Current topicInfluence of Endurance Exercise and Diet on Human Placental Development and Fetal Growth☆
Introduction
In recent years it has become apparent that both the maternal environment and maternal lifestyle factors influence many of the maternal physiological adaptations to pregnancy that regulate feto-placental growth. The purpose of this paper is to review what is known about the interaction amongst two maternal lifestyle variables (specific types of physical activity and dietary intake) and feto-placental growth in the human. It begins with a brief discussion of current growth-regulatory concepts and mechanisms that may mediate these interactions. This is followed by a review of the effects of maternal exercise and diet on the physiological variables of interest. Then, some of the descriptive and intervention studies, which address the effects of exercise and diet on feto-placental growth, will be discussed. Finally, the potential preventive and/or therapeutic value of maternal exercise and diet in the health care of those at risk for disorders of placentation or growth in utero due to social, environmental or medical circumstance is addressed. The review ends with a brief discussion of exercise prescription for healthy women experiencing uncomplicated pregnancies.
Section snippets
Mechanism of feto-placental growth regulation
A large amount of experimental data reviewed elsewhere [1], [2], [3], [4], [5], indicates that the availability and rate of delivery of oxygen and nutrient at the maternal–fetal interphase are major regulators of feto-placental growth in multiple animal species and the human. For instance, the early observations of Ziegler [6] suggested that increased maternal intake of processed carbohydrate stimulated fetal growth rate in the human. This hypothesis was tested experimentally by Mellor [7]. In
Maternal physiological variables of interest
The rate of placental bed blood flow, hemoglobin content, the partial pressure of oxygen and the concentration of nutrient in maternal arterial blood are the basic physiological determinants of the availability or rate of delivery of oxygen and substrate at the maternal–fetal interphase.
Normal pregnancy adaptations that increase placental bed blood flow include hormonally mediated vascular growth and remodeling, changes in vascular tone and distensibility, trophoblastic invasion, decreased
Acute and chronic effects of exercise and diet on placental bed blood flow and nutrient delivery
During acute exercise the rate of visceral blood flow decreases as flow rate to the exercising muscle and skin increases [24], [25]. The magnitude of the decrease varies with the type (intermittent versus sustained, weight bearing versus non-weight bearing, muscle mass utilized, etc.), intensity and duration of the exercise. The magnitude of the exercise-associated decrease in the rate of placental bed blood flow during human pregnancy has not been directly ascertained. However, animal studies,
Effect of maternal exercise on placental growth and development
Studies assessing the effect of maternal exercise on placental growth and functional capacity are limited but all indicate that regular weight-bearing forms of exercise influence placental growth and anatomic indices of functional capacity [36], [37], [38], [39], [40]. The exact reason for this remains unclear but, as discussed earlier, it is likely that the exercise-induced intermittent fluctuations in substrate and oxygen delivery produce a recurrent stimulus which evokes a different overall
Effect of maternal exercise on size at birth and neonatal lean body mass and fat mass
The placental effects detailed above would be expected to alter nutrient transfer, fetal growth rate, size at birth and neonatal morphometrics. Our experience indicates that is indeed the case. Although many studies reviewed elsewhere have not identified an effect on size at birth [3], [34], [43], our experience indicates that these specific effects on growth are obvious at birth. The results of our prospective, randomized studies indicate that the reasons for this discrepancy are threefold.
Effect of diet on maternal blood glucose levels, placental development, size at birth, neonatal fat mass and lean body mass
Our studies on the effects of maternal sustained, weight-bearing exercise on fetal growth and development began over 20 years ago. Initially, we attributed the exercise effects on maternal weight gain and size at birth entirely to excessive energy expenditure and the recurrent exercise-induced decreases in maternal blood glucose levels and placental bed blood flow which limited delivery of oxygen and substrate to the placental site [47], [48]. After 10 years experience, however, it became clear
The potential clinical value of modifying maternal exercise and diet
Exercise and diet are two easily modifiable lifestyle variables that have been shown to influence various aspects of feto-placental growth and to specifically reduce the risk of small-for-gestational age newborns in an at-risk populace [4], [30], [31], [38], [39], [40], [43], [56]. Furthermore, maternal benefits are clear and follow-up studies have demonstrated that both have either neutral or positive effects on neurodevelopment and growth in infancy and childhood [43], [58], [59], [60].
Thus,
Summary
In summary, these findings indicate that both maternal physical activity and dietary glycemic load modify several of the physiological adaptations to pregnancy that are coincidentally important acute and chronic regulators of the availability of oxygen and substrate at the maternal–fetal interphase. The latter appears to be the major factor that initiates a growth-regulatory sequence which balances feto-placental growth rate with the availability of substrate and oxygen from the maternal
References (74)
- et al.
Aspects of human fetoplacental vasculogenesis and angiogenesis. 1. Molecular regulation
Placenta
(2004) - et al.
Maternal adaptation to high-altitude pregnancy: an experiment of nature – a review
Placenta
(2004) The effects of maternal exercise on fetal oxygenation and feto-placental growth
Eur J Obstet Gynecol Reprod Biol
(2003)Nutritional and placental determinants of fetal growth rate in sheep and consequences for the newborn lamb
Br Vet J
(1983)- et al.
Mechanism of oxygen sensing in human trophoblast cells
Placenta
(2002) - et al.
Maternal IGF-I levels reflect placental mass and fetal fat mass
Am J Obstet Gynecol
(2004) - et al.
Human placental growth hormone causes severe insulin resistance in transgenic mice
Am J Obstet Gynecol
(2002) - et al.
