Tracey L Weissgerber

Mayo Clinic - Rochester, Rochester, Minnesota, United States

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Publications (23)62.39 Total impact

  • Kidney international. 08/2014; 86(2):445.
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    ABSTRACT: Background: Free vascular endothelial growth factor (VEGF) is undetectable in plasma during human pregnancy. However, studies examining pregnant rats have reported both low (8-29 pg/mL) and high (527-1030 pg/mL) free VEGF. These discrepancies cast uncertainty over the use of rat models to study angiogenic factors in pregnancy and preeclampsia. This study investigates methodological factors that may explain these discrepancies. Methods: Plasma VEGF in non-pregnant, day 7 pregnant and day 19 pregnant rats was measured using rat and mouse ELISAs. Results: The rat ELISA detected VEGF in plasma from non-pregnant rats, but not in plasma from day 19 pregnant rats. The mouse ELISA detected higher VEGF concentrations than the rat ELISA in every sample tested. This discrepancy was greater in day 19 pregnant rats (Median: 2,273 vs. 0 pg/mL) than in non-pregnant (97 vs. 20 pg/mL) and day 7 pregnant (66 vs. 2 pg/mL) rats. Recovery of recombinant rat VEGF (rrVEGF) spiked into plasma from non-pregnant and day 7 pregnant rats was high for the rat ELISA (82-105%), but low for the mouse ELISA (17-22%). The rat ELISA did not recover rrVEGF in plasma from day 19 pregnant rats, suggesting that this ELISA measures free VEGF. Conclusions: The use of the rat vs. mouse ELISA likely explains the differences in reported VEGF concentrations in pregnant rats. While the rat ELISA appears to measure free VEGF, plasma concentrations are below the assay sensitivity limit. As most previous studies of pregnant rats used the mouse VEGF ELISA, this data should be interpreted cautiously.
    AJP Regulatory Integrative and Comparative Physiology 03/2014; · 3.28 Impact Factor
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    ABSTRACT: Pre-eclampsia is a pregnancy-specific hypertensive disorder that may lead to serious maternal and fetal complications. It is a multisystem disease that is commonly, but not always, accompanied by proteinuria. Its cause(s) remain unknown, and delivery remains the only definitive treatment. It is increasingly recognized that many pathophysiological processes contribute to this syndrome, with different signaling pathways converging at the point of systemic endothelial dysfunction, hypertension, and proteinuria. Different animal models of pre-eclampsia have proven utility for specific aspects of pre-eclampsia research, and offer insights into pathophysiology and treatment possibilities. Therapeutic interventions that specifically target these pathways may optimize pre-eclampsia management and may improve fetal and maternal outcomes. In addition, recent findings regarding placental, endothelial, and podocyte pathophysiology in pre-eclampsia provide unique and exciting possibilities for improved diagnostic accuracy. Emerging evidence suggests that testing for urinary podocytes or their markers may facilitate the prediction and diagnosis of pre-eclampsia. In this review, we explore recent research regarding placental, endothelial, and podocyte pathophysiology. We further discuss new signaling and genetic pathways that may contribute to pre-eclampsia pathophysiology, emerging screening and diagnostic strategies, and potential targeted interventions.Kidney International advance online publication, 26 February 2014; doi:10.1038/ki.2014.17.
    Kidney International 02/2014; · 8.52 Impact Factor
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    ABSTRACT: Abstract Objective: The anti-oxidant and proangiogenic protein haptoglobin (Hp) is believed to be important for implantation and pregnancy, although its specific role is not known. The three phenotypes (1-1, 2-1 and 2-2) differ in structure and function. Hp 2-2 is associated with increased vascular stiffness in other populations. We examined whether Hp phenotype is associated with abnormal uterine artery Doppler (UAD) in pregnancy. Methods: We conducted a secondary analysis of a preeclampsia prediction cohort nested within a larger placebo-controlled randomized clinical trial of antioxidants for prevention of preeclampsia. We determined Hp phenotype in 2184 women who completed UAD assessments at 17 weeks gestation. Women with notching were re-evaluated for persistent notching at 24 weeks' gestation. Logistic regression was used to assess differences in UAD indices between phenotype groups. Results: Hp phenotype did not significantly influence the odds of having any notch (p = 0.32), bilateral notches (p = 0.72), or a resistance index (p = 0.28) or pulsatility index (p = 0.67) above the 90th percentile at 17 weeks' gestation. Hp phenotype also did not influence the odds of persistent notching at 24 weeks (p = 0.25). Conclusions: Hp phenotype is not associated with abnormal UAD at 17 weeks' gestation or with persistent notching at 24 weeks.
