Objective Cardiac output, a fundamental parameter of cardiovascular function, has consistently been shown to increase across healthy pregnancy; however, the time course and magnitude of adaptation remains equivocal within published literature. The aim of the present meta-analyses was to comprehensively describe the pattern of change in cardiac output during healthy pregnancy. Method A series of meta-analyses of previously published cardiac output data during healthy, singleton pregnancies was completed. PubMed and Scopus databases were searched for studies published between 1996 and 2014. Included studies reported absolute values during a predetermined gestational age (non-pregnant, late first trimester, early and late second trimester, early and late third trimester, early and late postpartum). Cardiac output was measured through echocardiography, impedance cardiography or inert gas rebreathing. Observational data were meta-analysed at each gestational age using a random-effects model. If reported, related haemodynamic variables were evaluated. Results In total, 39 studies were eligible for inclusion, with pooled sample sizes ranging from 259 to 748. Cardiac output increased during pregnancy reaching its peak in the early third trimester, 1.5 L/min (31%) above non-pregnant values. The observed results from this study indicated a non-linear rise to this point. In the early postpartum, cardiac output had returned to non-pregnant values. Conclusion The present results suggest that cardiac output peaks in the early third trimester, following a non-linear pattern of adaptation; however, this must be confirmed using longitudinal studies. The findings provide new insight into the normal progression of cardiac output during pregnancy.

Background Clinical guidelines recommend pregnant women without contraindication engage in regular physical activity. This is based on extensive evidence demonstrating the safety and benefits of prenatal exercise. However, certain medical conditions or contraindications warrant a reduction, modification or cessation of activity due to potential health risks. Aim To review and evaluate the evidence related to medical disorders which may warrant contraindication to prenatal exercise. Methods Online databases were searched up to 5 April 2019. Forty-four unique studies that reported data on our Population (pregnant women with contraindication to exercise), Intervention (subjective/objective measures of acute or chronic exercise), Comparator (not essential) and Outcomes (adverse maternal or fetal outcomes) were included in the review. Key findings We found that the majority of medical conditions listed as contraindications were based on expert opinion; there is minimal empirical evidence to demonstrate harm of exercise and benefit of activity restriction. We identified 11 complications (eg, gestational hypertension, twin pregnancy) previously classified as contraindications where women may in fact benefit from regular prenatal physical activity with or without modifications. However, the evidence suggests that severe cardiorespiratory disease, placental abruption, vasa previa, uncontrolled type 1 diabetes, intrauterine growth restriction, active preterm labour, severe pre-eclampsia and cervical insufficiency are associated with strong potential for maternal/fetal harm and warrant classification as absolute contraindications. Conclusion Based on empirical evidence, we provide a call to re-evaluate clinical guidelines related to medical disorders that have previously been considered contraindications to prenatal exercise. Removing barriers to physical activity during pregnancy for women with certain medical conditions may in fact be beneficial for maternal–fetal health outcomes.

This study has identified that sympathetically mediated blood pressure regulation is reduced following ascent to high altitude. Additionally, we show that high-altitude Andean natives have reduced blood pressure responsiveness to sympathetic nervous activity (SNA) outflow compared with Nepalese Sherpa. However, basal sympathetic activity is inversely related to the magnitude of SNA-mediated fluctuations in blood pressure regardless of population or condition. These data set a foundation to explore more precise mechanisms of blood pressure control under conditions of persistent sympathetic activation and hypoxia.

Background: Structural remodeling of the right ventricle (RV) is widely documented in athletes. However, functional adaptation, including RV pressure generation and systolic free-wall longitudinal mechanics, remains equivocal. This meta-analysis compared RV pressure and function in athletes and controls. Methods: A systematic review of online databases was conducted up to June 4, 2020. Meta-analyses were performed on RV systolic pressures, at rest and during exercise, tricuspid annular plane systolic displacement, myocardial velocity (S’), and global and regional longitudinal strain. Bias was assessed using Egger regression for asymmetry. Data were analyzed using random-effects models with weighted mean difference and 95% CI. Results: Fifty-three studies were eligible for inclusion. RV systolic pressure was obtained from 21 studies at rest ( n =1043:1651; controls:athletes) and 8 studies during exercise ( n =240:495) and was significantly greater in athletes at rest (weighted mean difference, 2.9 mmHg [CI, 1.3–4.5 mmHg]; P =0.0005) and during exercise (11.0 [6.5–15.6 mm Hg]; P <0.0001) versus controls. Resting tricuspid annular plane systolic displacement ( P <0.0001) and S’ ( P =0.001) were greater in athletes. In contrast, athletes had similar RV free-wall longitudinal strain (17 studies; n =450:605), compared with controls but showed greater longitudinal apical strain (16 studies; n =455:669; 0.9%, 0.1%–1.8%; P =0.03) and lower basal strain (−2.5% [−1.4 to −3.5%]; P <0.0001). Conclusions: Functional RV adaptation, characterized by increased tricuspid annular displacement and velocity and a greater base-to-apex strain gradient, is a normal feature of the athlete’s heart, together with a slightly elevated RV systolic pressure. These findings contribute to our understanding of RV in athletes and highlight the importance of considering RV function in combination with structure in the clinical interpretation of the athlete’s heart.