Chalk and Brown (2014) hypothesized that exercising during pregnancy can permanently alter offspring epigenetics. Epigenetics is literally defined as ‘above genetics’ and includes all heritable variation in gene activity that is not due to changes in the underlying DNA sequence. One such epigenetic mechanism is called DNA methylation, which is the addition of methyl groups to DNA that can alter a gene’s expression patterns (e.g., DNA methylation at a gene’s promoter can lead to silencing of a gene’s expression).
Despite an absence of evidence in humans, Chalk and Brown (2014) suggest that DNA methylation in human offspring may be altered by maternal exercise during pregnancy. Their reasons for this hypothesis are threefold. Firstly, DNA methylation in offspring can be altered by maternal exercise in rats. Secondly, maternal exercise alters offspring phenotypes in humans. Thirdly, exercise is a form of stress, and it is well known that the epigenome is a sensitive barometer of stress experiences during pregnancy in mice.
So how much exercise is too much for a pregnant mother? There appear to be dose-dependent phenotypic effects of maternal exercise during pregnancy. Specifically, too much maternal exercise can have negative effects on offspring. Below is a graph depicting the hypothesized dose-response relation between maternal exercise and offspring epigenetics.
Clearly more research is needed on this topic given that the epigenome between rodents and humans is likely very different based on species-specific evolutionary and ecological histories. From an applied perspective, the dose-response curve will be needed to ensure maximal safety and benefits from maternal exercise on the fetal epigenome.
Below is a reprint to learn more about this important area of research:
Exercise epigenetics and the fetal origins of disease.
Chalk TE, Brown WM. Epigenomics. 2014;6(5):469-72. doi: 10.2217/epi.14.38.