Journal of Sports Science and Medicine
Journal of Sports Science and Medicine
ISSN: 1303 - 2968   
Ios-APP Journal of Sports Science and Medicine
Androit-APP Journal of Sports Science and Medicine
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©Journal of Sports Science and Medicine (2022) 21, 616 - 624   DOI: https://doi.org/10.52082/jssm.2022.616

Research article
Resistance Exercise-Induced Increases in Muscle Myostatin mRNA and Protein Expression Are Subsequently Decreased in Circulation in the Presence of Increased Levels of the Extracellular Matrix Stabilizing Protein Decorin
Darryn S. Willoughby1,2, , Thomas D. Cardaci3, Steven B. Machek4, Dylan T. Wilburn2, Jeffery L. Heileson5
Author Information
1 School of Exercise and Sport Science, University of Mary Hardin-Baylor, Belton, TX, USA
2 Department of Health and Human Performance, Baylor University, Waco, TX, USA
3 Department of Pathology, Microbiology, and Immunology, University of South Carolina School of Medicine, Columbia, SC, USA
4 Department of Kinesiology, California State University Monterey Bay, Seaside, CA, USA
5 Nutrition Services Division, Walter Reed National Military Medical Center, Bethesda, MD, USA

Darryn S. Willoughby
‚úČ School of Exercise and Sport Science, University of Mary Hardin-Baylor, Belton, TX, USA
Email: dwilloughby@umhb.edu
Publish Date
Received: 25-10-2022
Accepted: 23-11-2022
Published (online): 01-12-2022
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ABSTRACT

Resistance exercise (RE) activates cell signaling pathways associated with myostatin. Decorin is located in the extracellular matrix (ECM) and can block the inhibitory effect of myostatin. This study sought to determine the impact of low-load (LL) and high-load (HL) RE on myostatin mRNA and protein expression along with changes in muscle decorin and circulating follistatin. Ten resistance-trained men performed a LL (50% 1RM) and HL (80% 1RM) RE session using the angled leg press and leg extension with load and volume equated. Venous blood samples and muscle biopsies were obtained prior to and at 3h and 24h following each RE session. Muscle myostatin mRNA expression was increased at 24h post-exercise (p = 0.032) in LL and at 3h (p = 0.044) and 24h (p = 0.003) post-exercise in HL. Muscle decorin was increased at 24h post-exercise (p < 0.001) in LL and HL; however, muscle myostatin was increased at 24h post-exercise (p < 0.001) only in HL. For muscle Smad 2/3, no significant differences were observed (p > 0.05). Serum follistatin was increased and myostatin decreased at 24h post-exercise (p < 0.001) in LL and HL. Muscle myostatin gene and protein expression increased in response to HL RE. However, serum myostatin was decreased in the presence of increases in decorin in muscle and follistatin in circulation. Therefore, our data suggest a possible mechanism may exist where decorin within the ECM is able to bind to, and decrease, myostatin that might otherwise enter the circulation for activin IIB (ACTIIB) receptor binding and subsequent canonical signaling through Smad 2/3.

Key words: Follistatin, Smad 2/3, extracellular matrix, mechanotransduction


           Key Points
  • With volume equated, high-load RE increased muscle myostatin mRNA at both 3h and 24h post-exercise and muscle myostatin and decorin protein at 24h post-exercise.
  • Significant decreases in serum myostatin and increases in follistatin at 24h post-exercise was observed in both high- and low-load RE conditions.
  • RE apparently creates a mechanotransductive mechanism where decorin within the ECM is able to bind to and subsequently decrease the amount of myostatin that might otherwise enter the circulation and negatively impact the response of skeletal muscle to RE.
 
 
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