    The journal of maternal-fetal & neonatal medicine: the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians 01/2014; · 1.36 Impact Factor
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    ABSTRACT: Context: Research examining the source of excess sFLT1 in preeclampsia has focused on the placenta. The potential contribution of the releasable store of sFLT1 in the systemic vasculature is unknown. Objective: We asked if the non-placental releasable store of sFLT1 is larger in women with previous preeclampsia than in women with a previous uncomplicated pregnancy. Design: We administered heparin to nulligravid women, and women with previous preeclampsia or a previous uncomplicated pregnancy. We compared post-heparin sFLT1 concentrations with those observed in uncomplicated pregnancy and preeclampsia. Setting: Magee-Womens Hospital Patients: Nulligravidas (n=8), women 6-24 months post-partum (Previous uncomplicated pregnancy: n=16; Previous preeclampsia: n=15), pregnant women (Uncomplicated pregnancy: n=30; Preeclampsia: n=25) Intervention: Non-pregnant women received an unfractionated heparin bolus. Main Outcome Measures: Pre- and post-heparin plasma sFLT1, placental growth factor (PGF) and vascular endothelial growth factor (VEGF). Results: In non-pregnant women, heparin increased plasma sFLT1 by 250-fold (p<0.01), increased PGF by 7-fold (p<0.01), and decreased free VEGF (p<0.01). These changes did not differ between nulligravidas, women with previous preeclampsia and women with a previous uncomplicated pregnancy. Post-heparin sFLT1 in non-pregnant women was higher than sFLT1 in uncomplicated pregnancy, but lower than sFLT1 in preeclampsia. Baseline and post-heparin sFLT1 were positively correlated (r(2)=0.19, p<0.01). Heparin increased the concentration of the 100 kD sFLT1 isoform. Adding heparin to whole blood or plasma did not increase sFLT1. Conclusions: Non-pregnant women have a significant vascular store of releasable sFLT1. The size of this store does not differ between women with previous preeclampsia vs. previous uncomplicated pregnancy.
    The Journal of clinical endocrinology and metabolism 12/2013; · 6.50 Impact Factor
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    ABSTRACT: Objective The phenotype of the antioxidant and pro-angiogenic protein haptoglobin (Hp) predicts cardiovascular disease risk and treatment response to antioxidant vitamins in individuals with diabetes. Our objective was to determine whether Hp phenotype influences pre-eclampsia risk, or the efficacy of vitamins C and E in preventing pre-eclampsia, in women with type-1 diabetes. DesignThis is a secondary analysis of a randomised controlled trial in which women with diabetes received daily vitamins C and E, or placebo, from 8 to 22 weeks of gestation until delivery. SettingTwenty-five antenatal metabolic clinics across the UK (in north-west England, Scotland, and Northern Ireland). PopulationPregnant women with type-1 diabetes. Methods Hp phenotype was determined in white women who completed the study and had plasma samples available (n = 685). Main outcome measurePre-eclampsia. ResultsCompared with Hp 2-1, Hp 1-1 (OR 0.59, 95% CI 0.30–1.16) and Hp 2-2 (OR 0.93, 95% CI 0.60–1.45) were not associated with significantly decreased pre-eclampsia risk after adjusting for treatment group and HbA1c at randomisation. Our study was not powered to detect an interaction between Hp phenotype and treatment response; however, our preliminary analysis suggests that vitamins C and E did not prevent pre-eclampsia in women of any Hp phenotype (Hp 1-1, OR 0.77, 95% CI 0.22–2.71; Hp 2-1, OR 0.81, 95% CI 0.46–1.43; Hp 2-2, 0.67, 95% CI 0.34–1.33), after adjusting for HbA1c at randomisation. Conclusions The Hp phenotype did not significantly affect pre-eclampsia risk in women with type-1 diabetes.
