Point:counterpoint Comments

To the Editor: The Point:Counterpoint concerning the issue of mechanoreceptor vs. metaboreceptor control of sympathetic nerve activity (SNA) in chronic heart failure (CHF; Refs. 1, 2) relates exclusively to input from exercising skeletal muscle. Although both sides make cogent points on the basis of published data, in our opinion the debate has not been conclusively settled and will not be using the types of experiments carried out in human subjects. First, it is certainly not clear if passive exercise simulates true dynamic exercise and, second, if capsaicin injections simulate the ischemic stimulus observed during exercise in the CHF state. We offer an alternative hypothesis as to the mechanism for exaggerated SNA during exercise in the CHF state. Clearly exercise evokes a stimulus from muscle but also may increase neural signaling from cardiac and chemoreflexes in the heart and in the arterial system. Cardiac sympathetic afferents respond to ischemic metabolites, which are likely to be elevated in CHF patients during exercise. These largely c-fiber afferents are sensitized in animals with CHF (5). The cardiac sympathetic afferent reflex is clearly augmented in CHF (6). In addition to this particular sympathoexcitatory reflex, the arterial chemoreflex is sensitized in CHF (3). It is not inconceivable that carotid hypoxia during exercise (perhaps as a result of pulmonary interstitial edema) evoking an increase in carotid body activity acts as another sympathoexcitatory reflex. Because both of these afferent pathways appear to be enhanced even under normoxic resting conditions and because our recent data indicate that these inputs to the nucleus of the solitary tract augment sympathoexcitatory stimuli (4), they can not be excluded as potential contributors to the exaggerated SNA responses to exercise.