Cerebrovascular Reserve: The Link Between Fitness and Cognitive Function
In this review article from the July 2012 issue of Exercise and Sport Sciences Reviews, the authors discuss recent evidence relating changes in cerebrovasculature function with cerebrovasculature reserve and the potential consequences for cognitive function (2). It has been recently demonstrated that higher levels of aerobic fitness in older individuals are associated with improved cognition, greater cerebrovascular conductance at rest, which is a measure of basal brain perfusion, and increased cerebrovascular reserve or the ability of the cerebral blood vessels to respond to stimuli. Data suggest that the association between fitness and cognition is mediated, at least in part, by processes that involve cerebral circulation. While the brain only makes up 2% of the body’s weight, it uses 15% of total cardiac output and up to 20% of the oxygen and nutrients supplied by the cardiovascular system. Owing to a high level of metabolism and a lack of energy stores, the brain relies on cerebral blood flow (CBF) being maintained. With advancing age, blood flow declines, and resting CBF decreases ∼4 mL·min·yr−1 after the third decade. This coincides with an increase in oxidative stress with age. Reactive oxygen species are believed to decrease nitric oxide (NO) bioavailability in the vasculature, leading to endothelial dysfunction. Reactive oxygen species-mediated inhibition of NO production is positively correlated with decreased basal cerebral perfusion. Although the decline in resting CBF associated with normal aging is not sufficient to cause major ischemic injury, it might result in hypoperfusion that could prevent sufficient nutrients from reaching areas of high metabolic need and in exacerbating age-associated degenerative changes. The article then reviews the currently available research supporting regular aerobic exercise as an effective method to enhance endothelial function (and thereby arterial compliance) and decrease arterial stiffness, oxidative stress, and vascular inflammation. Regular exercise leads to a number of favorable adaptations in the vascular system, including decreases in blood pressure and oxidative stress and increases in antioxidant activity, which all contribute to improved cerebrovascular function. The elevated levels of markers such as NO as a result of improved cerebrovascular reserve serve to promote neurogenesis, angiogenesis, and synaptogenesis, thereby potentially providing a substrate for preserving or even improving cognitive function. By elucidating these effects, the authors propose that exercise has the ability to maintain CBF, which, in turn, can theoretically protect cognition in the aging population. The authors suggest intervention studies as the next step to determine the extent to which cerebrovascular reserve might explain the association between increased fitness and improved cognition. If this is indeed confirmed in efficacy studies, the potential for physical fitness to prevent and/or delay cognitive decline and dementia through vascular-mediated mechanisms has enormous implications for both preventive and therapeutic strategies.
Bottom line: Better physical fitness in later life is positively associated with cognitive functioning. The data thus far suggest that this association is mediated in part by increases in brain perfusion and the ability of cerebral blood vessels to respond to demand.
Is Exercise a Viable Treatment for Depression?
This article in the July/August 2012 edition of ACSM’s Health & Fitness Journal® reviews the literature available supporting the use of exercise in the treatment of depression (1). With depression being a common disorder that is associated with compromised quality of life, increased health care costs, and greater risk for a variety of medical conditions, having exercise as a viable treatment alternative to frequently expensive medications and their associated adverse effects offers huge benefits to patients. With regard to the available exercise research, the authors acknowledge that, while many studies exist, they are limited by the fact that few studies have used high-quality methodologies in which treatment allocation is concealed, intention-to-treat analyses are used, a control group is included in the design, and depression is assessed by clinical interview in which the assessor is blinded to the treatment group. Several of the larger studies available are reviewed including the one Cochrane review where the primary analyses were limited to those trials comparing exercise treatment with no treatment or a control intervention (n = 25). Here they found large, clinically meaningful improvements associated with an exercise in comparison with controls (standardized mean difference (SMD) = −0.82, 95% confidence interval (CI) = −1.12 to −0.51). However, when the analyses were further limited to those trials using intention-to-treat analyses and blinded outcome assessment, the effect was slightly weaker, suggesting only a moderate antidepressant effect associated with exercise. In addition, when analyses were conducted among the five trials that collected long-term follow-up data, the effects of treatment were again slightly weaker, consistent with a moderate clinical improvement (SMD = −0.44, 95% CI = −0.71 to −0.18). Although the research becomes weaker when good-quality measures are put in place, the authors also then remind the reader that, in comparative studies, exercise is able to go head to head with other treatment modalities. The Mead meta-analysis examined several of these comparative effectiveness analyses, conducting sensitivity analyses of those trials comparing established treatments with exercise. Comparison with exercise and cognitive behavioral therapy showed no difference between exercise and cognitive therapy (SMD = −0.17, 95% CI = −0.51 to 0.18). An additional sensitivity analysis was conducted comparing the results of exercise compared with antidepressant medication. Only two studies, both from researchers at Duke University, compared the effectiveness of exercise with pharmacotherapy. No differences between exercise and antidepressant medication were noted (SMD = −0.04, 95% CI = −0.31 to 0.24). While limited studies exist as to the appropriate exercise “dose” for treatment of depression, data that are available suggest that higher intensity has a greater effect than lower intensity but that there is little difference between 3 d·wk−1 of exercise compared to 5 d·wk−1.
Bottom line: This is a concise review that includes methods for assessing depression, discusses current treatment approaches, evaluates the supporting evidence that aerobic exercise is an effective treatment option for patients with major depression, and offers practical suggestions for helping patients initiate and maintain exercise in their daily lives.
The author declares no conflict of interest and does not have any financial disclosures.
1. Blumenthal JA, Smith PJ, Hoffman B. Opinion and evidence: is exercise a viable treatment for depression? Health Fit. J. 2012; 16: 14–21.
2. Davenport MH, Hogan DB, Eskes GA, Longman RS, Poulin MJ. Cerebrovascular reserve: the link between fitness and cognitive function? Exerc. Sport Sci. Rev. 2012; 40: 153–158.