Tschakovsky ME, Matusiak K, Vipond C, McVicar L. Lower limb-localized vascular phenomena explain initial orthostatic hypotension upon standing from squat. Am J Physiol Heart Circ Physiol 301: H2102-H2112, 2011. First published August 19, 2011 doi:10.1152/ajpheart.00571.2011.-The cause(s) of initial orthostatic hypotension (transient fall in blood pressure within 15 s upon active rising) have not been established. We tested the hypothesis that this hypotension is due to local vascular phenomena in contracting leg muscles from the brief effort of standing up. Seventeen young healthy subjects (2 male and 15 female, 22.5 Ϯ 1.0 years) performed an active rise from resting squat after a 10-s squat, a 1-min squat, or a 5-min squat. Beat-by-beat arterial blood pressure, cardiac output, heart rate, and stroke volume (Finometer finger photoplethysmography) and right common femoral artery blood flow (Doppler and Echo ultrasound) were recorded. Data are means Ϯ SE. Quiet standing before squat represented baseline. Peak increases in lower limb and total vascular conductance (ml·min Ϫ1 ·mmHg Ϫ1 ) upon standing were not different within squat conditions (10-s squat, 50.0 Ϯ 12.4 vs. 44.3 Ϯ 5.0; 1-min squat, 54.7 Ϯ 9.2 vs. 50.5 Ϯ 4.5; 5-min squat, 67.4 Ϯ 13.7 vs. 58.8 Ϯ 3.9; all P Ͼ 0.574). Mean arterial blood pressure (in mmHg) fell to a nadir well below standing baseline in all conditions despite increases in cardiac output. The hypotension predicted by the increase in leg vascular conductance accounted for this hypotension [observed vs. predicted (in mmHg): 10-s squat, Ϫ17.1 Ϯ 2.1 vs. Ϫ18.3 Ϯ 5.5; 1-min squat, Ϫ22.0 Ϯ 3.8 vs. Ϫ25.3 Ϯ 4.9; 5-min squat, Ϫ28.3 Ϯ 4.0 vs. Ϫ29.2 Ϯ 6.7]. We conclude that rapid contraction induced dilation in leg muscles with the effort of standing, along with a minor potential contribution of elevated lower limb arterio-venous pressure gradient, outstrips compensatory cardiac output responses and is the cause of initial orthostatic hypotension upon standing from squat. blood pressure; syncope; muscle blood flow; muscle contraction; sympathetic withdrawal; cardiopulmonary baroreflex

Obesity in the childbearing population is increasingly common. Obesity is associated with increased risk for a number of maternal and neonatal pregnancy complications. Some of these complications, such as gestational diabetes, are risk factors for long-term disease in both mother and baby. While clinical practice guidelines advocate for healthy weight prior to pregnancy, there is not a clear directive for achieving healthy weight before conception. There are known benefits to even moderate weight loss prior to pregnancy, but there are potential adverse effects of restricted nutrition during the periconceptional period. Epidemiological and animal studies point to differences in offspring conceived during a time of maternal nutritional restriction. These include changes in hypothalamic-pituitary-adrenal axis function, body composition, glucose metabolism, and cardiovascular function. The periconceptional period is therefore believed to play an important role in programming offspring physiological function and is sensitive to nutritional insult. This review summarizes the evidence to date for offspring programming as a result of maternal periconception weight loss. Further research is needed in humans to clearly identify benefits and potential risks of losing weight in the months before conceiving. This may then inform us of clinical practice guidelines for optimal approaches to achieving a healthy weight before pregnancy.

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