Sarah Hissen (Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital, Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital), Ryosuke Takeda (Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital, Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital), Jeung-Ki Yoo (Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital, Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital), Mark Badrov (Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital, Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital), Andrew Tomlinson (Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital, Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital), Safia Khan (University of Texas Southwestern Medical Center), David Nelson (University of Texas Southwestern Medical Center), Tony Babb (Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital, Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital), Qi Fu (Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital, Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital)
Speaker University of Texas Southwester Medical Center
Maternal obesity increases the risk of adverse pregnancy outcomes. The mechanisms that contribute to this elevated risk are unclear but may be related to overactivation of the sympathetic nervous system. Indeed, sympathetic activation during pregnancy is now regarded as a normal adaptation to maintain homeostasis. However, sympathetic overactivation is associated with gestational hypertensive disorders. It is unknown whether the health related problems linked to maternal obesity (i.e., inflammation, insulin resistance, dyslipidemia) results in sympathetic overactivation during pregnancy. We hypothesized that maternal obesity would induce greater increases in resting muscle sympathetic nerve activity (MSNA) during pregnancy when compared with normal-weight women.
Blood pressure (BP), heart rate and MSNA (microneurography) were recorded during 5 min of supine rest in 14 normal-weight (Age 30±1.6 [SE] yrs; BMI 22.1±0.6 kg/m2) and 14 obese (Age 28±0.8 yrs; BMI 33.9±1.0 kg/m2) women during early pregnancy (5-12 weeks), late pregnancy (32 to 34 weeks) and 6-10 weeks postpartum.
Gestational weight gain from early to late pregnancy was not significantly different between groups (11.8±0.9 kg vs. 9.2±2.1 kg, P=0.23). Resting MSNA burst frequency was not different between normal-weight and obese groups during early pregnancy (17±3 bursts/min vs. 22±4 bursts/min, P=0.35) or postpartum (10±2 bursts/min vs. 8±2 bursts/min P=0.74) but was significantly greater in the obese group during late pregnancy (23±4 bursts/min vs. 35±4 bursts/min, Figure A, P=0.031). There were no significant changes in resting MSNA from early to late pregnancy in the normal-weight group (P=0.67) whereas the obese group had significant increases in MSNA from early to late pregnancy (P=0.002). These findings were also apparent when MSNA was characterized as burst incidence and total activity (Figure B and C). Although still within the normotensive range, women with obesity had greater levels of systolic BP when compared with normal-weight women across all time points (Figure D, group main effect P=0.002). Diastolic BP was lower during pregnancy when compared with postpartum and this was similar between groups (Figure E, gestation main effect Plt;0.001). Heart rate was greater during early pregnancy when compared with postpartum and increased similarly in both groups during late pregnancy (Figure F, gestation main effect Plt;0.001).
These findings suggest that maternal obesity is associated with greater increases in sympathetic activation even during normotensive pregnancy and may play a role in the increased risk of adverse maternal and fetal outcomes in women with obesity.
Supported by the R21HL088184, R01 HL142605 and American Heart Association Postdoctoral Fellowship (826095).
Figure. Resting A) muscle sympathetic nerve activity (MSNA) burst frequency, B) MSNA burst incidence, C) MSNA total activity, D) systolic blood pressure, E) diastolic blood pressure and F) heart rate during early and late pregnancy and postpartum in normal-weight and obese women. Values are mean±SE. Circles depict normal-weight group and squares depict obese group. Mixed effects model with repeated measures was used to compare group and gestation. * significantly different between groups.
