Grant: Doctoral Award - Frederick Banting and Charles Best Canada Graduate Scholarships

The loss of skeletal muscle mass is an inevitable consequence of age, and often results in impaired mobility and a lowered quality of life. Many components of skeletal muscle are thought to foster this progressive degeneration, with mitochondria proving to be one of the most critical contributors. Located within the cell, this organelle generates energy required for movement and metabolism. Studies show that muscle mitochondrial content deteriorates with age, and may be linked to the muscle atrophy observed. Accordingly, much interest surrounds the search for mechanisms to maintain or enhance skeletal muscle mitochondrial content in an ever-increasing aging population. Recent studies have found exercise to be a stimulant for mitochondrial synthesis in aged skeletal muscle. Specifically, molecular pathways have found that exercise is able to trigger the activity of signalling molecules that activate genes required for organelle synthesis. Not yet known are the alternative pathways following gene activation that may also contribute to mitochondrial synthesis. Thus, the purpose of this project will be to utilize both animal studies and cells in culture to examine the effects of exercise and aging on the alternative pathways regulating skeletal muscle mitochondrial content. We hypothesize that these processes are likely rendered dysfunctional with age, leading to abnormal and reduced mitochondria. We further hypothesize that exercise will prove to be protective against such changes, promoting the maintenance of mitochondria with increasing age. The present research is unique as it aims to provide information regarding the use of exercise as a potential therapy to be used in the prevention of age-induced muscle loss.