Exercise Improves Vascular Function, but does this Translate to the Brain?

Jill N Barnes, Adam T Corkery, Jill N Barnes, Adam T Corkery

Abstract

The number of adults with Alzheimer's disease (AD) or related dementia is expected to increase exponentially. Interventions aimed to reduce the risk and progression of AD and dementia are critical to the prevention and treatment of this devastating disease. Aging and cardiovascular disease risk factors are associated with reduced vascular function, which can have important clinical implications, including brain health. The age-associated increase in blood pressure and impairment in vascular function may be attenuated or even reversed through lifestyle behaviors. Greater volumes of habitual exercise and higher cardiorespiratory fitness are associated with beneficial effects on vascular health and cognition. Exercise and cardiorespiratory fitness may be most important during midlife, as physical activity and cardiorespiratory fitness during the middle-aged years are associated with future cognitive function. The extent to which exercise, and more specifically aerobic exercise, influences the cerebral circulation is not well established. In this review, we present our working hypothesis showing how cerebrovascular function may be a mediating factor underlying the association between exercise and cognition, as well as discuss recent studies evaluating the effect of exercise interventions on the cerebral circulation.

Keywords: Physical activity; blood flow; blood pressure; blood vessels; cognition.

Figures

Fig. 1.
Fig. 1.
The relationship between cardiorespiratory fitness (VO2max) and aortic pulse wave velocity (PWV), a measure of central arterial stiffness, in 53 healthy women. Adapted with permission from Tanaka, et al. [85].
Fig. 2.
Fig. 2.
The relationship between cardiorespiratory fitness (VO2max) and cerebrovascular function (CVRCO2) in older adults as a function of exercise training status. CVRCO2 indicates cerebral vasodilator responses to carbon dioxide. Adapted with permission from Bailey, et al. [114].
Fig. 3.
Fig. 3.
Scanning electron micrographs comparing cerebrovascular microstructure of sedentary and exercised middle-aged mice. A) Low magnification images of the middle cerebral artery (MCA) (single arrow) with branch (double arrow) in a sedentary (left) and exercised (right) mouse. Arteries are distinguished from veins (arrowhead) by the distinct impressions made by their endothelial cell nuclei (ECN). B) High magnification images of ECN imprints from the MCA in a sedentary (left) and exercised (right) mouse. C and D) Exercise increased the area of ECN in the MCA and its associated branches. *p < 0.005, t-test. Adapted with permission from Latimer, et al. [128].
Fig. 4.
Fig. 4.
Our working hypothesis showing that aging is associated with an adverse cardiovascular profile, including increased blood pressure, arterial stiffness, and endothelial dysfunction, which could all contribute to cerebrovascular dysfunction, and ultimately, cognitive decline. Individuals at elevated risk of cognitive decline may experience “accelerated aging”. Aerobic exercise appears to attenuate vascular aging and may be directly or indirectly associated with preserved cerebrovascular function throughout the lifespan. Solid lines represent mechanisms with strong support from the literature. Dashed lines represent mechanisms that require further research to be definitively established.

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Source: PubMed

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