A Single Session of Exercise Reduces Blood Pressure Reactivity to Stress: a Systematic Review With Meta-analysis

Stressful situations are common in everyday life and disturb homeostasis. So, an exercise session is a strategy to mitigate blood pressure (BP) peaks in response to stress (i.e., BP reactivity), decreasing the cardiovascular risk of these individuals. This is a systematic review with a meta-analysis that aims to verify the effects of a single session of physical exercises on BP reactivity to stress. The searches were realized in digital databases (PUBMED, LILACS, EMBASE and PsycInfo) and 28 studies were included, totaling 846 individuals (meta-analysis stage: k = 24, n = 710). As for exercise characteristics, 23 of the 28 studies focused on aerobic exercises, and 24 studies focused on low to moderate intensities. Favorable metanalytic results (standardized mean differences through random-effects approach) for the exercises were found, with attenuated reactivity in systolic BP (pooled effect size = -0.35 [-0.46; -0.23], representing average reductions of 3.8 ± 3.5 mmHg), diastolic BP (pooled effect size = -0.49 [-0.68; -0.30], representing average reductions of 3.1 ± 3.6 mmHg), and mean BP (pooled effect size = -0.48 [-0.70; -0.26], representing average reductions of 4.1 ± 3.0 mmHg). So, acute physical exercise lowers systolic, diastolic, and mean blood pressure reactivity in response to stressor tasks.

Case Studies in Physiology: Cardiovascular function during triplet pregnancy

Pregnancy is recognized as a natural physiological stressor to the maternal cardiovascular system. Cardiovascular adaptation is markedly greater in twin compared to singleton pregnancy; however, these changes are sparsely documented in triplet pregnancy. The aim of this case series was to compare maternal cardiac function, cardioautonomic regulation and blood pressure reactivity in healthy singleton, twin, and triplet pregnancies. Resting cardiac structure and function (echocardiography), beat-by-beat blood pressure variability (BPV; photoplethysmography) and heart rate variability (HRV; electrocardiogram) were measured in two triplet, three twin and three singleton pregnancies (matched for maternal age, pre-pregnancy BMI and gestational age). Hemodynamic responses to a 3-minute cold pressor test were also recorded to assess blood pressure reactivity. Due to the small sample size of this case series, statistical comparisons were not made between groups. Compared to singleton and twin pregnancies, individuals pregnant with triplets had greater resting cardiac output but lower cardiac deformation (longitudinal strain, basal circumferential strain, and torsion), sympathetic dominance in cardioautonomic regulation (lower HRV and higher BPV) and elevated blood pressure reactivity in response to the cold pressor test. Taken together, these observations suggest that females with triplet pregnancies may have reduced cardiovascular function, which may contribute to the heightened risk of complications in multifetal pregnancies.

Increased vascular α1-adrenergic receptor sensitivity in older adults with posttraumatic stress disorder

Posttraumatic stress disorder (PTSD) is an independent risk factor for the development of hypertension and cardiovascular disease. Patients with PTSD have heightened blood pressure and sympathetic nervous system reactivity; however, it is unclear if patients with PTSD have exaggerated vasoconstriction in response to sympathetic nerve activation that could also contribute to increased blood pressure reactivity. Therefore, we hypothesized that patients with PTSD have increased sensitivity of vascular α1-adrenergic receptors (α1ARs), the major mediators of vasoconstriction in response to release of norepinephrine at sympathetic nerve terminals. To assess vascular α1AR sensitivity, we measured the degree of venoconstriction in a dorsal hand vein in response to exponentially increasing doses of the selective α1AR agonist, phenylephrine (PE), in 9 patients with PTSD (age = 59 ± 2 yr) and 10 age-matched controls (age = 60 ± 1 yr). Individual dose-response curves were generated to determine the dose of PE that induces 50% of maximal venoconstriction (i.e., PE ED50) reflective of vascular α1AR sensitivity. In support of our hypothesis, PE ED50 values were lower in PTSD compared with controls (245 ± 54 ng/min vs. 1,995 ± 459 ng/min, P = 0.012), indicating increased vascular α1AR sensitivity in PTSD. The PTSD group also had an increase in slope of rise in venoconstriction, indicative of an altered venoconstrictive reactivity to PE compared with controls (19.8% ± 1.2% vs. 15.1% ± 1.2%, P = 0.009). Heightened vascular α1AR sensitivity in PTSD may contribute to augmented vasoconstriction and blood pressure reactivity to sympathoexcitation and to increased cardiovascular disease risk in this patient population.

Is stressor-evoked cardiovascular reactivity a pathway linking positive and negative emotionality to carotid intima-media thickness?

Stressor-evoked cardiovascular reactivity, trait positive emotionality, and negative emotionality are all associated with cardiovascular disease. It is unknown, however, whether cardiovascular reactivity may constitute a pathway by which trait positive or negative emotionality relates to disease risk. Accordingly, this study modeled the cross-sectional relationships between trait positive and negative emotionality, stressor-evoked cardiovascular reactivity, and severity of a subclinical vascular marker of cardiovascular risk, carotid artery intima-media thickness (CA-IMT). The sample consisted of healthy, midlife adults free from clinical cardiovascular disease (N = 286; ages 30-54; 50% female). Trait positive and negative emotionality were measured by three questionnaires. Heart rate and blood pressure reactivity were assessed across three stressor tasks. CA-IMT was assessed by ultrasonography. Latent factors of positive and negative emotionality, blood pressure reactivity, heart rate reactivity, and CA-IMT were created using structural equation modeling. Greater negative emotionality was marginally associated with more CA-IMT (β = .21; p = .049), but lower blood pressure reactivity (β = -.19; p = .03). However, heightened blood pressure (β = .21; p = .03), but not heart rate reactivity (β = -.05; p = .75), associated with greater CA-IMT. Positive emotionality was uncorrelated with cardiovascular reactivity (blood pressure: β = -.04; p = .61; heart rate: β = .16; p = .11) and CA-IMT (β = .16; p = .07). Although trait negative emotionality associates with a known marker of cardiovascular disease risk, independent of positive emotionality, it is unlikely via a stressor-evoked cardiovascular reactivity pathway.