy and cardiovascular disease patients, those with and without reduced ejection fraction, remains unknown. Here it was found that in the absence of symptoms associated with irregular heartbeats, such as dizziness or hypotension, single, multiple non-sustained and sustained irregular heartbeats influence cerebral haemodynamics in a population-specific, arrhythmia-type and organ-dependent manner. Relative deficits in the index of cerebral blood flow normalized to relative deficits in blood pressure were greatest in patients with heart failure with reduced ejection and inversely related with cognitive performance. Chronic arrhythmias may exacerbate existing cerebral hypoperfusion in heart failure with reduced ejection fraction, thereby providing a mechanistic link between otherwise benign irregular heartbeats and cognitive dysfunction, independent of embolism.

Association of Arterial Stiffness Index and Brain Structure in the UK Biobank: A 10-Year Retrospective Analysis.

Arterial stiffening and changes in brain structure both occur with normal aging and can be exacerbated via acquired health conditions. While cross-sectional associations exist, the longitudinal relationship between arterial stiffness and brain structure remains unclear. In this study, we investigated 1) associations between baseline arterial stiffness index (ASI) and brain structure (global and regional grey matter volumes (GMV), white matter hyperintensities (WMH)) 10-years post-baseline (10.4±0.8 years) and 2) associations between the 10-year change in ASI from baseline and brain structure 10-years post-baseline in 650 healthy middle- to older-aged adults (53.4±7.5 years) from the UK Biobank. We observed significant associations between baseline ASI and GMV (p<0.001) and WMH (p=0.0036) 10-years post-baseline. No significant associations between 10-year change in ASI and brain structure (global GMV p=0.24; WMH volume p=0.87) were observed. There were significant associations of baseline ASI in 2 of 60 regional brain volumes analyzed (right posterior superior temporal gyrus p=0.001; left superior lateral occipital cortex p<0.001). Strong associations with baseline ASI, but not changes in ASI over 10-years, suggest arterial stiffness at the entry point of older adulthood is more impactful on brain structure 10-years later compared to age-related stiffening. Based on these associations, we suggest clinical monitoring and potential intervention for reducing arterial stiffness should occur in midlife to reduce vascular contributions to structural changes in the brain, supporting a healthy trajectory of brain aging. Our findings also support use of ASI as a surrogate for gold standard measures in showing overall relationships between arterial stiffness and brain structure.

What are the effects of acute exercise and exercise training on cerebrovascular hemodynamics following stroke? A systematic review and meta-analysis.

Limited data exist regarding the effects of acute exercise and exercise training on cerebrovascular hemodynamic variables after stroke. This systematic review and meta-analysis 1) examined the effects of acute exercise and exercise training on cerebrovascular hemodynamic variables reported in the stroke exercise literature and 2) synthesized the peak middle cerebral artery blood velocity (MCAv) achieved during an acute bout of moderate-intensity exercise in individuals after stroke. Six databases (Medline, Embase, Web of Science, CINAHL, PsycINFO, AMED) were searched from inception to December 1st, 2021 for studies that examined the effect of acute exercise or exercise training on cerebrovascular hemodynamics in adults after stroke. Two reviewers conducted title and abstract screening, full-text evaluation, data extraction, and quality appraisal. Random-effects models were used in meta-analysis. Nine studies, including four acute exercise (n = 61) and five exercise training studies (n = 193), were included. Meta-analyses were not statistically feasible for several cerebrovascular hemodynamic variables. Descriptive analysis reveals that exercise training may increase cerebral blood flow and cerebrovascular reactivity to carbon dioxide among individuals after stroke. Meta-analysis of three acute exercise studies revealed no significant changes in MCAv during acute moderate-intensity exercise [n = 48 participants, mean difference = 5.2 cm/s, 95% confidence interval (CI) [-0.6, 11.0], P = 0.08] compared with resting MCAv values. This review suggests that individuals after stroke may have attenuated cerebrovascular hemodynamics as measured by the MCAv during acute moderate-intensity exercise. Aerobic exercise training is beneficial for improving cardiovascular health and function after stroke; higher-quality research utilizing agreed-upon hemodynamic variables is needed to synthesize the effects of exercise training on poststroke cerebrovascular hemodynamics.