PGC-1α Methylation, miR-23a, and miR-30e Expression as Biomarkers for Exercise- and Diet-Induced Mitochondrial Biogenesis in Capillary Blood from Healthy Individuals: A Single-Arm Intervention

Abstract

Healthy mitochondria and their epigenetic control are essential to maintaining health, extending life expectancy, and improving cardiovascular performance. Strategies to maintain functional mitochondria during aging include training; cardiovascular exercise has been suggested as the best method, but strength training has also been identified as essential to health and healthy aging. We therefore investigated the effects of concurrent exercise training and dietary habits on epigenetic mechanisms involved in mitochondrial (mt) functions and biogenesis. We analyzed epigenetic biomarkers that directly target the key regulator of mitochondrial biogenesis, PGC-1α, and mtDNA content. Thirty-six healthy, sedentary participants completed a 12-week concurrent training program. Before and after the intervention, dried blood spot samples and data on eating habits, lifestyle, and body composition were collected. MiR-23a, miR-30e expression, and mtDNA content were analyzed using real-time quantitative polymerase chain reaction (qPCR) analysis. PGC-1α methylation was analyzed using bisulfite pyrosequencing. MiR-23a, miR-30e expression, and PGC-1α methylation decreased after the intervention (p < 0.05). PGC-1α methylation increased with the consumption of red and processed meat, and mtDNA content increased with the ingestion of cruciferous vegetables (p < 0.05). Our results indicate that concurrent training could improve mitochondrial biogenesis and functions by altering the epigenetic regulation. These alterations can also be detected outside of the skeletal muscle and could potentially affect athletic performance.

MiRNA-based “fitness score” to assess the individual response to diet, metabolism, and exercise

“…Furthermore, elite athletes, individuals who participated vigorously in competitive sports (for the past 2 years), and anyone with a history of chronic illness or medication use have been excluded from participation. The participants received a 12-week training intervention that included both endurance and strength training, as previously published by Krammer et al 2022 [ 55 ]. During their training sessions, they were supervised by the gym trainers and our staff and had to keep a training log.…”

Nutritional supplements for athletes and personalization; a short review

“…It was found that PGC-1α methylation decreased after the intervention, while PGC-1α methylation increased with the consumption of red and processed meat, and mtDNA content increased with the ingestion of cruciferous vegetables. These results indicate that concurrent training could improve mitochondrial biogenesis and its functions by altering the epigenetic regulation [7]. Exercise changes the mitochondrial content and quality, which is beneficial for metabolic health.…”

“…Adaptation to exercise leads to a release of miRNAs from muscle tissue and other organs into our blood circulation [7,9]. This has the potential to affect signaling pathways such as the IGF1/PI3K/AKT/mTOR axis, which are changing rapidly during exercise and recovery.…”

Epigenomic and Other Evidence for Cannabis-Induced Aging Contextualized in a Synthetic Epidemiologic Overview of Cannabinoid-Related Teratogenesis and Cannabinoid-Related Carcinogenesis

“…Since mitochondria supply energy and epigenomic substrates to the nucleus and interact with it closely via mitohormetic and mitonuclear balance systems [ 148 , 149 ] metabolic inhibition implies epigenomic disruption. Mitochondrial inhibition is well established as one of the key hallmarks of aging [ 1 , 150 , 151 , 152 , 153 , 154 , 155 , 156 , 157 , 158 ] and implicated pathophysiological pathways include such novel mechanisms as the leakage of mitochondrial DNA into the cytosol and stimulation of innate γ-interferon-dependent immunity via the cGAS-STING pathway [ 156 ].…”