Exercise Intolerance in Chronic Heart Failure

xercise intolerance is a major clinical manifestation in patients with chronic heart failure (CHF). It was originally considered to be the result of a failure of perfusion to the exercising musculature and consequent early onset of intramuscular acidosis. Under this theory, cardiotonic agents were administered to improve symptoms and exercise tolerance in patients with CHF. However, the therapy had no effect on exercise capacity despite hemodynamic improvement.1,2 Subsequently, the discrepancy between exercise tolerance and indices of left ventricular function has been reported.3,4 With this evidence, the study target shifted from central hemodynamics to the peripheral circulation and skeletal muscle condition. The purpose of the present review is to summarize the widespread skeletal muscle abnormalities originating from reduced perfusion and additive factors in patients with CHF, and to discuss the mechanisms for such alterations and their relation to established therapeutic tools, angiotensin-converting enzyme (ACE) inhibitors, angiotensin-receptor blockers (ARB), β-blockers, and exercise training.