During the past decade, cachexia in the setting of severe CHF has gained considerable attention. Loss of skeletal muscle mass as well as structural and functional changes, however, occur already early in the disease process. Interestingly, even after correction for reduced muscle mass, it appears that muscle quality is also affected. This has led investigators to launch the concept of "heart failure myopathy". Energetic deprivation has been attributed a key role in the pathophysiological cascade of events. Amongst a whole series of recently discovered adipokines, adiponectin may well play a fundamental role in the energy – deprived status in CHF. Recent data provided evidence of a functional adiponectin resistance at the level of the skeletal muscle in CHF patients. The aim of this study is to explore the role of adiponectin in CHF, in particular the underlying mechanisms of adiponectin resistance and this, for the first time, in an in vitro setting.