Myokine Secretion following an Aerobic Exercise Intervention in Individuals with Type 2 Diabetes with or without Exercise Resistance

Author:

Garneau Léa12ORCID,Mulvihill Erin E.13ORCID,Smith Steven R.4ORCID,Sparks Lauren M.4,Aguer Céline1256ORCID

Affiliation:

1. Faculty of Medicine, Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON K1H 8M5, Canada

2. Institut du Savoir Montfort, Ottawa, ON K1K 0T2, Canada

3. University of Ottawa Heart Institute, Ottawa, ON K1Y 4W7, Canada

4. Translational Research Institute for Metabolism and Diabetes, AdventHealth Orlando, Orlando, FL 32804, USA

5. Faculty of Medicine and Health Sciences, Department of Physiology, McGill University–Campus Outaouais, Gatineau, QC J8V 3T4, Canada

6. Faculty of Health Sciences, School of Human Kinetics, University of Ottawa, Ottawa, ON K1N 6N5, Canada

Abstract

Type 2 diabetes (T2D) is characterized by muscle metabolic dysfunction that exercise can minimize, but some patients do not respond to an exercise intervention. Myokine secretion is intrinsically altered in patients with T2D, but the role of myokines in exercise resistance in this patient population has never been studied. We sought to determine if changes in myokine secretion were linked to the response to an exercise intervention in patients with T2D. The participants followed a 10-week aerobic exercise training intervention, and patients with T2D were grouped based on muscle mitochondrial function improvement (responders versus non-responders). We measured myokines in serum and cell-culture medium of myotubes derived from participants pre- and post-intervention and in response to an in vitro model of muscle contraction. We also quantified the expression of genes related to inflammation in the myotubes pre- and post-intervention. No significant differences were detected depending on T2D status or response to exercise in the biological markers measured, with the exception of modest differences in expression patterns for certain myokines (IL-1β, IL-8, IL-10, and IL-15). Further investigation into the molecular mechanisms involving myokines may explain exercise resistance with T2D; however, the role in metabolic adaptations to exercise in T2D requires further investigation.

Funder

Société Francophone du Diabète

Heart and Stroke New Investigator Award

American Diabetes Association

Fonds de Recherche du Québec—Santé

Publisher

MDPI AG

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