    BJOG An International Journal of Obstetrics & Gynaecology 09/2013; 120(10). · 3.76 Impact Factor
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    ABSTRACT: BACKGROUND: An ankle-brachial index (ABI) (the ratio of ankle to brachial artery systolic blood pressure) value ≤0.9 identifies patients with peripheral arterial disease (PAD) and elevated cardiovascular event risk. This study examined whether women with a history of hypertension in pregnancy are more likely to have an ABI ≤0.9 decades after pregnancy. METHODS AND RESULTS: ABI was measured in nulliparous women (n = 144), and women with a history of normotensive (n = 1272) or hypertensive (n = 281) pregnancies who participated in the Genetic Epidemiology Network of Arteriopathy (GENOA) study [non-Hispanic white (39%) and black (61%) women, 60 (mean) ± 10 (SD) years of age]. Relationships between PAD and pregnancy history were examined by logistic regression. Compared to women with a history of normotensive pregnancy, women with a history of hypertensive pregnancy had greater odds of PAD (1.61 (odds ratio); 1.04-2.49 (95% confidence interval), p = 0.03, adjusted for age, race, height and heart rate). Additional adjustment for ever smoking, hypertension, diabetes, dyslipidemia, a family history of hypertension or coronary heart disease, body mass index and education did not attenuate this relationship (1.63; 1.02-2.62, p = 0.04). PAD risk did not differ between women with a history of normotensive pregnancy and nulliparous women (1.06; 0.52-2.14, p = 0.87). CONCLUSIONS: Hypertension in pregnancy is an independent risk factor for PAD decades after pregnancy after adjusting for race, age, height, heart rate, ever smoking, hypertension, diabetes, dyslipidemia, a family history of hypertension or coronary heart disease, body mass index and education.
    Atherosclerosis 04/2013; · 3.71 Impact Factor
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    ABSTRACT: Haptoglobin's (Hp) antioxidant and pro-angiogenic properties differ between the 1-1, 2-1, and 2-2 phenotypes. Hp phenotype affects cardiovascular disease risk and treatment response to antioxidant vitamins in some non-pregnant populations. We previously demonstrated that preeclampsia risk was doubled in white Hp 2-1 women, compared to Hp 1-1 women. Our objectives were to determine whether we could reproduce this finding in a larger cohort, and to determine whether Hp phenotype influences lack of efficacy of antioxidant vitamins in preventing preeclampsia and serious complications of pregnancy-associated hypertension (PAH). This is a secondary analysis of a randomized controlled trial in which 10,154 low-risk women received daily vitamin C and E, or placebo, from 9-16 weeks gestation until delivery. Hp phenotype was determined in the study prediction cohort (n = 2,393) and a case-control cohort (703 cases, 1,406 controls). The primary outcome was severe PAH, or mild or severe PAH with elevated liver enzymes, elevated serum creatinine, thrombocytopenia, eclampsia, fetal growth restriction, medically indicated preterm birth or perinatal death. Preeclampsia was a secondary outcome. Odds ratios were estimated by logistic regression. Sampling weights were used to reduce bias from an overrepresentation of women with preeclampsia or the primary outcome. There was no relationship between Hp phenotype and the primary outcome or preeclampsia in Hispanic, white/other or black women. Vitamin supplementation did not reduce the risk of the primary outcome or preeclampsia in women of any phenotype. Supplementation increased preeclampsia risk (odds ratio 3.30; 95% confidence interval 1.61-6.82, p<0.01) in Hispanic Hp 2-2 women. Hp phenotype does not influence preeclampsia risk, or identify a subset of women who may benefit from vitamin C and E supplementation to prevent preeclampsia.