Portal vein blood flow – effects of pregnancy, gravity and exercise
Am J Obstet Gynecol
(2000) - et al.
Cardiovascular function before, during, and after the first and subsequent pregnancies
Am J Cardiol
(1997) - et al.
Effect of recreational exercise on mid-trimester placental growth
Am J Obstet Gynecol
(1992)
The effects of maternal aerobic exercise on human placental development: placental volumetric composition and surface areas
Placenta
The changing glycemic response to exercise during pregnancy
Am J Obstet Gynecol
Beginning regular exercise in early pregnancy: effect on fetoplacental growth
Am J Obstet Gynecol
Continuing regular exercise during pregnancy: effect of exercise volume on fetoplacental growth
Am J Obstet Gynecol
Running throughout pregnancy: effect on placental villous vascular volume and cell proliferation
Placenta
Maternal insulin-like growth factor-I levels reflect placental mass and neonatal fat mass
Am J Obstet Gynecol
Maternal and fetal responses to a maternal aerobic exercise program
Am J Obstet Gynecol
Neonatal morphometrics after endurance exercise in pregnancy
Am J Obstet Gynecol
A clinical approach to exercise in pregnancy
Clin Sports Med
The use of the glycemic index in predicting the blood glucose response to mixed meals
Am J Clin Nutr
International table of glycemic index and glycemic load values
Am J Clin Nutr
Glycemic control in diabetes mellitus – how tight is tight enough: small for gestational age versus large for gestational age
Am J Obstet Gynecol
Maternal carbohydrate metabolism and its relationship to fetal growth and body composition
Am J Obstet Gynecol
NICHD diabetes in early pregnancy study. Maternal postprandial glucose levels and infant birth weight: the diabetes and early pregnancy study
Am J Obstet Gynecol
The neonatal behavioral profile of the offspring of women who continued to exercise regularly throughout pregnancy
Am J Obstet Gynecol
One year morphometric and neurodevelopmental outcome of offspring of women who continued to exercise regularly throughout pregnancy
Am J Obstet Gynecol
The morphometric and neurodevelopmental outcome at 5 years of the offspring of women who continued to exercise throughout pregnancy
J Pediatr
Randomized trial of diet vs. diet plus cardiovascular conditioning on glucose levels in gestational diabetes
Am J Obstet Gynecol
Resistance exercise decreases the need for insulin in overweight women with gestational diabetes mellitus
Am J Obstet Gynecol
Energy metabolism during pregnancy: influence of maternal energy status
Am J Clin Nutr
Physiology of pregnancy and nutrient metabolism
Am J Clin Nutr
Energy adaptations in human pregnancy: limits and long-term consequences
Am J Clin Nutr
Effect of energy and protein intakes during pregnancy outcome: an overview of the research evidence from controlled clinical trials
Am J Clin Nutr
Maternal carbohydrate intake and pregnancy outcome
Proc Nutr Soc
Physiological adaptation to intrauterine growth retardation
Sugar consumption and prenatal acceleration. I. Studies in the history of medicine on the coincidence and connection of these 2 secular phenomena
Helv Paediatr Acta
Studies of babies born at high altitude
Am J Dis Child
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Heat loss responses at rest and during exercise in pregnancy: A scoping review.
2021, Journal of Thermal BiologyCitation Excerpt :Throughout pregnancy, heat transfer between mother and fetus occurs predominantly via the placental wall and uterine blood flow (Ziskin and Morrissey, 2011). In circumstances when maternal core temperature increases, there is evidence of reduced uterine blood flow demonstrated in pregnant ewes (Chandler and Bell, 1981; Clapp, 1980), although maternal-fetal protective mechanisms exist to maintain nutrient supply to the fetus (Clapp, 2006; Lotgering et al., 1983; Curet et al., 1976). Fetal heat balance is maintained by a temperature difference of ~0.5 °C greater in fetus compared to mother, most of the heat dissipation occurs via convective cooling in umbilical and placental blood circulation (Schröder and Power, 1997; Asakura, 2004; Power, 1989) and ~15% happens through conductive cooling via amniotic fluids (Asakura, 2004).
Maternal Inactivity Programs Skeletal Muscle Dysfunction in Offspring Mice by Attenuating Apelin Signaling and Mitochondrial Biogenesis
2020, Cell ReportsCitation Excerpt :Physical exercise is highly accessible and a prominent therapeutic tool to combat diet-induced obesity in adults (Peres Valgas da Silva et al., 2019). Based on epidemiological studies, exercise during pregnancy is beneficial for maternal health and neonatal outcomes (Barakat et al., 2015; Davenport et al., 2018; Gustafsson et al., 2016; Nascimento et al., 2012), which is supported by animal and human studies (Clapp, 2006; Hopkins and Cutfield, 2011; Mangwiro et al., 2018; Moyer et al., 2016; Son et al., 2019b). However, these available studies focus on measurements of offspring outcomes due to ME of obese dams (Stanford et al., 2015, 2017).
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2020, TheriogenologyA risk-benefit analysis of maintaining an aerobic-endurance triathlon training program during pregnancy: A review
2018, Science and SportsCitation Excerpt :There is an increase in cell proliferation in the placenta of mothers who continued to run throughout pregnancy [28]. The mechanism thought responsible is a transient reduction in placental blood flow during exercise stimulating the vascular endothelial growth factor (VEGF) system that promotes angiogenesis [14]. As a result of exercise, placental growth occurs and oxygen and substrate delivery is increased at rest.
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Supported by NIH grants HD21268, RR00080, RR00109 and MetroHealth Medical Center.