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J Am Coll Cardiol, 1996; 28:1092-1102
© 1996 by the American College of Cardiology Foundation
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Exercise limitation in chronic heart failure: central role of the periphery

AL Clark, PA Poole-Wilson, and AJ Coats

Department of Cardiac Medicine, National Heart and Lung Institute, London, England, United Kingdom.

The symptoms of chronic heart failure (CHF) are predominantly shortness of breath and fatigue during exercise and reduced exercise capacity. Disturbances of central hemodynamic function are no longer considered to be the major determinants of exercise capacity. The two symptoms of fatigue and breathlessness are often considered in isolation. A pulmonary abnormality is usually considered to be the cause of abnormal ventilation, and increased dead space ventilation has come to be accepted as a major cause of the increased ventilation relative to carbon dioxide production seen in CHF. Rather than decreased skeletal muscle perfusion, an intrinsic muscle abnormality is considered to be responsible for fatigue. Another abnormality seen in CHF is persistent sympathetic nervous system activation, which is difficult to explain on the basis of baroreflex activation. There is increasing evidence for the importance of skeletal muscle ergoreceptors or metaboreceptors in CHF. These receptors are sensitive to work performed, and activation results in increased ventilation and sympathetic activation. The ergoreflex appears to be greatly enhanced in CHF. We put forward the "muscle hypothesis" as an explanation for many of the pathophysiologic events in CHF. Impaired skeletal muscle function results in ergoreflex activation. In turn, this causes increased ventilation, thus linking the symptoms of breathlessness and fatigue. Furthermore, ergoreflex stimulation may be responsible for persistent sympathetic activation.


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J. Appl. Physiol.Home page
G. C. M. Beaufort-Krol, W. G. Zijlstra, J. Takens, M. C. Molenkamp, K. J. Meuzelaar, G. B. Smid, and J. R. G. Kuipers
Lactate kinetics at rest and during exercise in lambs with aortopulmonary shunts
J Appl Physiol, March 1, 1999; 86(3): 832 - 839.
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CirculationHome page
K. Okita, K. Yonezawa, H. Nishijima, A. Hanada, M. Ohtsubo, T. Kohya, T. Murakami, and A. Kitabatake
Skeletal Muscle Metabolism Limits Exercise Capacity in Patients With Chronic Heart Failure
Circulation, November 3, 1998; 98(18): 1886 - 1891.
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J Am Coll CardiolHome page
J. Niebauer, C.-D. Pflaum, A. L. Clark, C. J. Strasburger, J. Hooper, P. A. Poole-Wilson, A. J. S. Coats, and S. D. Anker
Deficient insulin-like growth factor I in chronic heart failure predicts altered body composition, anabolic deficiency, cytokine and neurohormonal activation
J. Am. Coll. Cardiol., August 1, 1998; 32(2): 393 - 397.
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Cardiovasc ResHome page
K. R Sipido, T. Stankovicova, W. Flameng, J. Vanhaecke, and F. Verdonck
Frequency dependence of Ca2+ release from the sarcoplasmic reticulum in human ventricular myocytes from end-stage heart failure
Cardiovasc Res, February 1, 1998; 37(2): 478 - 488.
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HeartHome page
A L CLARK and T MCDONAGH
The origin of symptoms in chronic heart failure
Heart, November 1, 1997; 78(5): 429 - 430.
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