Physical activity in the prevention of human diseases: role of epigenetic modifications

Abstract

Epigenetic modification refers to heritable changes in gene function that cannot be explained by alterations in the DNA sequence. The current literature clearly demonstrates that the epigenetic response is highly dynamic and influenced by different biological and environmental factors such as aging, nutrient availability and physical exercise. As such, it is well accepted that physical activity and exercise can modulate gene expression through epigenetic alternations although the type and duration of exercise eliciting specific epigenetic effects that can result in health benefits and prevent chronic diseases remains to be determined. This review highlights the most significant findings from epigenetic studies involving physical activity/exercise interventions known to benefit chronic diseases such as metabolic syndrome, diabetes, cancer, cardiovascular and neurodegenerative diseases.

Keywords: DNA methylation; Disease prevention; Exercise; Histone modification.

Fig. 1

Small-scale intervention protocols from human and animal studies focusing on the exercise-related epigenetic modulations in human diseases and/or in specific disease candidate genes. * Exercise-induced hypermethylation (ADAMT59, CPEB4, GRB14, ITPR2, LY86, LYPLAL1, MAP2K5, MSRA, MTIF3, MRXN3, PRKD1, SOCCAG8, STAB1, TBX15, TMEM160, ZNF608) or hypomethylation (GPRC58, TUB) in obesity candidate genes [85]. **Exercise-induced hypermethylation (ADAMT59, ADCY5, ARAP1, BCL11A, CDKAL1, CDKN2A, DGKB, DUSP8, FTO, HHEX, HMGA2, IGF2BP2, JAZF1, KCNQ1, PRC1, PROX1, PTPRD, TCF7L2, THADA, WFS1, ZBED3) or hypomethylation (KCNQ1, TCF7L2) in T2D candidate genes [85]