ObjectiveTo determine efficacy of aerobic exercise for cognitive function in younger healthy adults. MethodsIn a randomized, parallel-group, observer-masked, community-based clinical trial, 132 cognitively normal individuals aged 20-67 with below median aerobic capacity were randomly assigned to one of two 6-month, 4-times-weekly conditions: aerobic exercise and stretching/ toning. Efficacy measures included aerobic capacity; cognitive function in several domains (executive function, episodic memory, processing speed, language, and attention), everyday function, body mass index (BMI), and cortical thickness. ResultsAerobic capacity increased significantly (β = 2.718; p = 0.003), and BMI decreased significantly (β = −0.596; p = 0.013) in the aerobic exercise but not in the stretching/toning condition. Executive function improved significantly in the aerobic exercise condition; this effect was moderated by age (β = 0.018 SD/y; p = 0.028). At age 40, the executive function measure increased by 0.228 SD (95% confidence interval [CI] 0.007-0.448), and by 0.596 SD (95% CI 0.219-0.973) at age 60. Cortical thickness increased significantly in the aerobic exercise group in a left frontal region and did not interact with age. Controlling for age and baseline performance, individuals with at least one APOE e4 allele showed less improvement in executive function with aerobic exercise (β = 0.5129, 95% CI 0.0381-0.988; p = 0.0346). ConclusionsThis randomized clinical trial demonstrates the efficacy of aerobic exercise for cognition in adults age 20-67. The effect of aerobic exercise on executive function was more pronounced as age increased, suggesting that it may mitigate age-related declines. Increased cortical thickness suggests that aerobic exercise contributes to brain health in individuals as young as age 20.Clinicaltrials.gov identifier NCT01179958. Classification of evidenceThis study provides Class II evidence that for adults age 20-67 with below median aerobic capacity, aerobic exercise significantly improves executive function but not other measures of cognitive function.

Objective Evidence from both laboratory and observational studies suggests that acute and chronic smoking leads to reduced high frequency heart rate variability (HF-HRV), a measure of cardiac vagal regulation. We utilized ecological momentary assessment (EMA) to study the effect of smoking on concurrent HF-HRV in a trial measuring the effects of hostility reduction, and compared 24-hour HF-HRV in smokers and non-smokers. Method Ambulatory ECG data were collected pre-randomization from 149 healthy, individuals with high hostility levels (20–45 years, BMI ≤ 32 kg/m2) and paired with concurrent EMA ratings of smoking, and physical position during waking hours. A multilevel mixed model was estimated associating ln(HF-HRV) from smoking status (between-person factor) and person-centered momentary smoking (within-person factor, treated as a random effect), adjusting for momentary physical position, medication use, and consumption of alcohol and caffeine. Results 35 smokers and 114 non-smokers provided both EMA and HF-HRV data. Within smokers, ln HF-HRV was reduced by 0.31 ms2 (p=0.04) when participants reported having recently smoked cigarettes, compared to when they had not. The 24-hour HF-HRV was significantly lower in smokers (mean = 5.24 ± SD = 0.14 ms2) than non-smokers (5.63 ± 0.07 ms2; p=0.01)." Conclusion In healthy, smokers with high hostility levels used as their own controls during daily living, smoking acutely reduced HF-HRV. HF-HRV was also reduced in smokers as compared to non-smokers. Although limited by a small sample of individuals with high hostility levels, these findings nonetheless provide additional evidence that cardiac vagal regulation is lowered by cigarette smoking, which may be one of the numerous pathophysiological effects of smoking.

HS completion robustly predicts mortality by ages 55 years and 75 years. Dq-r personality traits predict mortality by age 75 years, accounting, in part, for Dq-r mortality.

Objective Elevated cardiovascular reactivity to, and reduced recovery from, challenging events may increase the risk of cardiovascular disease, and exercise training may reduce this reactivity. However, in a randomized controlled trial of aerobic versus strength training in sedentary, healthy young adults, we found no training group differences in reactivity or recovery. Because strength training also may have a reactivity-reducing effect, we conducted a secondary analysis of data from another trial, this time with a wait-list control condition. Methods One hundred nineteen healthy, young, sedentary adults were randomized to a 12-week aerobic training program or wait-list control. Before (T1) and after (T2) training and after 4 weeks of sedentary deconditioning (T3), we measured heart rate (HR), heart rate variability, and blood pressure at rest and in response to and recovery from psychological and orthostatic challenge. Data were analyzed using a group (aerobic versus wait-list) by session (T1, T2, and deconditioning) and by period (baseline, psychological challenge, recovery, standing) three-way analysis of variance with prespecified contrasts. Results Aerobic capacity significantly increased at T2 and decreased at T3 only in the aerobic training group. The groups did not differ on HR, heart rate variability, or blood pressure reactivity to or recovery from challenge. Without baseline adjustment, there were no significant treatment differences in response to challenges. With baseline adjustment, there were significant treatment by session effects for HR (Cohen d = 0.54, p = .002), systolic blood pressure (d = 0.44, p = .014), diastolic blood pressure (d = 0.74, p = .002), and root mean squared successive difference (d = 0.48, p = .006) reactivity from T1 to T2 only for orthostatic challenge: at T2, reactivity in the aerobic group was nonsignificantly reduced, compared with T1. In the wait-list group, reactivity significantly increased after T1. Conclusions This study raises further doubt about attenuation of cardiovascular reactivity or enhancement of recovery as a cardioprotective mechanism of aerobic exercise training. Clinical Trial Registration: ClinicalTrials.gov Unique identifier: NCT01335737.