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Circulation. 1995;91:559-561

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(Circulation. 1995;91:559-561.)
© 1995 American Heart Association, Inc.


Articles

Exercise Intolerance in Heart Failure

Importance of Skeletal Muscle

John R. Wilson, MD

From the Cardiology Division, Vanderbilt University Medical Center, Nashville, Tenn.

Correspondence to John R. Wilson, MD, Cardiology Division, RM CC-2218 MCN, Vanderbilt University Medical Center, Nashville, TN 37232-2170.


Key Words: Editorials • heart failure • muscles • exercise • respiration


*    Introduction
 
For over a century, investigators have sought to define the mechanisms responsible for exercise intolerance in heart failure. At the outset, this mission appeared a simple one. Exertional dyspnea was attributed to exercise-induced increases in pulmonary wedge pressure. Exertional fatigue was attributed to an inadequate cardiac output. Over the past decade, however, it has become clear that the link between cardiac dysfunction and exertional symptoms in heart failure is far more complex. This understanding has led investigators to explore novel treatment options in heart failure. In this issue of Circulation, Mancini and coworkers describe one such new treatment option: selective respiratory muscle training.

At first glance, respiratory muscle training would appear of little value since it targets the skeletal muscle rather than the circulatory system. However, recent observations increasingly suggest that abnormalities of the skeletal muscle system are important contributors to exertional symptoms in patients with heart failure. Indeed, there is growing evidence that the sensations of exertional fatigue and dyspnea are linked, in part, via the skeletal muscle system. The first evidence that noncirculatory factors contribute to exertional symptoms in heart failure came from observations that acutely altering hemodynamic parameters did not alter exertional symptoms. The traditional presumption that dyspnea is caused by elevated intrapulmonary pressures was tested by measuring symptomatic and ventilatory responses to exercise before and after pharmacologic manipulation of the pulmonary wedge pressure; excessive ventilatory levels during exercise have been viewed as a hallmark of lung dysfunction during exercise. Acute reductions in the pulmonary wedge . . . [Full Text of this Article]




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