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Exercise During Pregnancy: Developmental Origins of Disease Prevention?

Donovan, Elise L.; Miller, Benjamin F.

Exercise and Sport Sciences Reviews: July 2011 - Volume 39 - Issue 3 - p 111
doi: 10.1097/JES.0b013e31821f7d78
Commentaries to Accompany

Health and Exercise Science, Colorado State University, Fort Collins, CO

Authors for this section are recruited by Commentary Editor: George A. Brooks, Ph.D., FACSM, Department of Integrative Biology, University of California, Berkeley, CA 94720 (E-mail: gbrooks@berkeley.edu).

David Barker hypothesized that poor nutrition in utero can influence a fetus' chance of developing chronic disease later in life. Subsequent research has shown that overfeeding and maternal obesity also predispose offspring to metabolic disease. Offspring of obese and diabetic mothers and offspring born to mothers who consume a high-fat diet are more likely to be large for gestational age, have higher body fat, and be at risk for early development of metabolic disease (5). There is evidence that these outcomes are direct effects of a suboptimal nutritional milieu (excess calories and fat leading to increased fat deposition) and altered epigenetic programming of metabolic pathways (2). In addition, the high-fat maternal diet itself can alter proteins that mediate epigenetic modification such as histone deacetylases (1). Many of the genes epigenetically influenced by nutrition also are affected by exercise or are involved in metabolic processes that are modulated by exercise. It is therefore reasonable to hypothesize that exercise during pregnancy also could mediate future health outcomes through epigenetic modifications (6). In the current issue of Exercise and Sport Sciences Reviews, Hopkins and Cutfield consider how exercise during pregnancy affects developing offspring both in utero and postnatally (5).

The authors review the evidence that favorable health outcomes are likely to result from modest reductions in birth weight within a healthy range, as large for gestational age and small for gestational age are both associated with increased risk for later chronic disease. Hopkins et al. (3,4) have recently published two studies showing a modest decrease in offspring weight and percent fat with moderate-intensity aerobic exercise during the second half of pregnancy. In the same cohort, maternal insulin sensitivity was not affected by exercise but insulin-like growth factors I and II were lower in offspring cord blood. In addition, serum leptin increased in response to exercise during late gestation, and there was a trend toward exercise blunting increases in serum free fatty acids that were observed in a nonexercising group. The population in these studies was healthy and had normal weight, which leads one to wonder if exercise in overweight women would have more profound effects. Furthermore, it leads one to question why there is a paucity of studies examining the potential epigenetic programming effects of exercise during pregnancy. Future research questions include whether epigenetic programming is altered in response to changes in energy balance as a combination of diet and exercise manipulation, whether a high volume of exercise without concomitant changes in diet could lead to inadequate fetal nutrition, or if exercise can favorably change the potential epigenetic programming of an obese or insulin-resistant mother.

Benefits of exercise to the individual are well documented, and the information reviewed by Hopkins and Cutfield indicates that these benefits may carry over to the fetus. In an obese mother, or a mother who is hyperglycemic, hyperinsulinemic, or dyslipidemic, exercise may be more important if it can help normalize the metabolic milieu that the fetus is exposed to, change programming effects, and reduce offspring susceptibility to disease. As we better understand the consequences of changes in the in utero environment for the offspring, interventions including exercise programs can be developed and implemented to minimize offspring health and disease risk. The study of the developmental origins of disease could then include the developmental origins of disease prevention.

Elise L. Donovan

Benjamin F. Miller

Health and Exercise Science

Colorado State University

Fort Collins, CO

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References

1. Aagaard-Tillery KM, Grove K, Bishop J, et al. Developmental origins of disease and determinants of chromatin structure: maternal diet modifies the primate fetal epigenome. J. Mol. Endocrinol. 2008; 41:91-102.
2. Hanson M, Godfrey KM, Lillycrop KA, Burdge GC, Gluckman PD. Developmental plasticity and developmental origins of non-communicable disease: theoretical considerations and epigenetic mechanisms. Prog. Biophys. Mol. Biol. 2011; doi: 10.1016/j.pbiomolbio.2010.12.008.
3. Hopkins SA, Baldi JC, Cutfield WS, McCowan L, Hofman PL. Effects of exercise training on maternal hormonal changes in pregnancy. Clin. Endocrinol. (Oxf). 2011; 74:495-500.
4. Hopkins SA, Baldi JC, Cutfield WS, McCowan L, Hofman PL. Exercise training in pregnancy reduces offspring size without changes in maternal insulin sensitivity. J. Clin. Endocrinol. Metab. 2011; 95:2080-8.
5. Hopkins SA, Cutfield WS. Exercise in pregnancy: weighing up the long-term impact on the next generation. Exerc. Sport Sci. Rev. 2011; 39:120-7.
6. McGee SL, Fairlie E, Garnham AP, Hargreaves M. Exercise-induced histone modifications in human skeletal muscle. J. Physiol. 2009; 587:5951-8.
©2011 The American College of Sports Medicine