Mechanisms of Exercise Intolerance in Patients with Chronic Heart Failure

Summary

In patients with chronic heart failure, aerobic exercise capacity is decreased as reflected by decreases in the maximal oxygen uptake and anaerobic threshold. This decrease in the maximal aerobic power is attributed primarily to a decrease in the blood flow to exercising muscles and consequent reduction in the oxygen availability in active tissues. An inadequate pressor response, due to impairments of inotropic and chronotropic responses of the failing heart to sympathetic activation during exercise, plays a central role in the reduced blood flow to exercising muscles. In normal subjects, the venous pressure drop by means of muscle venous pump has been demonstrated to play an important role in increasing the skeletal muscle blood flow through an increase in the arteriovenous pressure gradient and local venoarteriolar reflex-mediated vasodilation. In patients with chronic heart failure, muscle venous pump is attenuated due to an elevated central venous pressure, and this may also be a flow-limiting factor in chronic heart failure. Other mechanisms such as metabolic abnormalities in skeletal muscle may also account for exercise intolerance, by decreasing oxygen utilization. Thus, the exercise intolerance in patients with chronic heart failure may be induced by multifactorial abnormalities.