Findings suggest that exercise-based interventions are effective in reducing systolic blood pressure, fasting glucose, and fasting insulin, and increasing high-density lipoprotein cholesterol after stroke or transient ischemic attack, providing evidence for their implementation as a strategy for secondary prevention.

Endothelial function, assessed using brachial artery flow-mediated dilation (FMD), predicts future cardiovascular disease (CVD) risk. This study established age- and sex-specific reference intervals for brachial artery FMD in healthy individuals and examined the relation with CVD risk factors. In a retrospective study design, we pooled brachial artery FMD (acquired according to expert-consensus guidelines for FMD protocol and analysis) and participant characteristics/medical history from 5362 individuals (4–84 years; 2076 females). Healthy individuals (n=1403 [582 females]) were used to generate age-/sex-specific percentile curves. Subsequently, we included individuals with CVD risk factors, without overt disease (unmedicated n=3167 [1247 females] and medicated n=792 [247 females]). Multiple linear regression tested the relation of CVD risk factors (body mass index, blood pressure, cholesterol, diabetes, dyslipidemia, and smoking) with FMD. Healthy males showed a negative, curvilinear relation between FMD and age, while females revealed a negative linear relation that started higher but declined at a faster rate than males. Age- and sex-specific differences in FMD relate, at least partly, to baseline artery diameter. FMD was related to CVD risk factors in unmedicated (eg, systolic/diastolic blood pressure) and medicated individuals (eg, diabetes/dyslipidemia). Sex mediated some of these effects ( P <0.05), with normalization of FMD in medicated men, but not women with dyslipidemia. In conclusion, sex alters the age-related decline in FMD, which may partly be explained through differences in baseline diameter. Sex also alters the influence of some CVD risk factors and medication on FMD. This work improves interpretation and future use of the FMD technique.

We measured acute vascular responses to heat stress to examine the hypothesis that macrovascular endothelial-dependent dilation is improved in a shear-dependent manner, which is further modified by skin temperature. Twelve healthy males performed whole-body heating (+1.5°C esophageal temperature), bilateral forearm heating (~38°C skin temperature), and a time-matched (~60 min) control condition on separate days in counterbalanced order. Bilateral assessments of blood flow and brachial artery flow-mediated dilation (FMD) were performed before and 10 min after each condition protocols with duplex Doppler ultrasound. To isolate the influence of shear stress, a pneumatic cuff was inflated (~90 mmHg) around the right forearm during each condition to attenuate heat-induced rises in blood flow and shear stress. After forearm heating, FMD increased [cuffed: 4.7 (2.9) to 6.8 (1.5)%, non-cuffed: 5.1 (2.8) to 6.4 (2.6)%] in both arms (time P<0.01). Whole-body heating also increased FMD in the non-cuffed arm from 3.6 (2.2) to 9.2 (3.2)% and in the cuffed arm from to 5.6 (3.0)% to 8.6 (4.9)% (time P<0.01). After the time control, FMD decreased [cuffed: 6.3 (2.4) to 4.7 (2.2)%, non-cuffed: 6.1 (3.0) to 4.5 (2.6)%] in both arms (time P=0.03). Multiple linear regression (adjusted r2=0.263, P=0.003) revealed that changes in esophageal temperature, skin temperatures, and heart rate explained the majority of the variance in this model (34%, 31% and 21%, respectively). Our findings indicate that, in addition to shear stress, skin and core temperatures are likely important contributors to passive heating-induced vascular adaptations.