There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.
Abstract
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.