Skeletal muscle is a highly adaptable tissue but its capacity to maintain protein balance and regenerate/repair diminishes with physical inactivity, chronic disease and aging which impair mobility and function. Our study will use a unique animal model of different genetic backgrounds and divergent adaptive capacity to gain new information on mechanisms regulating skeletal muscle mass. We will compare the muscle response to overload, disuse atrophy and repair after injury in selectively-bred rats with contrasting muscle metabolism and exercise capacity. This study will identify mechanisms and specific targets that protect skeletal muscle mass and promote growth/regeneration to counteract muscle wasting. The findings from this study extend across sports science and clinical research applications, and will also have implications for repair and regeneration from injury.

Failure to attain and maintain peak muscle mass predisposes an individual to greater risk of disability and loss of functional capacity with aging, injury or disease. Moreover, the accelerated muscle wasting in many chronic diseases has debilitating health consequences additive to the primary disease pathology. It is imperative to develop and implement effective therapeutic strategies to combat muscle loss, particularly if the goal is to close the gap between life expectancy and healthy, functional life expectancy. While knowledge gained from transgenic models is important to identify therapeutic targets, translational studies in appropriate biological model systems are essential to determine the efficacy and/or validity of their potential. The proposed study will be the first to use an innovative inbred strain of rodents artificially selected for exercise training responses to determine adaptive/maladaptive responses that modulate skeletal muscle mass.

Project lead

  • Associate Professor Vernon Coffey

Project collaborators

  • Dr. Jonathan Peake QUT
  • Dr. Roland Steck QUT
  • Dr. Daniel West UC Davis
  • Dr. Hayley O’Neill Bond University

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