Abstract des Autors

Many different types of exercise and physical activity induce mechanical, hormonal, and metabolic stimuli that lead to adaptions in almost every tissue and cell type. Recent research has shown that both acute exercise and chronic exercise are potential epigenetic modifiers (affecting DNA methylation, posttranslational histone modifications, and the expression of microRNAs) that change the functional genome in gametes, muscle, blood, and fat cells in brain tissue as well as in cells of the cardiovascular system. The results of these studies reveal that exercise-induced epigenetic modifications may counteract pathophysiological alterations of the epigenome in diseased states (e.g., cancer, neurodegenerative disorders, cardiovascular diseases). It is hypothesized that the beneficial preventative and rehabilitative effects of exercise are at least partly driven by epigenetic modifications, which contribute to reduced systemic inflammation and local adaptions, such as the demethylation of tumor suppressor genes. Furthermore, data show that responders to certain exercise programs (e.g., resistance training) have different epigenetic patterns compared to non-responders. Additionally, different types and intensities of exercise exhibit specific epigenetic responses that can be directly measured in muscle tissue and the circulation. Therefore, epigenetic adaptions may be used in clinical trials or in the field as markers for exercise conducting and controlling in the future. However, more research is needed to generate meaningful knowledge about exercise-induced epigenetic modifications in particular tissues as well as the local and systemic consequences of these modifications. As exercise seems to provoke different responses throughout the life span—and considering the popular belief that exercise can rewind the “epigenetic clock”—age should always be considered as a covariate in further studies.