One Size Does Not Fit All: Personalised Exercise Strategies To Improve Cardiovascular And Metabolic Health In Patients With Non-alcoholic Fatty Liver Disease.
Funder
National Health and Medical Research Council
Funding Amount
$318,768.00
Summary
Non-alcoholic fatty liver disease (NAFLD) affects one third of Australian adults and is linked with numerous chronic health conditions. Regular exercise reduces NAFLD, even without weight loss. However, response to exercise therapy is highly variable and there is a need for more personalised approaches. This research will identify which personalised exercise strategies effectively treat NAFLD, and, which measures can accurately monitor the progression of the disease in clinical practice.
Nutrient-training Interactions In Human Skeletal Muscle
Funder
National Health and Medical Research Council
Funding Amount
$53,659.00
Summary
Skeletal muscle accounts for 50% of total body mass with critical roles in body movement and blood glucose regulation. Exercise is a potent stimulus for maintaining/ increasing muscle mass, an effect that is augmented when combined with protein ingestion. The aims of this proposal are to better understand this exercise-nutrient interaction to optimize the prescription of programs and recovery strategies as a countermeasure for muscle degeneration with aging and disease.
IS NITRIC OXIDE A CENTRAL REGULATOR OF EXERCISE-INDUCED SKELETAL MUSCLE MITOCHONDRIAL BIOGENESIS?
Funder
National Health and Medical Research Council
Funding Amount
$340,750.00
Summary
Mitochondria are the energy producing parts of the cell and are the major controllers of metabolism. There is now good evidence that reduced muscle mitochondrial size contributes to diabetes. Exercise is good for diabetics due partly to increasing muscle mitochondrial production (mitochondrial biogenesis). Unfortunately, little is known about the mechanisms involved in increased muscle mitochondrial biogenesis following exercise. It has been shown recently that nitric oxide (NO), a gas made by m ....Mitochondria are the energy producing parts of the cell and are the major controllers of metabolism. There is now good evidence that reduced muscle mitochondrial size contributes to diabetes. Exercise is good for diabetics due partly to increasing muscle mitochondrial production (mitochondrial biogenesis). Unfortunately, little is known about the mechanisms involved in increased muscle mitochondrial biogenesis following exercise. It has been shown recently that nitric oxide (NO), a gas made by muscle during exercise, plays a role in mitochondrial biogenesis in fat cells. This project will determine whether NO is a central regulator of exercise-induced mitochondrial biogenesis in skeletal muscle. If we find that NO increases mitochondrial biogenesis in muscle, drugs designed to mimic these exercise effects may prevent or improve diabetes. We will firstly establish if specific drug treatments that alter NO levels in muscle cells grown in culture alter mitochondrial biogenesis. These results will help us to clarify the role of NO in mitochondrial biogenesis. However, it is difficult to directly examine the effects of exercise in cultured cells. Therefore, further studies will then use real life models such as rodents that have been exercised to examine the role of NO and exercise on mitochondrial biogenesis. We will feed a drug to decrease NO levels in normal rats; and use mice, genetically altered to be lacking in NO to determine if these treatments decrease mitochondrial biogenesis that is normally seen following endurance exercise. Furthermore, since defects in mitochondrial biogenesis have such an important impact on diabetic humans, we will use humans to examine if differences in NO levels in skeletal muscle among type 2 diabetics or endurance-trained athletes correlate with mitochondrial biogenesis. Finally, we will infuse a drug into type 2 diabetics that increases NO in muscle to determine if it also increases mitochondrial biogenesis.Read moreRead less