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J Appl Physiol 102: 502, 2007. First published November 9, 2006; doi:10.1152/japplphysiol.01256.2006
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POINT-COUNTERPOINT COMMENTS

Increased mechanoreceptor/metaboreceptor stimulation explains the exaggerated exercise pressor reflex seen in heart failure

Mary G. Garry,1 Scott A. Smith,2 and Jere H. Mitchell1

1Internal Medicine
2Physical Therapy
University of Texas Southwestern Medical Center
Dallas, Texas
e-mail: mary.garry{at}utsouthwestern.edu

The following letter is 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: There can be no more debate as to the validity of the skeletal muscle hypothesis. This peripheral paradigm revealed in the elegant studies of Piepoli and Coats (3) and based on the classic study of McCloskey and Mitchell (1) has set the stage for new insights into the mechanisms of abnormal cardiovascular responses to exercise in heart failure. Our current research confirms these findings as we are able to invoke exaggerations in the exercise pressor reflex by inducing a peripheral abnormality by ablating group IV afferent neurons in normal neonatal rat pups (6). When these animals reached adulthood we observed abnormal increases in mean arterial pressure and heart rate in response to exercise, yet these animals displayed normal left ventricular function. These data indicate that abnormal responses to exercise can be generated by peripheral abnormalities in primary afferent neurons in the absence of cardiac dysfunction. Middlekauff et al. (2) showed in humans and we (5) showed in rats that the mechanoreflex mediates the abnormal responses to exercise in heart failure and we (5) showed the same in animals lacking group IV afferent neurons. Additionally, we (5) demonstrated that the metaboreflex is blunted in these rats just as it is in rats in heart failure. These latter data are consistent with the observations of Sinoway and colleagues (4) in both humans and rats. We hypothesize that the blunting of the metaboreflex that occurs in heart failure initiates a series of events that results in the overactivity of the mechanoreflex.

REFERENCES

  1. McCloskey DI, Mitchell JH. Reflex cardiovascular and respiratory responses originating in exercising muscle. J Physiol 224: 173–186, 1972.[Abstract/Free Full Text]
  2. Middlekauff HR, Nitzsche EU, Hoh CK, Hamilton MA, Fonarow GC, Hage A, Moriguchi JD. Exaggerated muscle mechanoreflex control of reflex renal vascoconstriction in heart failure. J Appl Physiol 90: 1714–1719, 2001.[Abstract/Free Full Text]
  3. Piepoli M, Ponikowski P, Clark AL, Banasiak W, Capucci A, Coats AJ. A neural link to explain the "muscle hypothesis" of exercise intolerance in chronic heart failure. Am Heart J 137: 1050–1056, 1999.[CrossRef][ISI][Medline]
  4. Sinoway LI, Li J. A perspective on the muscle reflex: implications for congestive heart failure. J Appl Physiol 99: 5–22, 2005.[Abstract/Free Full Text]
  5. Smith SA, Mitchell JH, Naseem RH, Garry MG. Mechanoreflex mediates the exaggerated exercise pressor reflex in heart failure. Circulation 112: 2293–2300, 2005
  6. Smith SA, Williams MA, Mitchell JH, Mammen PP, Garry MG. The capsaicin-sensitive afferent neuron in skeletal muscle is abnormal in heart failure. Circulation 111: 2056–2065, 2005.




This Article
Right arrow Full Text (PDF) Free
Right arrow All Versions of this Article:
102/1/502    most recent
01256.2006v1
Right arrow Submit a response
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Google Scholar
Right arrow Articles by Garry, M. G.
Right arrow Articles by Mitchell, J. H.
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PubMed
Right arrow PubMed Citation
Right arrow Articles by Garry, M. G.
Right arrow Articles by Mitchell, J. H.

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