Skeletal muscle disorders in heart failure

Heart failure is associated with reduction of exercise capacity that cannot be solely ascribed to reduced maximal oxygen uptake ((V) over dot O-2max). Therefore, research has focused on changes in skeletal muscle morphology, metabolism and function. Factors that-can cause such changes in skeletal mu scle comprise inactivity, malnutrition, constant or repeated episodes of in adequate oxygen delivery and prolonged exposure to altered neurohumoural st imuli. Most of these factors are not specific for the heart failure conditi on. On the other hand, heart failure is more than one clinical condition. C ongestive heart failure (CHF) develops gradually as a result of deteriorati ng contractility of the viable myocardium, myocardial failure. Is it possib le that development of this contractile deficit in the myocardium is parall eled by a corresponding contractile deficit of the skeletal muscles? This q uestion cannot be answered today. Both patient studies and experimental stu dies support that there is a switch to a faster muscle phenotype and energy metabolism balance is more anaerobic. The muscle atrophy seen in many pati ents is not so evident in experimental studies. Few investigators have stud ied contractile function. Both fast twitch and slow twitch muscles seem to become slower, not faster as might be expected, and this is possibly linked to slower intracellular Ca2+ cycling. The neurohumoural stimuli that can c ause this change are not known, but recently it has been reported that seve ral cytokines are increased in CHF patients. Thus, the changes seen in skel etal muscles during CHF are partly secondary to inactivity, but the possibi lity remains that the contractility is altered because of intracellular cha nges of Ca2+ metabolism that are also seen in the myocardium.