Researchers have discovered a gene that enhances muscular strength when activated by physical activity, opening the door to the creation of healing therapies that mimic some of the advantages of exercise.
The University of Melbourne-led research, published in Cell Metabolism, demonstrated how various forms of exercise modify the molecules in our muscles, leading to the identification of the novel C18ORF25 gene, which is triggered with all types of exercise and is responsible for boosting muscular strength. Animals lacking C18ORF25 perform poorly during activity and have weaker muscles.
Dr Benjamin Parker, project leader, said that by activating the C18ORF25 gene, the study team could witness muscles grow significantly stronger without necessarily being larger.
Identifying this gene may impact how we manage healthy aging, diseases of muscle atrophy, sports science and even livestock and meat production. This is because promoting optimal muscle function is one of the best predictors of overall health.”
Dr Benjamin Parker, Project Leader, Department of Anatomy & Physiology, The University of Melbourne
Dr Parker added, “We know exercise can prevent and treat chronic diseases including diabetes, cardiovascular disease and many cancers. Now, we hope that by better understanding how different types of exercise elicits these health promoting effects at the molecular level, the field can work towards making new and improved treatment options available.”
The team was able to recognize the molecular similarities and differences between different types of exercise in human muscle biopsies by analyzing proteins and how they change within cells in the study, which was a partnership between Dr Parker and Professors Erik Richter and Bente Kiens of the University of Copenhagen, Denmark.
To identify how genes and proteins are activated during and after different exercises, we performed an analysis of human skeletal muscle from a cross-over intervention of endurance, sprint and resistance exercise.”
Dr Benjamin Parker, Project Leader, Department of Anatomy & Physiology, The University of Melbourne
Researchers were able to evaluate signaling responses across exercise modalities in the same person, compared to their pre-exercise level, thanks to the experimental design. This allowed them to see how a person reacted to various forms of exercise directly in their muscles.
It also enabled the research team to identify genes and proteins that alter consistently across all persons and kinds of exercise, leading to the identification of the new gene.
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Journal reference:
Blazev, R., et al. (2022) Phosphoproteomics of three exercise modalities identifies canonical signaling and C18ORF25 as an AMPK substrate regulating skeletal muscle function. Cell Metabolism. doi.org/10.1016/j.cmet.2022.07.003.