[Pathophysiology of heart failure: peripheral vascular and muscular mechanisms]

Exercise tolerance in patients with congestive heart failure correlates poorly with measures of systolic left-ventricular function and is determined by disturbances of the regulation of skeletal muscle perfusion and structural and metabolic changes of skeletal muscle itself. The increase in minimal vascular resistance in skeletal muscle is due to increased activities of the sympathetic nervous system, the renin-angiotensin and vasopressin systems and decreased and increased endothelium-mediated vasodilation and vasoconstriction, respectively. In addition, skeletal muscle atrophy, decreased oxidative capacity and a relative increase of easily fatiguable glycolytic muscle fibres also contribute to the reduction of exercise tolerance. The disturbances of skeletal muscle perfusion and changes of skeletal muscle are at least in part reversible by vasodilator therapy or, in the extreme situation, by cardiac transplantation.