Exercise Responsiveness in Obese Adults

Kevin Gries, Corey Hart, Hawley Kunz, Zachary Ryan, Xiaoyan Zhang, Mojtaba Parvizi, Yuanhang Liu, Surendra Dasari, Ian Lanza

Research output: Contribution to journalArticlepeer-review

Abstract

Obesity is associated with several skeletal muscle impairments which can be improved through an aerobic exercise prescription. The possibility that exercise responsiveness is diminished in people with obesity has been suggested but not well-studied. PURPOSE: The purpose of this study was to investigate how obesity influences acute exercise responsiveness within skeletal muscle. METHODS: Non-obese (NO; n=19; 10F/9M; BMI=25.1 ± 2.8 kg/m2 ) and Obese (O; n=21; 14F/7M; BMI=37.3 ± 4.6 kg/m2 ) adults performed 30 minutes of single-leg cycling at 70% of VO2 peak. Serial muscle biopsies (vastus lateralis) were collected before exercise and 3 and 6 hours post-exercise to measure protein synthesis and gene expression. RESULTS: The exercise-induced fold change in mixed muscle protein synthesis trended (p=0.058) higher in NO (1.28 ± 0.54-fold) compared to O (0.95 ± 0.42-fold) and was inversely related to BMI (r=-.374, p=0.027). RNA sequencing revealed 331 and 280 genes that were up or downregulated after exercise in NO and O, respectively. Gene set enrichment analysis showed O had blunted post-exercise pathways related to MAPK signaling, chemokine-mediated signaling, FC receptor mediated stimulation signaling, cell proliferation, apoptosis, and RNA polymerase II promotion. Quantitative polymerase chain reaction of select metabolic (PGC1a, PGC1b, TFAM, PDK4, IRS, MAPK, and PRKAA1) and muscle growth (SLC, TBC, MSTN, MyoD, TRIM32, FOX03, and FBXO3) genes were similar between groups 3 and 6 hours after exercise. CONCLUSION: These data highlight several unique pathways in individuals with obesity that result in a blunted exercise response.

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

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