    PLoS ONE 04/2013; 8(4):60479-. · 3.73 Impact Factor
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    ABSTRACT: Objective We sought to determine whether haptoglobin (Hp) phenotype is related to preeclampsia risk, or to plasma concentrations of soluble endoglin (sEng), soluble fms-like tyrosine kinase 1 (sFlt-1), and placental growth factor (PlGF). Study design Hp phenotype was retrospectively determined in primiparous women with uncomplicated pregnancies (n = 309), gestational hypertension (n = 215), and preeclampsia (n = 249). Phenotype was assessed by peroxidase staining following native polyacrylamide gel electrophoresis of hemoglobin-supplemented serum. Results Compared with Hp 1-1, Hp 2-1 was associated with a significantly increased risk of preeclampsia (odds ratio, 2.11; 95% confidence interval, 1.07–4.18) and term preeclampsia (odds ratio, 2.45; 95% confidence interval, 1.07–5.83) in Caucasian women. Hp phenotype was not associated with preeclampsia risk in African Americans. Preeclamptic women had higher plasma sEng and sFlt-1, and lower PlGF, than control subjects. sEng, sFlt-1, and PlGF did not differ among women of different Hp phenotypes. Conclusion Hp 2-1 is associated with higher preeclampsia risk in primiparous Caucasian women.
    American Journal of Obstetrics and Gynecology 02/2012; · 3.88 Impact Factor
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    ABSTRACT: We sought to determine whether haptoglobin (Hp) phenotype is related to preeclampsia risk, or to plasma concentrations of soluble endoglin (sEng), soluble fms-like tyrosine kinase 1 (sFlt-1), and placental growth factor (PlGF). Hp phenotype was retrospectively determined in primiparous women with uncomplicated pregnancies (n = 309), gestational hypertension (n = 215), and preeclampsia (n = 249). Phenotype was assessed by peroxidase staining following native polyacrylamide gel electrophoresis of hemoglobin-supplemented serum. Compared with Hp 1-1, Hp 2-1 was associated with a significantly increased risk of preeclampsia (odds ratio, 2.11; 95% confidence interval, 1.07-4.18) and term preeclampsia (odds ratio, 2.45; 95% confidence interval, 1.07-5.83) in Caucasian women. Hp phenotype was not associated with preeclampsia risk in African Americans. Preeclamptic women had higher plasma sEng and sFlt-1, and lower PlGF, than control subjects. sEng, sFlt-1, and PlGF did not differ among women of different Hp phenotypes. Hp 2-1 is associated with higher preeclampsia risk in primiparous Caucasian women.
    American journal of obstetrics and gynecology 01/2012; 206(4):358.e10-8. · 3.28 Impact Factor
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    Tracey L Weissgerber, Gregory A L Davies, Michael E Tschakovsky
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    ABSTRACT: Whether brachial artery FMD (flow-mediated dilation) is altered in pregnancy by 28-35 weeks compared with non-pregnant women remains controversial. The controversy may be due to limitations of previous studies that include failing to: (i) test non-pregnant controls in the mid-late luteal phase, (ii) account for effects of pregnancy on the dilatory shear stimulus, (iii) account for physical activity or (iv) control for inter-individual variation in the time to peak FMD. In the present study, brachial artery FMD was measured in 17 active and eight sedentary pregnant women (34.1±1.6 weeks of gestation), and in 19 active and 11 sedentary non-pregnant women (mid-late luteal phase). Decreased vascular tone secondary to increased shear stress contributes minimally to pregnancy-induced increases in baseline brachial artery diameter, as shear stress removal during distal cuff inflation in pregnant women did not reduce diameter to baseline levels observed in non-pregnant controls. Neither the shear stimulus nor the percentage FMD was affected by pregnancy or regular exercise. Continuous diameter measurements are required to control for delayed peak dilation during pregnancy (57±15 compared with 46±15 s; P=0.012), as post-release diameter measured at 60 or 55-65 s post-release underestimated FMD to a greater extent in non-pregnant than in pregnant women.
