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Skeletal muscle dysfunction and exercise intolerance in heart failure

Author
Wilson S Colucci, MD
Section Editor
Stephen S Gottlieb, MD
Deputy Editor
Susan B Yeon, MD, JD, FACC

INTRODUCTION

The hallmark of heart failure (HF) is exercise intolerance due to dyspnea and fatigue. These symptoms were, in the past, thought to result entirely from central hemodynamic derangements, which might be reversed by inotropic agents and/or vasodilators. (See "Inotropic agents in heart failure with reduced ejection fraction" and "ACE inhibitors in heart failure with reduced ejection fraction: Therapeutic use".)

However, it is now clear that significant skeletal muscular pathology is also present in HF and may contribute to the associated symptoms [1]. The evidence associating skeletal muscular abnormalities and exercise intolerance, and the beneficial effects of cardiac rehabilitation for patients with HF will be reviewed here. An overview of normal exercise physiology, the use of measurement of peak oxygen uptake (peak Vo2) to assess exercise capacity and prognosis, and the ability of cardiac rehabilitation to improve exercise capacity in patients with mild to moderate HF are discussed separately. (See "Exercise physiology" and "Exercise capacity and VO2 in heart failure" and "Cardiac rehabilitation in patients with heart failure".)

IMPACT OF MEDICAL THERAPY ON EXERCISE TOLERANCE

Exercise capacity is reduced even in mild heart failure. Exercise intolerance and fatigue may be the result of a reduction in cardiac output, which is due primarily to impaired myocardial function, and may be exaggerated by decreased plasma and blood volumes caused by excessive diuresis [2]. Although the cardiac output may be relatively normal at rest, it is usually unable to increase adequately with even mild exertion [3]. As in normal subjects, peak Vo2 in patients with heart failure (HF) is directly related to peak exercise cardiac output and muscle blood flow (figure 1). However, the inability to appropriately increase cardiac output in HF results in an insufficient increase in perfusion to exercising muscle, which can cause early anaerobic metabolism, an inadequate increase in muscle strength, and muscle fatigue [4].

With the success of medical therapy for HF in the early 1980s, several investigators evaluated the acute impact of inotropic agents and vasodilators on exercise capacity in patients with HF. As an example, one study evaluated 11 patients with New York Heart Association (NYHA) class III HF and a mean left ventricular ejection fraction (LVEF) of 20 percent who underwent exercise on a bicycle ergometer before and during infusion of dobutamine [5]. Although dobutamine improved peak exercise cardiac output (6.5 versus 7.4 L/min, p <0.01) and reduced pulmonary capillary wedge pressure (PCWP), it failed to significantly increase exercise duration (5.5 versus 5.8 minutes).

Another study investigated the effect of the potent vasodilator hydralazine on blood flow to exercising skeletal muscle and exercise capacity in 10 patients with NYHA class III HF and a mean LVEF of 19 percent [6]. Hydralazine, administered intravenously, substantially increased peak cardiac output during exercise on a bicycle ergometer (5.6 versus 6.7 L/min, p <0.01) and improved femoral venous flow, indicating improved femoral arterial flow and delivery of oxygen to the exercising skeletal muscle. However, maximal oxygen consumption (Vo2max) was unaffected because of a reduction in systemic and leg oxygen extraction after hydralazine administration.

        

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Literature review current through: Nov 2016. | This topic last updated: Wed Apr 29 00:00:00 GMT+00:00 2015.
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