1. Obesity and exercise training alter inflammatory pathway skeletal muscle small extracellular vesicle microRNAs
- Author
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Brian P. Sullivan, Yaohui Nie, Sheelagh Evans, Chris K. Kargl, Zach R. Hettinger, Ron T. Garner, Monica J. Hubal, Shihuan Kuang, Julianne Stout, and Timothy P. Gavin
- Subjects
Inflammation ,Nutrition and Dietetics ,Physiology ,Interleukin-8 ,General Medicine ,Extracellular Vesicles ,MicroRNAs ,Phosphatidylinositol 3-Kinases ,Physiology (medical) ,Humans ,Obesity ,RNA, Messenger ,Muscle, Skeletal ,Exercise - Abstract
What is the central question of this study? Is 1 week of exercise training sufficient to reduce local and systemic inflammation? Do obesity and short-term concurrent aerobic and resistance exercise training alter skeletal muscle extracellular vesicle (EV) contents? What is the main finding and its importance? Obesity alters skeletal muscle small EV microRNAs targeting inflammatory and growth pathways. Exercise training alters skeletal muscle small EV microRNAs targeting inflammatory pathways, indicative of reduced inflammation. Our findings provide support for the hypotheses that EVs play a vital role in intercellular communication during health and disease and that EVs mediate many of the beneficial effects of exercise.Obesity is associated with chronic inflammation characterized by increased levels of inflammatory cytokines, whereas exercise training reduces inflammation. Small extracellular vesicles (EVs; 30-150 nm) participate in cell-to-cell communication in part through microRNA (miRNA) post-transcriptional regulation of mRNA. We examined whether obesity and concurrent aerobic and resistance exercise training alter skeletal muscle EV miRNA content and inflammatory signalling. Vastus lateralis biopsies were obtained from sedentary individuals with (OB) and without obesity (LN). Before and after 7 days of concurrent aerobic and resistance training, muscle-derived small EV miRNAs and whole-muscle mRNAs were measured. Pathway analysis revealed that obesity alters small EV miRNAs that target inflammatory (SERPINF1, death receptor and Gα
- Published
- 2022