A neural link to explain the "muscle hypothesis" of exercise intolerance in chronic heart failure

Background In chronic heart failure the cause of exercise imitation it still unclear: ergoreceptors, muscle afferents sensitive to exercise metabolites, are proposed as a neural link between muscular abnormalities and the limited exercise responses in this syndrome. Methods In 92 stable patients with heart failure (34 in New York Heart Association class 1, 27 in class II, and 31 in class III) and 28 age-matched normal controls, we assessed exercise tolerance (maximal upright bicycle) and ergoreflex activity (2 dynamic handgrips, one control and one followed by 3 minutes of local circulatory occlusion to isolate the ergoreflex component by metabolite trapping). Results Patients, with respect to the controls. showed reduced exercise tolerance (peak (V) over dot O-2 20 vs 33 mL/kg/min), increased ergoreflex effects on ventilation (9 vs 4 L/min), systolic pressure (37 vs 13 mm Hg), and leg vascular resistance (45 vs 22 units) tall P <.005); with the progression of the symptoms, a progressive increase in ergoreflex contribution to the ventilatory response to exercise was observed. The indexes of exercise limitation during arm and leg exercise tie, peak (V) over dot O-2 (V) over dot/(V) over dot CO2 slope) correlated highly with the ergoreflex contribution to ventilatory response during handgrip test (r less than or equal to 0.7 P <.0001) but weakly with left ventricular election fraction (r less than or equal to 0.5). Conclusion In chronic heart failure, the overactivity of the ergoreflex is related to a degree of functional limitation and appears, through direct ventilatory and cardiovascular responses, to contribute to the abnormal responses to exercise, explaining the "muscle hypothesis."