Abstract
ObjectiveTo determine the effects of combined aerobic and resistance exercise training during the second half of pregnancy on endothelial NOS expression (eNOS), nitric oxide (NO) production and oxygen metabolism in human placenta.MethodsThe study included 20 nulliparous in gestational week 16–20, attending prenatal care at three tertiary hospitals in Colombia who were randomly assigned into one of two groups: The exercise group (n = 10) took part in an exercise session three times a week for 12 weeks which consisted of: aerobic exercise at an intensity of 55–75% of their maximum heart rate for 60 min and 25 mins. Resistance exercise included 5 exercise groups circuit training (50 repetitions of each) using barbells (1–3 kg/exercise) and low-to-medium resistance bands. The control group (n = 10) undertook their usual physical activity. Mitochondrial and cytosol fractions were isolated from human placental tissue by differential centrifugation. A spectrophotometric assay was used to measure NO production in cytosolic samples from placental tissue and Western Blot technique to determine eNOS expression. Mitochondrial superoxide levels and hydrogen peroxide were measured to determine oxygen metabolism.ResultsCombined aerobic and resistance exercise training during pregnancy leads to a 2-fold increase in eNOS expression and 4-fold increase in NO production in placental cytosol (p = 0.05). Mitochondrial superoxide levels and hydrogen peroxide production rate were decreased by 8% and 37% respectively in the placental mitochondria of exercising women (p = 0.05).ConclusionRegular exercise training during the second half of pregnancy increases eNOS expression and NO production and decreases reactive oxygen species generation in human placenta. Collectively, these data demonstrate that chronic exercise increases eNOS/NO production, presumably by increasing endothelial shear stress. This adaptation may contribute to the beneficial effects of exercise on the vascular and antioxidant system and in turn reduce the risk of preeclampsia, diabetes or hypertension during pregnancy.
Highlights
Pregnancy is a physiological state characterized by hemodynamic changes, such as an increase in heart rate at rest, increased cardiac output and diminished peripheral vascular resistance [1]
A decreased production or an increased inactivation of nitric oxide (NO) has been linked to the endothelial dysfunction that characterizes pre-eclampsia, gestational diabetes and hypertension [2]
We developed a special protocol by flow cytometry in order to detect superoxide anion not consumed by the MnSOD in isolated mitochondria
Summary
Pregnancy is a physiological state characterized by hemodynamic changes, such as an increase in heart rate at rest, increased cardiac output and diminished peripheral vascular resistance [1]. These adaptations appear to be mediated to a great extent by an increased endothelium-dependent vasodilation. The endothelial release of nitric oxide (NO) has been proposed as the main factor responsible for the decreased systemic vascular resistance observed during pregnancy [1]. A decreased production or an increased inactivation of NO has been linked to the endothelial dysfunction that characterizes pre-eclampsia, gestational diabetes and hypertension [2]. Placental mitochondria are one of the a major source of oxidative stress in pre-eclampsia [3,4]
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