    Clinical Science 10/2011; 121(8):355-65. · 4.86 Impact Factor
  • Tracey L Weissgerber, Gregory A L Davies, James M Roberts
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    ABSTRACT: This cross-sectional study examined mechanisms through which exercise might alter preeclampsia risk by estimating the effects of acute and chronic exercise on angiogenic markers in healthy pregnant women with different amounts of regular exercise participation. Serum-soluble fms-like tyrosine kinase-1 (sFlt-1), placental growth factor (PlGF), and soluble endoglin (sEng) were measured before and after 20 min of moderate-intensity cycle ergometry in normotensive, nonsmoking pregnant (16 active, 9 inactive, 34.1+/-1.6 wk gestation) and nonpregnant (15 active, 12 inactive, midlate luteal phase) women. Inactive women did not regularly exercise at an intensity that was sufficient to cause sweating. Active women exercised for at least 3 h/wk. Inactive pregnant women had significantly lower PlGF concentrations [median (interquartile range): 268 (159, 290) vs. 278 (221, 647) pg/ml, P=0.014] and higher sFlt-1 [5,180 (4,540, 5,834) vs. 4,217 (2,014, 5,481) pg/ml, P=0.005] and sEng concentrations [9.1 (7.7, 16.7) vs. 7.8 (6.5, 10.1) ng/ml, P=0.025] than active pregnant women. This effect of regular exercise participation was not observed in nonpregnant women. Acute exercise in pregnancy was not associated with antiangiogenic changes that might contribute to preeclampsia; rather, there was a small, but statistically significant, increase in PlGF following acute exercise in active pregnant women [278 (221, 647) vs. 335 (245, 628) pg/ml, P=0.014]. sFlt-1 increased significantly following acute exercise in inactive nonpregnant women [90 (86, 100) vs. 106 (101, 116) pg/ml, P=0.012], but not in active nonpregnant women. Regular exercise during pregnancy is associated with higher serum PlGF and lower sFlt-1 and sEng concentrations in late gestation, a difference that is unlikely to have predated the pregnancy.
    Journal of Applied Physiology 03/2010; 108(5):1217-23. · 3.48 Impact Factor
  • Tracey L Weissgerber, Gregory A L Davies, Michael E Tschakovsky
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    ABSTRACT: Radial artery diameter decreases when a wrist cuff is inflated to stop blood flow to distal tissue. This phenomenon, referred to as low flow-mediated vasoconstriction (L-FMC), was proposed as a vascular function test. Recommendations that L-FMC be measured concurrently with flow-mediated dilation (FMD) were based on radial artery data. However, cardiovascular disease prediction studies traditionally measure brachial artery FMD. Therefore, studies should determine whether L-FMC occurs in the brachial artery. The hypothesis that reduced shear causes L-FMC has not been tested. Brachial and radial artery L-FMC and FMD were assessed in active nonpregnant (n=17), inactive nonpregnant (n=10), active pregnant (n=15, 34.1+/-1.2 wk gestation), and inactive pregnant (n=8, 34.2+/-2.2 wk gestation) women. Radial artery diameter decreased significantly during occlusion in all groups (nonpregnant, -4.4+/-4.2%; pregnant, -6.4+/-3.2%). Brachial artery diameter did not change in active and inactive nonpregnant, and inactive pregnant women; however, the small decrease in active pregnant women was significant. Occlusion decreased shear rate in both arteries, yet L-FMC only occurred in the radial artery. Radial artery L-FMC was not correlated with the reduction in shear rate. L-FMC occurs in the radial but not the brachial artery and is not related to changes in shear rate. Positive correlations between L-FMC (negative values) and FMD (positive values) suggest that radial artery FMD may be reduced among women who experience greater L-FMC. Studies should clarify the underlying stimulus and mechanisms regulating L-FMC, and test the hypothesis that endothelial dysfunction is manifested as enhanced brachial artery L-FMC, but attenuated radial artery L-FMC.
