The goal of the project is to provide a deeper understanding of the mechanisms responsible for the beneficial effects of exercise in chronic heart failure, using a novel approach of investigating the role of yet unrecognized potential contributors (mitochondria and KATP channels). These factors were chosen based on the current knowledge that exercise can affect the function of both the mitochondria, the energy producing organelles within the cell, and KATP channels, important metabolic sensors that couple metabolic demand to the cellular excitability. For that purpose, a rat model of chronic heart failure and a number of state-of-the-art methodologies will be used that will enable identification of the effects of exercise at subcellular and molecular level. It is expected that this project will provide insight into the complex mechanism whereby exercise improves the function of the diseased heart and that mitochondria and KATP channels will be identified as important contributing factors. The majority of scientific research will be conducted in University of Split Medical School in tight collaboration with Faculty of Medicine at Norwegian University of Science and Technology (Trondheim, Norway) and Medical College of Wisconsin (Milwaukee, USA). Besides their clinical relevance, the results from this project will provide a base for submission of international projects and further extension of international collaboration of the University of Split Medical School.

Adopt a gene transfer technology targeted to DRG nociceptive neurons, and with the help of this methodology strengthen previous and gain new collaborations, increase our research and innovation capacities and attract international funding.