New research identifies protein that affects muscle health during exercise
Faculty of Health Professor David Hood, Canada Research Chair in Cell Physiology, has led a study that determined that Parkin, a protein that breaks down or degrades unneeded proteins, is present and active in the degradation of muscle mitochondria during exercise.
“Mitochondria are the energy-supplying powerhouses of all cells. When they lose their ability to generate energy, they must be removed and degraded, or they will generate harmful free radicals (or reactive oxygen species) that can lead to premature cellular aging and death. The removal process is termed mitophagy,” Hood explains.
Exercise is a stimulus that can accelerate mitophagy, thereby improving the quality of mitochondria within muscle. This exercise effect can only happen if the protein Parkin is present. It is well-known that mutations in Parkin cause one hereditary form of Parkinson’s disease, a central nervous system disorder, but the function of Parkin in muscle was not established until now. In the absence of Parkin, muscle accumulates non-working, dysfunctional mitochondria.
This research, funded by the Natural Sciences & Engineering Research Council of Canada, was published in the American Journal of Physiology, Endocrinology and Metabolism (2018).
Hood’s area of expertise
Hood is the director of the Muscle Health Research Centre. This centre, based in the Faculty of Health, provides a centralized and focused research emphasis on the importance of skeletal muscle to the overall health and well-being of Canadians. It facilitates the integrated study of muscle biology in the broadest terms, including muscle development, disease, metabolism, blood supply, injury and regeneration, and adaptation to acute and chronic exercise. Approaches used by faculty and graduate students for the study of muscle include molecular, cellular and whole-body techniques.
Exercise is important for everyone, especially as we age. Physical inactivity contributes to metabolic disorders including Type 2 diabetes, obesity and cardiovascular disease. In fact, regular exercise is a common prescription to combat against these disorders. “The benefits of regular exercise for the human body are well known as they relate to cardiovascular health, burning fat and strengthening muscles,” explains Hood.
Aging, exercise and the ability of muscles to respond to exercise
The ability of muscles to respond to exercise – muscle plasticity – and the benefits of exercise is a large and rapidly evolving area of research. This is Hood’s area of expertise. Additional but related research foci include skeletal muscle and heart biochemistry and molecular biology, adaptations in muscle subject to chronic activity and cardiac muscle adaptations to thyroid hormone.
Study investigated the role of Parkin
Hood’s research team hypothesized that Parkin may play an increasing role in regulating skeletal muscle function and mitochondrial degradation with age. Therefore, the objectives of this study were to investigate the role of Parkin in acute exercise-induced mitophagy and possible age-related alterations brought about by endurance exercise.
Hood’s team discovered that Parkin was important to facilitate muscle mitochondrial degradation. Its absence was found to reduce the ability of muscle to breakdown dysfunctional mitochondria during exercise, and the activity of Parkin in muscle appears to be lost with age.
“In this original study, we identified Parkin as the protein that’s facilitating the breakdown of poorly functioning mitochondria in muscle. It is an important component in mitophagy in muscles during exercise,” says Hood.
“Thus, our results provide a greater understanding of the cellular underpinnings of the positive effects of exercise on muscle health,” he adds.
By Megan Mueller, senior manager, research communications, Office of the Vice-President Research & Innovation, York University, email@example.com