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Learn MoreAcute aerobic exercise has been shown to improve skeletal muscle mitochondrial function and completeness of fatty acid -oxidation which contributes to reduction in lipid accumulation. We hypothesize that epigenetic regulation of mitochondrial genes due to exercise may lead to increased mitochondrial function in overweight/obese (Ov/Ob) individuals. 30 men, aged 19-30 years, were recruited and divided into two groups: lean (BMI<25, 18.5- 24.1 kg/m2, n=15) and Ov/Ob (BMI25, 25.5- 36.9 kg/m2, n=15). Four hours after eating a standardized high-carbohydrate breakfast (7 kcal/kg; 60% carbohydrate, 25% fat, 15% protein), they performed an acute bout of cycling exercise (50% VO2max, spending ~650 kcal). Thirty minutes before eating the breakfast, vastus lateralis muscle biopsy samples were collected (Pre). Biopsy samples were also collected immediately after (Post) exercise. In skeletal muscle, gene expression was determined by RNA-seq via the Illumina platform. For analysis, TopHat was used for sequence alignment and Cuffdiff for differential gene expression analysis. ~97% of all sequenced reads from RNA-seq aligned to the genome. As per RNA-seq analysis, in both lean and Ov/Ob, genes upregulated following exercise were enriched for GO terms related to lipid metabolism, mitochondrial biogenesis, function and insulin signaling. Pathway analysis revealed that the AMP-activated protein kinase (AMPK) signaling pathway was one of the pathways enriched in both lean Post and Ov/Ob Post. We found that exercise led the -1N nucleosome to repositioning away from the transcription start site in PGC-1 promoter in both lean and Ov/Ob in association with alterations in gene expression of genes involved in lipid metabolism and mitochondrial adaptations. SOURCE: Tara,M,Henagan (thenagan@purdue.edu) - Nutrition and Exercise Epigenetics Purdue University
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