The muscle hypothesis: a model of chronic heart failure

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The following article is based on a article written Rogers FJ (American journal of osteopathic association,2001)
Chronic heart failure is one of the most serious medical problems any where over the globe. There is no unifying hypothesis accepted to explain the signs and symptoms of chronic heart failure.
Two of the major in vogue models are: The cardiocirculatory and neurohormonal models.
These above two models place an emphasis on left ventricular ejection fraction and cardiac output.
While the major draw back is that they (cardiocirculatory and neurohormonal models) do not provide appropriate explanations for the symptoms of breathlessness and fatigue.
Enter the muscle hypothesis:

The muscle hypothesis supplements these conventional models. It proposes that:

1. Abnormal skeletal muscle in heart failure results in activation of muscle ergoreceptors, leading to an increase in ventilation and sensation of breathlessness, the perception of fatigue, and sympathetic activation.
2. 25% chronic heart failure are limited by skeletal muscle abnormalities rather than cardiac output.
3. Cardiac rehabilitation exercise can lead to an increase in exercise capacity that is superior to that gained from digitalis or angiotensin-converting enzyme inhibitors.
4. Exercise tends to reverse the skeletal muscle myopathy of chronic heart failure and reduces the abnormal ergoreflex.

Other possible interventions are:

Other interventions that have been shown to have a favorable outcome include localized muscle group training, respiratory muscle training, and dietary approaches. The possibility that osteopathic manipulative treatment might be of benefit is an attractive, but untested, possibility.

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