A new study out of York University has identified that the protein Parkin plays an important role in muscle health during exercise.
Professor David Hood and his research team from the School of Kinesiology and Health Science in the Faculty of Health published the findings in the study “Parkin is required for exercise-induced mitophagy in muscle: impact of aging” in the American Journal of Physiology Endocrinology and Metabolism.
The study examines aging muscle, disuse, weakness and how mitochondria contribute to this pathology. Physical inactivity is an increasing contributing factor to several metabolic disorders including Type 2 diabetes, obesity and cardiovascular disease, explains Hood, and regular exercise is a common prescription to combat against these disorders. However, the molecular mechanisms that underly the beneficial effects of exercise remain poorly understood.
Mitochondria are energy-producing components in skeletal muscle cells that are highly active in producing energy during exercise. However, when mitochondria are unable to generate energy efficiently, they are swiftly removed from the cell in a breakdown process known as mitophagy.
“In this study, we have identified Parkin, a protein mutated in Parkinson’s disease, as an important factor required for mitophagy in muscle during exercise,” said Hood. “We found that the absence of Parkin reduced the ability of muscle to breakdown dysfunctional mitochondria during exercise. Thus, our results describe an important function for Parkin in muscle, and provide a greater understanding of the cellular underpinnings of the positive effects of exercise on muscle health.”
The maintenance of muscle health with advancing age is dependent on mitochondrial homeostasis. The results of the study demonstrate that acute exercise-induced mitophagy is dependent on Parkin, and attenuated with age, which likely contributes to changes in mitochondrial content and quality in aging muscle.
The study was authored by Hood, Chris Chin Wah Chen, Avigail T. Erlich and Matthew J. Crilly.