BYLINE: Mario Boone
Rockville, Md. (November 16, 2023)—The reduction in mitochondrial-related gene expression observed during the thickening of muscle fibers (hypertrophy) matches changes in the muscle fibers’ DNA. In addition, the molecular changes match a reduction in muscle mitochondrial function measured by high-resolution respirometry (the measurement of oxygen consumption rate of living cells and tissues). Researchers from the University of Kentucky, University of Arkansas and The Karolinska Institute in Sweden published their findings in the journal Function.
Researchers used novel bioinformatics techniques that combine DNA and RNA data to achieve their findings. “On the surface, our findings may seem like a bad thing since mitochondria are the powerhouses of the cell,” said a spokesperson for the researchers. “However, rapidly dividing mononuclear cells such as those found in tumors undergo similar metabolic reprogramming, suppressing mitochondrial metabolism in favor of metabolism pathways that generate biosynthetic (‘building block’) molecules. We think differentiated multi-nuclear muscle fibers do the same thing when growing rapidly to support adaptation, at least in the short term.” Understanding the metabolic aspect of this rapid growth could lead to therapeutics to prevent muscle mass loss or promote muscle growth and adaptation in different conditions such as aging and disuse.
The research team consisted of the following physiologists:
- Ahmed Ismaeel, PhD, postdoctoral scholar, University of Kentucky
- Nick Thomas, MS, PhD candidate, University of Kentucky
- Yuan Wen, MD, PhD, assistant professor, University of Kentucky
- Kevin Murach, PhD, assistant professor, University of Arkansas
- Ferdinand von Walden, MD, PhD, The Karolinska Institute, Sweden
Read the full article, “Coordinated regulation of myonuclear DNA methylation, mRNA, and miRNA levels associates with the metabolic response to rapid synergist ablation-induced skeletal muscle hypertrophy in female mice,” published ahead of print in Function. Contact APS Media Relations or call 301.634.7314 to schedule an interview with a member of the research team.