tion explains the exaggerated exercise pressor reflex seen in heart failure.

following letters are in response to the Point:Counterpoint series “Increased mechanoreceptor/metaboreceptor stimulation explains the exaggerated exercise pressor reflex seen in heart failure ” that appears in this issue. To the Editor: The Point:Counterpoint concerning the issue of mechanoreceptor vs. metaboreceptor control of sympa-thetic 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 dy-namic exercise and, second, if capsaicin injections simulate the ischemic stimulus observed during exercise in the CH