Abigail S L Stickford1,2,3, Yoshiyuki Okada1,2, Stuart A Best1,2, Rosemary S Parker1, Benjamin D Levine1,2, Qi Fu4,5. 1. Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas, 7232 Greenville Ave, Dallas, TX, 75231, USA. 2. University of Texas Southwestern Medical Center, Dallas, TX, USA. 3. Department of Health and Exercise Science, Appalachian State University, Boone, NC, USA. 4. Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas, 7232 Greenville Ave, Dallas, TX, 75231, USA. qifu@texashealth.org. 5. University of Texas Southwestern Medical Center, Dallas, TX, USA. qifu@texashealth.org.
Abstract
PURPOSE: Women with a history of hypertensive pregnancy are at greater risk for future cardiovascular events; however, the mechanisms for this increased risk are unknown. Evidence suggests that an exercise stimulus unmasks latent hypertensive tendencies, identifying individuals at the greatest risk for developing cardiovascular disease. The current study examined the hypothesis that women with a hypertensive pregnancy history exhibit an augmented exercise pressor response. METHODS: Normotensive women with a history of healthy pregnancy (CON; n = 9) and hypertensive pregnancy (HP+; n = 12) were studied during the mid-luteal phase of the menstrual cycle. Heart rate (HR), systolic and diastolic blood pressure (SBP, DBP), and muscle sympathetic nerve activity (MSNA) were measured during a cold pressor test (CPT), and, following a sufficient period of recovery, during static handgrip to fatigue (SHG) and post-exercise circulatory arrest (PECA). RESULTS: The BP, HR, and MSNA responses to the CPT were similar between groups. The SBP response to SHG and PECA was similar between groups, but DBP and HR were significantly greater in HP+ women (both p < 0.05). MSNA burst frequency, but not burst incidence or total activity, tended to be elevated in HP+ women during the stressor (peak Δ from baseline 31 ± 13 vs. 23 ± 13 bursts/min; p for group = 0.06). CONCLUSION: Despite no clinical signs of cardiovascular disease or hypertension, women with a history of hypertensive pregnancy display an enhanced cardiovascular reactivity to an exercise stimulus compared to women with a healthy pregnancy history. This response may be indicative of impaired cardiovascular control that precedes the clinical manifestation of hypertension or cardiovascular events.
PURPOSE:Women with a history of hypertensive pregnancy are at greater risk for future cardiovascular events; however, the mechanisms for this increased risk are unknown. Evidence suggests that an exercise stimulus unmasks latent hypertensive tendencies, identifying individuals at the greatest risk for developing cardiovascular disease. The current study examined the hypothesis that women with a hypertensive pregnancy history exhibit an augmented exercise pressor response. METHODS: Normotensive women with a history of healthy pregnancy (CON; n = 9) and hypertensive pregnancy (HP+; n = 12) were studied during the mid-luteal phase of the menstrual cycle. Heart rate (HR), systolic and diastolic blood pressure (SBP, DBP), and muscle sympathetic nerve activity (MSNA) were measured during a cold pressor test (CPT), and, following a sufficient period of recovery, during static handgrip to fatigue (SHG) and post-exercise circulatory arrest (PECA). RESULTS: The BP, HR, and MSNA responses to the CPT were similar between groups. The SBP response to SHG and PECA was similar between groups, but DBP and HR were significantly greater in HP+ women (both p < 0.05). MSNA burst frequency, but not burst incidence or total activity, tended to be elevated in HP+ women during the stressor (peak Δ from baseline 31 ± 13 vs. 23 ± 13 bursts/min; p for group = 0.06). CONCLUSION: Despite no clinical signs of cardiovascular disease or hypertension, women with a history of hypertensive pregnancy display an enhanced cardiovascular reactivity to an exercise stimulus compared to women with a healthy pregnancy history. This response may be indicative of impaired cardiovascular control that precedes the clinical manifestation of hypertension or cardiovascular events.
Authors: H L Hambridge; S L Mumford; D R Mattison; A Ye; A Z Pollack; M S Bloom; P Mendola; K L Lynch; J Wactawski-Wende; E F Schisterman Journal: Hum Reprod Date: 2013-04-15 Impact factor: 6.918
Authors: Mark B Badrov; Sun Young Park; Jeung-Ki Yoo; Michinari Hieda; Yoshiyuki Okada; Sara S Jarvis; Abigail S Stickford; Stuart A Best; David B Nelson; Qi Fu Journal: Hypertension Date: 2019-02 Impact factor: 10.190
Authors: Michinari Hieda; Jeung-Ki Yoo; Dan-Dan Sun; Yoshiyuki Okada; Rosemary S Parker; Monique A Roberts-Reeves; Beverley Adams-Huet; David B Nelson; Benjamin D Levine; Qi Fu Journal: Am J Physiol Regul Integr Comp Physiol Date: 2018-06-13 Impact factor: 3.619