Vascular effects of aerobic exercise training in rat adult offspring exposed to hypoxia‐induced intrauterine growth restriction

Reyes, Laura M.; Morton, Jude S.; Kirschenman, Raven; DeLorey, Darren S.; Davidge, Sandra T.

doi:10.1113/jphysiol.2014.288449

Cited by 20 publications

(28 citation statements)

References 62 publications

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“…It has been shown that exercise training in IUGR animals improved the metabolic phenotype associated with being born growth restricted by increasing insulin sensitivity in female Sprague-Dawley rats (14) and by increasing relative islet surface area and ␤-cell mass in male Wistar-Kyoto rats (21). Furthermore, we found that aerobic exercise training had beneficial vascular effects in enhancing endothelium-derived hyperpolarization-mediated vasodilation in gastrocnemius muscle arteries from male IUGR offspring (26). The impact of aerobic exercise training on cardiac performance in IUGR offspring, however, remains unknown.…”

supporting

confidence: 49%

Aerobic exercise training reduces cardiac function in adult male offspring exposed to prenatal hypoxia

Reyes

Kirschenman

Quon

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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Intrauterine growth restriction (IUGR) has been associated with increased susceptibility to myocardial ischemia-reperfusion (I/R) injury. Exercise is an effective preventive intervention for cardiovascular diseases; however, it may be detrimental in conditions of compromised health. The aim of this study was to determine whether exercise training can improve cardiac performance after I/R injury in IUGR offspring. We used a hypoxia-induced IUGR model by exposing pregnant Sprague-Dawley rats to 21% oxygen (control) or hypoxic (11% oxygen; IUGR) conditions from gestational day 15 to 21. At 10 wk of age, offspring were randomized to a sedentary group or to a 6-wk exercise protocol. Transthoracic echocardiography assessments were performed after 6 wk. Twenty-four hours after the last bout of exercise, ex vivo cardiac function was determined using a working heart preparation. With exercise training, there was improved baseline cardiac performance in male control offspring but a reduced baseline cardiac performance in male IUGR exercised offspring (P < 0.05). In male offspring, exercise decreased superoxide generation in control offspring, while in IUGR offspring, it had the polar opposite effect (interaction P ≤ 0.05). There was no effect of IUGR or exercise on cardiac function in female offspring. In conclusion, in male IUGR offspring, exercise may be a secondary stressor on cardiac function. A reduction in cardiac performance along with an increase in superoxide production in response to exercise was observed in this susceptible group.

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supporting

confidence: 49%

Aerobic exercise training reduces cardiac function in adult male offspring exposed to prenatal hypoxia

Reyes

Kirschenman

Quon

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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“…, Reyes et al . ) and can therefore contribute to the microvascular complications that occur in some of these diseases. The development of well‐targeted therapeutics for ameliorating the effects of such diseases on EDH requires a detailed understanding of the particular processes involved in EDH hyperpolarization and relaxation that are impaired in disease.…”

Section: Endothelium‐dependent Vasorelaxationmentioning

confidence: 99%

Nonlinear effects of potassium channel blockers on endothelium-dependent hyperpolarization

2016

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In a number of published studies on endothelium-dependent hyperpolarization and relaxation, the results of the effects of K blockers have been difficult to interpret. When the effects of two blockers have been studied, often either blocker by itself had little effect, whereas the two blockers combined tended to abolish the responses. Explanations suggested in the literature include an unusual pharmacology of the K channels, and possible blocker binding interactions. In contrast, when we applied the same blockers to segments of small blood vessels under voltage clamp, the blockers reduced the endothelium-dependent K current in a linearly additive manner. Resolution of these contrasting results is important as endothelium-derived hyperpolarization (EDH) makes its greatest contribution to vasorelaxation in arterioles and small resistance arteries, where it can exert a significant role in tissue perfusion and blood pressure regulation. Furthermore, EDH is impaired in various diseases. Here, we consider why the voltage-clamp results differ from earlier free-running membrane potential and contractility studies. We fitted voltage-clamp-derived current-voltage relationships with mathematical functions and considered theoretically the effects of partial and total block of endothelium-derived K -currents on the membrane potential of small blood vessels. When the K -conductance was partially reduced, equivalent to applying a single blocker, the effect on EDH was small. Total block of the endothelium-dependent K conductance abolished the hyperpolarization, in agreement with various published studies. We conclude that nonlinear summation of the hyperpolarizing response evoked by endothelial stimulation can explain the variable effectiveness of individual K channel blockers on endothelium-dependent hyperpolarization and resulting relaxation.

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“…Exercise training in the offspring of rodent models of maternal nutrient restriction (131) or bilateral uterine artery ligation (207) has been shown to lead to beneficial metabolic effects on glucose and insulin handling. A recent study in growth-restricted offspring of hypoxia-exposed rats demonstrated a differential effect of aerobic exercise from 10 to 16 wk of age on the improvement of vascular function in males and females; these data suggested that exercise training in female offspring may not be beneficial in this population (322). It is possible that exercise may represent a secondary stressor that may not be well tolerated in developmentally programmed offspring.…”

Section: Exercisementioning

confidence: 99%

In Utero Origins of Hypertension: Mechanisms and Targets for Therapy

Morton

Cooke

Davidge³

2016

Physiological Reviews

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The developmental origins of health and disease theory is based on evidence that a suboptimal environment during fetal and neonatal development can significantly impact the evolution of adult-onset disease. Abundant evidence exists that a compromised prenatal (and early postnatal) environment leads to an increased risk of hypertension later in life. Hypertension is a silent, chronic, and progressive disease defined by elevated blood pressure (>140/90 mmHg) and is strongly correlated with cardiovascular morbidity/mortality. The pathophysiological mechanisms, however, are complex and poorly understood, and hypertension continues to be one of the most resilient health problems in modern society. Research into the programming of hypertension has proposed pharmacological treatment strategies to reverse and/or prevent disease. In addition, modifications to the lifestyle of pregnant women might impart far-reaching benefits to the health of their children. As more information is discovered, more successful management of hypertension can be expected to follow; however, while pregnancy complications such as fetal growth restriction, preeclampsia, preterm birth, etc., continue to occur, their offspring will be at increased risk for hypertension. This article reviews the current knowledge surrounding the developmental origins of hypertension, with a focus on mechanistic pathways and targets for therapeutic and pharmacologic interventions.

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Vascular effects of aerobic exercise training in rat adult offspring exposed to hypoxia‐induced intrauterine growth restriction

Cited by 20 publications

References 62 publications

Aerobic exercise training reduces cardiac function in adult male offspring exposed to prenatal hypoxia

Aerobic exercise training reduces cardiac function in adult male offspring exposed to prenatal hypoxia

Nonlinear effects of potassium channel blockers on endothelium-dependent hyperpolarization

In Utero Origins of Hypertension: Mechanisms and Targets for Therapy

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