Grant: Operating Grant

Mitochondrial dysfunction is a key factor driving the aging process. Impaired mitochondrial function has been linked with muscle diseases, such as sarcopenia (loss of muscle). Endurance exercise is well known to improve physical fitness, mitochondrial function, lipid profile and insulin sensitivity, which are impaired in aging population. Our search for genes modulated in the skeletal muscle by mild-exercise training, which can be easily and safely performed by elderly individuals, highlighted the importance of mitochondrial function and extracellular matrix (ECM) remodeling in the skeletal muscle after mild exercise training. One of the mild-exercise induced genes, secreted protein acidic and rich in cysteine (SPARC), controls ECM remodeling and plays an important role in skeletal muscle maturation. SPARC is also known to interact with a protein which induces mitochondrial biogenesis. Therefore, we hypothesized that SPARC is mediating enhanced muscle integrity promoted by mild-exercise training in elderly individuals, thus contributing to the improvement of sarcopenia and its related metabolic diseases. Our objectives are to 1) demonstrate the roles of SPARC in the link between ECM remodeling and mitochondrial function; 2) elucidate the effects of SPARC on exercise-induced changes in muscle growth and mitochondrial function 3) characterize the functional relevance of SPARC in sarcopenia and muscle adaptations to mild exercise in SPARC-deficient mice. This study may provide the functional characterization of SPARC controlling the beneficial effects of physical exercise against aging.