Skeletal muscle IGF-1 is lower at rest and after resistance exercise in humans with obesity
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ORIGINAL ARTICLE
Skeletal muscle IGF‑1 is lower at rest and after resistance exercise in humans with obesity Brian P. Sullivan1 · Jessica A. Weiss1 · Yaohui Nie1,2 · Ron T. Garner1 · Cathal J. Drohan3 · Shihuan Kuang1,2 · Julianne Stout4 · Timothy P. Gavin1 Received: 5 February 2020 / Accepted: 19 September 2020 © Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Purpose Obesity is associated with numerous changes in skeletal muscle including greater muscle mass and muscle fiber cross sectional area (FCSA), yet fasted muscle protein synthesis is lower. Activation of the IGF-1/Akt/mTOR pathway is critical for muscle mass maintenance, muscle hypertrophy, and muscle protein regulation. Resistance exercise (RE) increases muscle mass, FCSA, and IGF-1. Persons with obesity have greater skeletal muscle mass and larger skeletal muscle fiber cross sectional area. The IGF-1/Akt/mTOR pathway is critical for the regulation of skeletal muscle mass. Our study found men and women with obesity have lower skeletal muscle IGF-1 mRNA and protein and higher expression of miR-206 an epigenetic regulator of IGF-1, at rest and following an acute bout of resistance exercise. Despite this, Akt mediated signaling was maintained and maintenance of phosphorylation does not appear to be accounted for by compensatory pathways. Our findings suggest a possible negative feedback mechanism via increased miR-206 and in turn decreased IGF-1 to limit further skeletal muscle hypertrophy in persons with obesity. The current work investigated if: (1) obesity dysregulates basal skeletal muscle IGF-1 pathways; and (2) obesity augments the muscle IGF-1 pathway responses to acute RE. Methods Eight sedentary (no self-reported physical activity), lean (LN) and eight sedentary subjects with obesity (OB) had vastus lateralis biopsies taken at rest, and 15 min and 3 h post-acute RE for the measurement of the IGF-1 pathway and muscle FCSA. Results Type II FCSA was larger in OB vs. LN. Skeletal muscle IGF-1 mRNA and IGF-1 protein were lower in OB vs. LN at rest and post-exercise. Acute RE increased IGF-1 protein similarly in both groups. The expression of miR-206, a posttranscriptional inhibitor of IGF-1 expression, was higher in OB vs. LN and linked with lower IGF-1 mRNA (r = – 0.54). Conclusion In spite of greater muscle FCSA, muscle IGF-1 expression was lower in obesity suggesting negative feedback may be limiting muscle mass expansion in obesity. Keywords Obesity · AKT/mTOR · Wnt · MicroRNA
Communicated by William J. Kraemer. Electronic supplementary material The online version of this article (https://doi.org/10.1007/s00421-020-04509-z) contains supplementary material, which is available to authorized users. * Timothy P. Gavin [email protected] 1
Department of Health and Kinesiology and Max E, Wastl Human Performance Laboratory, Purdue University, 800 W. Stadium Ave, West Lafayette, IN 47907, USA
Department of Animal Sciences, Purdue University, West Lafayette, IN, USA
2
Abbreviations 1-RM One-repetition maximum ACC
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