Exercise, cognitive function, and aging

Abstract

Increasing the lifespan of a population is often a marker of a country's success. With the percentage of the population over 65 yr of age expanding, managing the health and independence of this population is an ongoing concern. Advancing age is associated with a decrease in cognitive function that ultimately affects quality of life. Understanding potential adverse effects of aging on brain blood flow and cognition may help to determine effective strategies to mitigate these effects on the population. Exercise may be one strategy to prevent or delay cognitive decline. This review describes how aging is associated with cardiovascular disease risks, vascular dysfunction, and increasing Alzheimer's disease pathology. It will also discuss the possible effects of aging on cerebral vascular physiology, cerebral perfusion, and brain atrophy rates. Clinically, these changes will present as reduced cognitive function, neurodegeneration, and the onset of dementia. Regular exercise has been shown to improve cognitive function, and we hypothesize that this occurs through beneficial adaptations in vascular physiology and improved neurovascular coupling. This review highlights the potential interactions and ideas of how the age-associated variables may affect cognition and may be moderated by regular exercise.

Keywords: brain; cardiovascular; physical activity; physiology.

Fig. 1.

Estimated number of Alzheimer's disease (AD) cases that could be prevented worldwide (A) or in the United States only (B) by a risk factor reduction of 10% or 25%. The risk factor reduction was estimated by multiplying present prevalence by 0.90 and 0.75, respectively, and subtracting the revised number of attributable cases from the original number. [This image is originally from Barnes and Yaffe (6) and used with permission.]

Fig. 2.

Modified version of the hypothetical model proposed by de la Torre (15). Cardiovascular disease risk factors, and more specifically vascular dysfunction, disrupt hemodynamics, which may cause either hypoperfusion or hyperperfusion and ultimately affect cognition. MMSE, mini-mental state examination. [This image is modified from de la Torre with permission (15).]

Fig. 3.

Age-associated reductions in cerebrovascular function. A: the increase in middle cerebral artery velocity (MCAv) relative to the stepped increases in end-tidal CO₂ (ETCO2) is greater in young healthy adults (age: 18–35 yr) compared with older healthy adults (age: 58–76 yr). The slope of the line indicates cerebrovascular reactivity. B: cerebrovascular reactivity is significantly lower in older healthy adults compared with young healthy adults. *P < 0.05. [This image is modified from Barnes et al. (7).]

Fig. 4.

There is a disconnect between AD pathology and clinical cognitive severity, which is moderated by cognitive reserve. Cognitive reserve is the idea that the brain tolerates structural AD pathology without a significant change in cognitive function. AD pathology ranges from mild to moderate. Individuals with high cognitive reserve may have moderate AD pathology, but they have not yet reached the diagnostic threshold to be considered demented. On the other hand, individuals with low cognitive reserve may be beyond the diagnostic threshold, despite mild AD pathology. MCI, mild cognitive impairment. [This image is originally from Stern et al. (48) and is used with permission.]

Fig. 5.

The potential interactions and ideas of how variables associated with aging may interact to affect cognition and how exercise may inhibit this process. The solid arrows indicate interactions backed by research, and the dotted arrows indicate potential interactions with less research focused on the association. CVD, cerebrovascular disease.