Andrew Sherwood

Aerobic Exercise and Neurocognitive Performance: A Meta-analytic Review of Randomized Controlled Trials

Objectives: To assess the effects of aerobic exercise training on neurocognitive performance. Although the effects of exercise on neurocognition have been the subject of several previous reviews and meta-analyses, they have been hampered by methodological shortcomings and are now outdated as a result of the recent publication of several large-scale, randomized, controlled trials (RCTs). Methods: We conducted a systematic literature review of RCTs examining the association between aerobic exercise training on neurocognitive performance between January 1966 and July 2009. Suitable studies were selected for inclusion according to the following criteria: randomized treatment allocation; mean age ≥18 years of age; duration of treatment >1 month; incorporated aerobic exercise components; supervised exercise training; the presence of a nonaerobic-exercise control group; and sufficient information to derive effect size data. Results: Twenty-nine studies met inclusion criteria and were included in our analyses, representing data from 2049 participants and 234 effect sizes. Individuals randomly assigned to receive aerobic exercise training demonstrated modest improvements in attention and processing speed (g = 0.158; 95% confidence interval [CI]; 0.055–0.260; p = .003), executive function (g = 0.123; 95% CI, 0.021–0.225; p = .018), and memory (g = 0.128; 95% CI, 0.015–0.241; p = .026). Conclusions: Aerobic exercise training is associated with modest improvements in attention and processing speed, executive function, and memory, although the effects of exercise on working memory are less consistent. Rigorous RCTs are needed with larger samples, appropriate controls, and longer follow-up periods. ITT = intention-to-treat; RCT = randomized controlled trial.

Exercise and Pharmacotherapy in the Treatment of Major Depressive Disorder

Objective: To assess whether patients receiving aerobic exercise training performed either at home or in a supervised group setting achieve reductions in depression comparable to standard antidepressant medication (sertraline) and greater reductions in depression compared to placebo controls. Methods: Between October 2000 and November 2005, we performed a prospective, randomized controlled trial (SMILE study) with allocation concealment and blinded outcome assessment in a tertiary care teaching hospital. A total of 202 adults (153 women; 49 men) diagnosed with major depression were assigned randomly to one of four conditions: supervised exercise in a group setting; home-based exercise; antidepressant medication (sertraline, 50–200 mg daily); or placebo pill for 16 weeks. Patients underwent the structured clinical interview for depression and completed the Hamilton Depression Rating Scale (HAM-D). Results: After 4 months of treatment, 41% of the participants achieved remission, defined as no longer meeting the criteria for major depressive disorder (MDD) and a HAM-D score of <8. Patients receiving active treatments tended to have higher remission rates than the placebo controls: supervised exercise = 45%; home-based exercise = 40%; medication = 47%; placebo = 31% (p = .057). All treatment groups had lower HAM-D scores after treatment; scores for the active treatment groups were not significantly different from the placebo group (p = .23). Conclusions: The efficacy of exercise in patients seems generally comparable with patients receiving antidepressant medication and both tend to be better than the placebo in patients with MDD. Placebo response rates were high, suggesting that a considerable portion of the therapeutic response is determined by patient expectations, ongoing symptom monitoring, attention, and other nonspecific factors. BDI = Beck Depression Inventory; CI = confidence interval; HAM-D = Hamilton Depression Rating Scale; ITT = intention-to-treat; MDD = major depressive disorder; SD = standard deviation; SSRIs = selective serotonin reuptake inhibitors; TSH = thyroid stimulating hormone.

Effects of the DASH diet alone and in combination with exercise and weight loss on blood pressure and cardiovascular biomarkers in men and women with high blood pressure: the ENCORE study.

BACKGROUND Although the DASH (Dietary Approaches to Stop Hypertension) diet has been shown to lower blood pressure (BP) in short-term feeding studies, it has not been shown to lower BP among free-living individuals, nor has it been shown to alter cardiovascular biomarkers of risk. OBJECTIVE To compare the DASH diet alone or combined with a weight management program with usual diet controls among participants with prehypertension or stage 1 hypertension (systolic BP, 130-159 mm Hg; or diastolic BP, 85-99 mm Hg). DESIGN AND SETTING Randomized, controlled trial in a tertiary care medical center with assessments at baseline and 4 months. Enrollment began October 29, 2003, and ended July 28, 2008. PARTICIPANTS Overweight or obese, unmedicated outpatients with high BP (N = 144). INTERVENTIONS Usual diet controls, DASH diet alone, and DASH diet plus weight management. OUTCOME MEASURES The main outcome measure is BP measured in the clinic and by ambulatory BP monitoring. Secondary outcomes included pulse wave velocity, flow-mediated dilation of the brachial artery, baroreflex sensitivity, and left ventricular mass. RESULTS Clinic-measured BP was reduced by 16.1/9.9 mm Hg (DASH plus weight management); 11.2/7.5 mm (DASH alone); and 3.4/3.8 mm (usual diet controls) (P < .001). A similar pattern was observed for ambulatory BP (P < .05). Greater improvement was noted for DASH plus weight management compared with DASH alone for pulse wave velocity, baroreflex sensitivity, and left ventricular mass (all P < .05). CONCLUSION For overweight or obese persons with above-normal BP, the addition of exercise and weight loss to the DASH diet resulted in even larger BP reductions, greater improvements in vascular and autonomic function, and reduced left ventricular mass. CLINICAL TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00571844.