    Journal of Applied Physiology 02/2010; 108(5):1097-105. · 3.48 Impact Factor
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    ABSTRACT: Evidence-based guidelines indicate that regular prenatal exercise is an important component of a healthy pregnancy. In addition to maintaining physical fitness, exercise may be beneficial in preventing or treating maternal-fetal diseases. Women who are the most physically active have the lowest prevalence of gestational diabetes (GDM), and prevention of GDM may decrease the incidence of obesity and type 2 diabetes in both mother and offspring. However, few studies have investigated the effectiveness of exercise in delaying or preventing GDM in at-risk women, and exercise prescriptions that optimize outcomes for women with GDM are lacking. Physically active women are also less likely to develop pre-eclampsia, and we have proposed the following 4 mechanisms that may explain this protective effect: enhanced placental growth and vascularity, reduced oxidative stress, reduced inflammation, and correction of disease-related endothelial dysfunction. Exercise may also prevent reproductive complications associated with maternal obesity. Obesity increases the risk of infertility and miscarriage, and weight loss programs that incorporate diet and exercise are a cost-effective fertility treatment that may also reduce the probability of obesity-related complications during pregnancy. Regular exercise following conception may prevent excessive gestational weight gain and reduce post-partum weight retention.
    Applied Physiology Nutrition and Metabolism 01/2007; 31(6):661-74. · 2.01 Impact Factor
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    ABSTRACT: This study determined the time course of changes in resting and exercising respiratory responses during the first half of human pregnancy, and examined the potential roles of plasma osmolality and the strong ion difference ([SID]) as mediators of pregnancy-induced increases in ventilation. Healthy active women (n = 11) were studied serially from 7 to 22 weeks gestation. Responses were compared with preconception data from 14 subjects (six of whom were tested in early pregnancy), and with late-gestation resting data from 10 additional women. Resting and exercising measurements included ventilation, PaCO2, progesterone, osmolality and [SID]. Results were analyzed using mixed-model linear regression. By 7 weeks gestation, increased ventilation resulted in a very large decrease in PaCO2 at rest and during moderate-intensity exercise. Large correlations (r > 0.5) between resting progesterone and PaCO2 support the traditional theory that circulating progesterone stimulates ventilation during pregnancy. The similar time course of changes and large correlations between raw and delta values of PaCO2 and each of plasma osmolality and [SID] also suggest that both variables may influence respiratory control at rest and during exercise in the first half of pregnancy. Future experiments should continue to explore the hypothesis that osmolality and [SID] contribute to pregnancy-induced respiratory changes.
    Respiratory Physiology & Neurobiology 08/2006; 153(1):39-53. · 2.05 Impact Factor
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    ABSTRACT: The primary objective of this study was to develop a cold pressor test (CPT) protocol to evaluate cardiac autonomic function. Secondary objectives were to assess CPT protocol reliability and to examine gender differences in response to orthostatic stress and the CPT. Healthy, normotensive men and women (n = 12 per group) completed 2 trials on different days in the left lateral decubitus and standing postures and during a 6 min CPT (hand immersion while seated). Measurements included R-R interval, blood pressure, ventilatory responses, spontaneous baroreflex sensitivity, and heart rate variability indices. During the CPT, blood pressure and the sympathetic nervous system (SNS) indicator increased significantly and low-frequency power, high-frequency power (normalized for tidal volume), and the parasympathetic nervous system (PNS) indicator decreased significantly. Standing caused significant increases in the SNS indicator and decreases in the R-R interval in both genders. The PNS indicator was higher in women than in men in the left lateral decubitus posture. The 6 min hand-immersion CPT provoked cardiac sympathetic activation and parasympathetic withdrawal; however, it is best suited to studies with a repeated measures design, as analysis of reliability suggests that responses are highly variable between individuals. Performing the CPT in the left lateral decubitus position may prevent vasovagal responses.
