Exercise induces mechanical and metabolic stimuli in tissue are involved in functional and structural adaption. The mechanical stimuli are transduced between cellular structure and extracellular structure in inside to outside and outside to inside direction. An important structure involved in these interactions at the cellular side are the focal adhesions which are composed by different molecules which contact extracellular matrix (ECM) to the cytoskeleton and contain mechanosensitive molecules, such as focal adhesion kinase or integrin linked kinase (ILK), which can transform mechanical stimuli in biochemical signals. The ECM is contacted to the cytoskeleton of cells beside of other structures by a molecular interaction of ECM with integrins and a complex of ILK associated molecules such as ß-Parvin and Pinch. It is shown that an alteration of this complex lead to structural and functional maladaptation in different cell types e.g. endothelial cells, cardiomyocyte and skeletal muscle fibers, which could be important targets in mechanotransduction of exercise performed stimuli. It is shown that the lack of ILK induces alteration of endothelial function, cardiac myopathy and skeletal muscle dystrophy. Less is known about the role of the ILK and their interaction partner for the response to different mechanical stimuli, which can be induced by different exercise conditions. In a set of new experiments using general and tissue specific knockout mice models for ILK and ß- Parvin we could identify the role of the focal adhesion molecules, ILK and ß-Parvin for differential functional and structural tissue adaption in dependency of kind and intensity of the mechanical load induced by exercise in skeletal muscle and cardiac muscle. A major finding was the identification of this complex as a central sensor for volume load dependent myocardial adaption induced by exercise.