A) The aim of the tender is to maintain and further increase the international competitiveness of the three institutions, which have already been successful in the field of skeletal and myocardium research, through the increased cooperation, renewed technical and personal conditions. Research is concentrated in four interlinked, mutually reinforcing strategic areas. These are: 1. Biochemical, molecular biological and electrophysiological characterisation of the regeneration and adaptability of skeletal muscles, in order to better understand the effects of training, nutrition, aging, muscle diseases, and to control and reverse adverse processes. In addition to sports, lifestyle, regeneration and recreation, the results also help economic, livestock (meat production) applications. 2. Molecular characterisation of the myocardial muscle adaptation, tolerance of hypoxia, interpretation of abnormal general metabolic conditions, effects of diseases on the heart muscle. Identification of the genetic determinants of adaptability to relieve and prevent the consequences of myocardial infarction and other myocardial damage. 3. In-depth study of channels, ion streams that determine the electrophysiological function of the myocardial muscle, for the prevention and treatment of cardiac arrests, for the development of possible drug strikes, effective compounds, which cause most cardiac deaths. 4. Identification of genetic constellations that cause childhood obesity and pathological metabolic conditions, accurate characterisation of risk factors for later metabolic and cardiac diseases, prevention programmes (diet, lifestyle, exercise). B) 1. We are looking at ways to restore and enhance myocardial and skeletal muscle performance. Performance enhancement is achieved through metabolic and signalling effects that have a potential therapeutic effect on the heart muscle but also on skeletal muscles (remote conditioning, electrical muscle stimulation, hypoxia-induced conditioning, “exercise mimetics”, eccentric muscle compression and eccentric motion). Our goal is to understand what is involved in these processes at molecular and cellular level. In physiological and pathological conditions, skeletal muscle can be regenerated significantly in size. Regenerative medicine is at the heart of medical-biological research. During the development and regeneration of the skeletal muscle, proliferating myoblasts formed from dormant satellite cells after their activation are differentiated into myocytes that fuse into myotubules. Many transcription factors and signal transmission molecules involved in myogenesis have been identified, and the control mechanisms are only partially known. For this reason, it is important to identify signals that regulate proliferation, differentiation and fusion, and to investigate the role of syndecan-4 mediated signal pathways. The background of inactivity associated with musculoskeletal disorders is the weakening and atrophy of the muscles. Any therapy that slows down old muscle atrophy or accelerates regeneration after injuries has a positive economic and social impact. The immobility and localisation of older people is a burden not only for themselves, but also for their families and their environment, which is expected to be reflected in increasing additional social and health costs due to an ageing population. At the same time, people with healthy but sedentary lifestyles are also characterised by reduced muscle performance and fatigue. This is also due to the phenomena that characterise old age or disease-related conditions. Our objective is to explore cellular mechanisms that increase the fatigue-bearing capacity of our muscles. Comparing the results thus obtained contributes to a better understanding of the background of fatigue and the development of new therapeutic interventions that increase muscle performance. 2. Major structural, metabolic and electrophysiological changes occur during ischemia due to narrowing or obstruction of coronary artery that supply the blood to the heart muscle, leading to damage to the heart muscle, severe arrhythmias that eventually cause the patient’s death. Pre-conditioning of the heart with short-term non-lethal stress stimuli, which trigger endogenous adaptive mechanisms, protects against the consequences of ischemic damage. In our studies, we aim to detect mechanisms that are activated after the pre-conditioning stimulus and play a role in the electrical and mechanical adaptation of the heart. Chronic complications of ischemic heart disease include hypertrophy and fibrotic reconstruction of the heart muscle, which eventually leads to chronic heart failure. Ischemic heart disease with other cardiovascular risk factors (hypercholesterolaemia, diabetes mellitus, hypertension, chronic renal failure