Social support and coronary heart disease: epidemiologic evidence and implications for treatment.

Objective: The present paper reviews theories of social support and evidence for the role of social support in the development and progression of coronary heart disease (CHD). Methods: Articles for the primary review of social support as a risk factor were identified with MEDLINE (1966–2004) and PsychINFO (1872–2004). Reviews of bibliographies also were used to identify relevant articles. Results: In general, evidence suggests that low social support confers a risk of 1.5 to 2.0 in both healthy populations and in patients with established CHD. However, there is substantial variability in the manner in which social support is conceptualized and measured. In addition, few studies have simultaneously compared differing types of support. Conclusions: Although low levels of support are associated with increased risk for CHD events, it is not clear what types of support are most associated with clinical outcomes in healthy persons and CHD patients. The development of a consensus in the conceptualization and measurement of social support is needed to examine which types of support are most likely to be associated with adverse CHD outcomes. There also is little evidence that improving low social support reduces CHD events. AMI = acute myocardial infarction; ANS = autonomic nervous system; CHD = coronary heart disease; ENRICHD = Enhancing Recovery in Coronary Heart Disease; HPA = hypothalamic pituitary adrenal; SES = socioeconomic status; SNS = sympathetic nervous system.

Gender differences in blood pressure control during a variety of behavioral stressors.

&NA; This study assessed gender differences in hemodynamic response patterns to behavioral stressors. In addition, the extent to which gender differences in cardiovascular reactivity were a function of the type of challenge was determined by employing tasks relying on stereotypically male areas of competence and a task relying on stereotypically female areas of competence. Sixteen female and 15 male graduate, medical or dental students were exposed to two speech tasks and two math tasks. While there were no significant differences in blood pressure reactivity between the genders, females exhibited significantly greater cardiac output increases across all tasks than males, while males tended to respond with greater increases in total peripheral resistance compared with females. Furthermore, during two of the tasks, significantly more females were classified as myocardial hyperreactors (based on increases in cardiac output), while significantly more males were vascular hyperreactors (based on increases in total peripheral resistance). A post hoc analysis also indicated an apparent association between oral contraceptive use and higher cardiovascular reactivity among the females tested. This association may have been a consequence of the decision to test all women during days 10 to 14 of the menstrual cycle when reactivity in women not using oral contraceptives may be suppressed.

Nighttime blood pressure dipping: The role of the sympathetic nervous system

There is a marked diurnal variation in blood pressure (BP), with BP dipping to its lowest levels during nighttime sleep. A day-night dip in systolic BP (SBP) of <10% has been used to characterize individuals as nondippers, and is associated with an increased risk for cardiovascular disease. The present study examined the contribution of the sympathetic nervous system (SNS) to BP dipping in a biracial sample of 172 men and women aged 25 to 45 years. Assessments included 24-h ambulatory BP monitoring and both waking and sleeping urinary catecholamines. In addition, cardiovascular alpha- and beta-adrenergic receptor (AR) responsiveness was determined by the doses of isoproterenol and phenylephrine required to attain an increase in heart rate of 25 points (CD25) and BP (PD25), respectively. Compared with dippers (n = 116), nondippers (n = 56) were more likely to be African American and to have a family history of hypertension as well as a higher body mass index (BMI). The nighttime fall in both norepinephrine (NE) and epinephrine (EPI) excretion rates was reduced in nondippers compared with dippers (NE dip 9.3 v 13.1 microg/mg; EPI dip 2.7 v 4.0 microg/mg; both P < .05). Nondippers also were characterized by heightened alpha1-AR responsiveness compared with dippers (PD25 = 252 v 321 microg, P < .05). These data suggest that the SNS may contribute to individual differences in nighttime BP dipping, and appears to account in part for blunted BP dipping in African Americans.

High stress responsivity predicts later blood pressure only in combination with positive family history and high life stress.