    Applied Physiology Nutrition and Metabolism 07/2006; 31(3):235-43. · 2.01 Impact Factor
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    Tracey L Weissgerber, Larry A Wolfe
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    ABSTRACT: After conception, the corpus luteum, placenta, and developing embryo release hormones, growth factors, and other substances into the maternal circulation. These substances trigger a cascade of events that transform the functioning of the maternal cardiovascular, respiratory, and renal systems, which in turn alter the physicochemical determinants of [H(+)]. Following implantation, maternal adaptations fulfill 4 important functions that support fetal growth. Increased availability of substrates and precursors for fetal-placental metabolism and hormone production is mediated by increases in dietary intake, as well as endocrine changes that increase the availability of glucose and low-density lipoprotein (LDL) cholesterol. Transport capacity is enhanced by increases in cardiac output, facilitating the transport of substrates and precursors to the placenta, and fetal waste products to maternal organs for disposal. Maternal-fetal exchange is regulated by the placenta after 10-12 weeks gestation, but it may occur through histiotrophic mechanisms before this time. Disposal of additional waste products (heat, carbon dioxide, and metabolic byproducts) occurs through peripheral vasodilation and increases in skin blood flow, ventilation, and renal filtration. The maternal physiological adaptations described above must meet the combined demands of maternal exercise and fetal growth. More research is needed to formulate evidence-based guidelines for healthy physical activity in early pregnancy.
    Applied Physiology Nutrition and Metabolism 03/2006; 31(1):1-11. · 2.01 Impact Factor
  • Tracey L Weissgerber, Larry A Wolfe, Gregory A L Davies
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    ABSTRACT: Preeclampsia affects 2-7% of pregnancies and is a leading cause of maternal and fetal morbidity and mortality. Despite extensive study, the etiology of preeclampsia is poorly understood. Abnormal placental development, predisposing maternal constitutional factors, oxidative stress, immune maladaptation, and genetic susceptibility have all been hypothesized to contribute to the development of preeclampsia. Physical conditioning and preeclampsia have opposite effects on critical physiological functions. This suggests that regular prenatal exercise may prevent or oppose the progression of the disease. Epidemiologic studies show that occupational and leisure-time physical activity is associated with a reduced incidence of preeclampsia. We hypothesize that this protective effect results from one of more of the following mechanisms: 1) stimulation of placental growth and vascularity, 2) reduction of oxidative stress, and 3) exercise-induced reversal of maternal endothelial dysfunction. Future research should include prospective epidemiological case-control studies that accurately measure occupational and leisure-time physical activity. Controlled randomized clinical trials examining the effects of prenatal exercise on biochemical markers for endothelial dysfunction, placental dysfunction, and oxidative stress are also needed. If future research supports the idea that exercise effectively protects against preeclampsia, this would provide a low-cost intervention that could dramatically improve prenatal care for women at risk of this disease.
    Medicine &amp Science in Sports &amp Exercise 01/2005; 36(12):2024-31. · 4.48 Impact Factor
  • Medicine and Science in Sports and Exercise - MED SCI SPORT EXERCISE. 01/2005; 37.
  • Larry A. Wolfe, Tracey L. Weissgerber, Gregory A. L. Davies
    Medicine and Science in Sports and Exercise - MED SCI SPORT EXERCISE. 01/2004; 36.

Publication Stats

194 Citations
62.39 Total Impact Points

Institutions

  • 2013
    • Mayo Clinic - Rochester
      Rochester, Minnesota, United States
  • 2010–2012
    • University of Pittsburgh
      • Department of Obstetrics, Gynecology and Reproductive Sciences
      Pittsburgh, PA, United States
  • 2010–2011
    • Magee-Womens Hospital
      Pittsburgh, Pennsylvania, United States
  • 2003–2007
    • Queen's University
      • Department of Kinesiology/ Physical and Health Education
      Kingston, Ontario, Canada