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Background: Regular, especially sustained exercise training plays an important role in the prevention and treatment of multiple chronic diseases. Some of the underlying molecular and cellular mechanisms behind the adaptive response to physical activity are still unclear, but recent findings suggest a possible role of epigenetic mechanisms, especially miRNAs, in the progression and management of exercise related changes. Due to the combination of the analysis of epigenetic biomarkers (miRNAs), the intake of food and supplements, and genetic dispositions, a “fitness sore” was evaluated to assess the individual response to nutrition, metabolism and exercise.Methods: In response to a 12-week sport intervention we analyzed genetic and epigenetic biomarkers in capillary blood, including Line-1 methylation, three SNPs and ten miRNAs using HRM and qPCR analysis. These biomarkers were also analyzed in a control group without intervention. Food frequency intake, including dietary supplement intake, and general health questionnaires were surveyed under the supervision of trained staff.Results: Exercise training decreased the expression of miR-20a, -22 and -505 (p < 0.02) and improved the “fitness score”, which estimates eight different lifestyle factors to assess, nutrition, inflammation, cardiovascular fitness, injury risk, regeneration, muscle- and hydration status as well as stress level. In addition, we were able to determine correlations between individual miRNAs, miR-20a, -22 and -101 (p < 0.04), and the genetic predisposition for endurance and / or strength and for obesity risk (ACE, ACTN3 and FTO), as well as between miRNAs and the body composition (p < 0.05). And we identified two miRNAs, miR-19b and -378a (p < 0.05), which could potentially provide information about the micronutrient / vitamin requirements of an athlete.Conclusions: Due to the detailed knowledge of individual regulatory mechanisms in the metabolism of sport intervention and / or nutritional behavior, this knowledge and our results can be used for personalized interventions and in the context of the new field of precision nutrition and precision training.

Introduction: Topical investigations have demonstrated that oxidative stress and inflammation play key roles in biological aging and determine incidence and course of age-related diseases. Lifestyle and environmental factors hugely impact epigenetic regulation and DNA stability with telomere attrition and epigenetic instability providing a potential record of the cumulative burden of endogenous and exogenous oxidative noxae. Certain physiologically active plant components exhibit antioxidative activities affecting epigenetic regulation of inflammation response and DNA repair. Methods: Against this background, the present study investigated green tea polyphenol epigallocatechin gallate (EGCG) in the context of telomere regulation in Caco-2 colorectal adenocarcinoma cells vs. ES-1 primary skin fibroblasts. Cell lines were treated with 20 and 200 µM EGCG for 36, 72 and 144 hours, respectively. Telomerase activity, relative telomere length as well as methylation status of hTERT and c-Myc from different culture conditions were assessed. Malondialdehyde (MDA) served as a surrogate marker of potential pro-oxidative effects of EGCG in a physiologically relevant tissue model. Results: EGCG incubation was associated with telomere shortening and decreased telomerase activity in Caco-2 cells, and relatively longer telomeres along with increased methylation of six 5'—C—phosphate—G—3' (CpG) sites in the promoter region of human Telomerase Reverse Transcriptase ( hTERT) in fibroblasts. At low concentrations, EGCG significantly decreased oxidative damage to lipids in Caco-2 cells and attenuated H 2 O 2 induced oxidation at higher concentrations. Conclusion: These results suggest differential EGCG-mediated telomeric modulation in cancer vs. primary cells and a specific antioxidant activity of EGCG against oxidative damage to lipids in abnormal cells. Keywords: Caco-2, epigallocatechin gallate, telomeres, hTERT, DNA methylation, telomerase, oxidative stress, malondialdehyde