High cardiovascular responsivity to stressors has not consistently improved prediction of later blood pressure increases beyond the predictive effects of baseline pressure. Animal models suggest that genetic susceptibility to hypertension and frequent stress exposure are important modulating factors in stress-related hypertension. Thus in 103 men originally tested at age 18 to 22 years and reassessed 10 years later, interactive effects of genetic susceptibility (defined as 1 or more hypertensive parents) with high stress responsivity (defined as top 25% on the basis of blood pressure and cardiac responses during both reaction time and cold pressor tasks) were examined in relation to follow-up systolic and diastolic levels and to change in blood pressure status from normal (diastolic<80 mm Hg) to marginally elevated (diastolic 85 to 95 mm Hg). Men with the combination of high stress response and hypertensive parents demonstrated higher systolic (P<0.05) and diastolic levels (P<0.05) at follow-up, and they showed a 7-fold increase (7.5, 95% confidence intervals 2.3, 24.3; P<0.001) in relative risk of change in blood pressure status versus men with no family history and a 3-fold increase (3.8, confidence intervals 1.5, 9.6; P<0.004) versus less stress-responsive men who also had hypertensive parents. In 65 men who also provided ratings of daily stress, family historyxstress responsivityxdaily stress interactions were significant in predicting follow-up systolic and diastolic levels (P<0.006 and 0.03, respectively), with highest pressure levels seen when high life stress was reported by high stress responders and/or men with hypertensive parents. In conclusion, results suggest that stress responsivity as a long-term predictor is modulated by both genetic and environmental factors.

Cardiovascular responses to an active coping challenge as predictors of blood pressure patterns 10 to 15 years later.

&NA; To assess the long‐term predictive importance of high cardiovascular reactivity in relation to subsequent blood pressure, 51 men from a pool of 204 men originally tested at age 18 to 22 years were recruited for blood pressure assessment 10 to 15 years later. Initial testing uniformly involved monitoring of systolic pressure, diastolic pressure, and heart rate during a reaction time task involving threat of shock. In 30 of the 51 men who participated at follow‐up, initial testing had also included separate visits to obtain relaxation‐only baseline levels of the cardiovascular indices. At follow‐up, in addition to clinic‐type stethoscopic determinations, blood pressure and heart rate were assessed during work and social and leisure activities via ambulatory monitoring. Men with higher levels of systolic pressure during the task showed higher stethoscopic and ambulatory systolic pressure at follow‐up. Likewise, men with higher levels of diastolic pressure during the task showed higher diastolic levels at follow‐up. In the 30 men with both good task and baseline data from initial testing, those with high heart rate reactivity (task minus baseline) showed higher systolic, diastolic, and heart rate levels at follow‐up than low heart rate reactors, even though their baseline blood pressures had not differed at initial testing. Similarly, men with high systolic reactivity showed higher diastolic pressure at follow‐up than low systolic reactors. Multiple regression analyses also demonstrated that systolic, diastolic, and heart rate reactivity improve prediction of follow‐up blood pressure when added to models incorporating the standard risk factors, baseline blood pressure, and parental history of hypertension.

Anxiety and vagal control of heart rate.

Objective Prospective studies have demonstrated that anxiety predicts sudden cardiac death, but the mechanism underlying this increased risk is unclear. This study examined whether anxiety is associated with reductions in vagal control of heart rate in healthy volunteers. Method Trait anxiety (T-ANX) was measured, using the Spielberger State-Trait Anxiety Inventory (STAI), in 93 healthy men and women 25 to 44 years of age. Power spectral analysis was used to measure two indices of vagal control: baroreflex control of heart rate (BRC) and respiratory sinus arrhythmia (RSA). Results High trait anxiety (T-ANX > 41, N = 23) was associated with significantly reduced vagal control of the heart, compared with low trait anxiety (T-ANX < 31, N = 22), as indicated by a 36% reduction in BRC (p < .001) and an 8% reduction in RSA (p < .05). Furthermore, T-ANX scores were negatively correlated with levels of BRC (r = -.30, p < .005), and levels of RSA (r = -.26, p < .05). Conclusions These findings provide evidence that trait anxiety is associated with reductions in vagal control of the heart. Additional studies are needed to examine whether low vagal control is involved in the increased risk of sudden cardiac death associated with anxiety.

Effects of perceived racism and anger inhibition on ambulatory blood pressure in African Americans.

Objective Hypertension is more prevalent in African Americans compared with Americans of European descent. Preliminary evidence indicates that perceived racism may play a role in elevated blood pressure in African Americans. The present study examined whether perceived racism was associated with higher ambulatory blood pressure measured during daily life. A potential contributing role for anger inhibition was also evaluated. Methods Twenty-four–hour ABP was obtained from 69 African American men and women with normal or mildly elevated blood pressure. ABP was averaged over waking and sleep periods, and clinic BP was also assessed. Perceived racism and anger expression were measured using self-report questionnaires. Results Greater perceived racism was related to higher ABP during waking hours for SBP (p < .01) and DBP (p < .05). Perceived racism was positively correlated with anger inhibition (r = .29, p < .05) but was not related to outwardly expressed anger (r = .01, NS). Anger inhibition was related to higher sleep DBP (p = .05) and a smaller drop in DBP from day to night (p < .05). Anger inhibition did not account for the relationship between perceived racism and blood pressure. Conclusions Perceived racism and anger inhibition are independently related to higher ABP. Both may contribute to the incidence of hypertension and hypertensive-related diseases observed in African Americans.