LETTERS TO THE EDITORLast Word: Point:Counterpoint authors respond to commentaries on “Increased mechanoreceptor/metaboreceptor stimulation explains the exaggerated exercise pressor reflex seen in heart failure”Holly R. Middlekauff, and Lawrence I. SinowayHolly R. Middlekauff, and Lawrence I. SinowayPublished Online:01 Jan 2007https://doi.org/10.1152/japplphysiol.01246.2006This is the final version - click for previous versionMoreSectionsPDF (28 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat To the Editor: We are grateful to Dr. Jerry Dempsey and the editors at the Journal of Applied Physiology for the opportunity to engage in this debate, which we feel has been overall illuminating, gratifying, and, at times, even surprising. Our first surprise was at the apparent incredulousness of our “adversaries” when they realized the debate was not over the validity of the Muscle Hypothesis. The debate, as conceived by the editors at the Journal of Applied Physiology, focused on the mechanisms—specifically the types of sensory neurons—underlying the Muscle Hypothesis. We have come a long way in the last 12 years when this novel and exciting concept was introduced by Coats, Piepoli, and colleagues (1), and we remain indebted to these scientists for their creativity. Therefore, we could not disagree more strongly with Dr. Clark (3), who “belittled” the topic of the debate, by comparing it to the “Big-Endians and Little-Endians in Gulliver's Travels.” On the contrary, the mechanisms underlying exercise dysfunction in heart failure are important and, in our estimation, will prove illuminating for the study of other diseases of the cardiovascular system. Already we see an example of this in the commentary: Dr. Guazzi (3) finds connections between mechanisms of exercise dysfunction in heart failure and atrial fibrillation. Likely this debate has implications across specialty lines as well, having relevance for the mechanisms underlying exercise dysfunction characteristic of other chronic conditions, including chronic obstructive lung disease and chronic renal insufficiency as well (2). Thus this debate has served the very important and gratifying purpose of bringing diverse groups of investigators together to shed new light and insights into the problem. Although some of the commentary was bogged down in the details of pitfalls inherent in both animal and human research (“Does passive exercise simulate true dynamic exercise? Do capsaicin injections simulate the ischemic stimulus?”), we would hope that this debate would transcend these details and focus on the question of whether the exercise dysfunction in heart failure is a consequence of abnormal muscle mechanoreceptor sensitivity to deformation or abnormal muscle metaboreceptor sensitivity to chemical stimulation. We feel we presented a compelling case that the exercise pressor reflex is augmented in heart failure based on enhanced mechanoreceptor sensitivity. This supposition is based on experimental data from a variety of laboratories using both animal models and human studies. We sincerely hope that this debate serves as a springboard to engage more investigators, both in and outside the heart failure field, to contribute new insights to this very important problem.REFERENCES1 Coats AJ, Clark AL, Piepoli M, Volterrani M, and Poole-Wilson PA. Symptoms and quality of life in heart failure: the muscle hypothesis. Br Heart J 72: S36–S39, 1994.Crossref | PubMed | Google Scholar2 Hsia CC. Coordinated adaptation of oxygen transport in cardiopulmonary disease. Circulation 104: 963–969, 2001.Crossref | ISI | Google Scholar3 Schultz HD, Zucker IH, Wang W, Guazzi M, Scott AC, Negrao CE, Rondon MUPB, Prakash ES, Clark AL, Crisafulli A, Concu A, Manisty CH, Francis DP. Comments on Point:Counterpoint: Increased mechanoreceptor/metaboreceptor stimulation explains the exaggerated exercise pressor reflex seen in heart failure. J Appl Physiol. In press.Google Scholar Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation Cited ByRenal vasoconstriction is augmented during exercise in patients with peripheral arterial disease7 November 2013 | Physiological Reports, Vol. 1, No. 6 More from this issue > Volume 102Issue 1January 2007Pages 504-504 Copyright & PermissionsCopyright © 2007 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.01246.2006History Published online 1 January 2007 Published in print 1 January 2007 Metrics