The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Exercise limitation in chronic heart failure: Central role of the periphery
Open accessAbstract
The symptoms of chronic heart failure (CHF) are predominantly shortness of breath and fatigue during exercise and reduced exercise capacity. Disturbances of central hemodynamic function are no longer considered to be the major determinants of exercise capacity. The two symptoms of fatigue and breathlessness are often considered in isolation. A pulmonary abnormality is usually considered to be the cause of abnormal ventilation, and increased dead space ventilation has come to be accepted as a major cause of the increased ventilation relative to carbon dioxide production seen in CHF. Rather than decreased skeletal muscle perfusion, an intrinsic muscle abnormality is considered to be responsible for fatigue. Another abnormality seen in CHF is persistent sympathetic nervous system activation, which is difficult to explain on the basis of baroreflex activation. There is increasing evidence for the importance of skeletal muscle ergoreceptors or metaboreceptors in CHF. These receptors are sensitive to work performed, and activation results in increased ventilation and sympathetic activation. The ergoreflex appears to be greatly enhanced in CHF. We put forward the "muscle hypothesis" as an explanation for many of the pathophysiologic events in CHF. Impaired skeletal muscle function results in ergoreflex activation. In turn, this causes increased ventilation, thus linking the symptoms of breathlessness and fatigue. Furthermore, ergoreflex stimulation may be responsible for persistent sympathetic activation.
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Cites
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Cited by
Authors/Task Force Members, Dickstein, K., Cohen-Solal, A., Filippatos, G., McMurray, J. J. V., Ponikowski, P., Poole-Wilson, P. A., Stromberg, A., van Veldhuisen, D. J., Atar, D., et al. (2008) · European Heart Journal · doi:10.1093/eurheartj/ehn309 · Cited by 2,696
Self-citationFerric Carboxymaltose in Patients with Heart Failure and Iron Deficiency
Anker, S. D., Comin Colet, J., Filippatos, G., Willenheimer, R., Dickstein, K., Drexler, H., Lüscher, T. F., Bart, B., Banasiak, W., Niegowska, J., et al. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0908355 · Cited by 2,083
Self-citationExercise Hemodynamics Enhance Diagnosis of Early Heart Failure With Preserved Ejection Fraction
Borlaug, B. A., Nishimura, R. A., Sorajja, P., Lam, C. S. P., & Redfield, M. M. (2010) · Circulation: Heart Failure · doi:10.1161/circheartfailure.109.930701 · Cited by 1,118
Piña, I. L., Apstein, C. S., Balady, G. J., Belardinelli, R., Chaitman, B. R., Duscha, B. D., Fletcher, B. J., Fleg, J. L., Myers, J. N., & Sullivan, M. J. (2003) · Circulation · doi:10.1161/01.cir.0000055013.92097.40 · Cited by 1,030
Endotoxin and immune activation in chronic heart failure: a prospective cohort study
Niebauer, J., Volk, H.-D., Kemp, M., Dominguez, M., Schumann, R. R., Rauchhaus, M., Poole-Wilson, P. A., Coats, A. J., & Anker, S. D. (1999) · The Lancet · doi:10.1016/s0140-6736(98)09286-1 · Cited by 877
Self-citation
Metadata
- Authors
- Clark, A. L., Poole-Wilson, P. A., & Coats, A. J. S.
- Venue
- Journal of the American College of Cardiology
- Publisher
- Elsevier BV
- Published
- 1996-11
- Volume
- 28
- Issue
- 5
- Pages
- 1092-1102
- ISSN
- 0735-1097 (ISSN-L)
- OpenAlex
- W1991209451
- Cited by
- 524
- References
- 8
- FWCI
- 35.14
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Clark, A. L., Poole-Wilson, P. A., & Coats, A. J. S. (1996). Exercise limitation in chronic heart failure: Central role of the periphery. Journal of the American College of Cardiology. https://doi.org/10.1016/s0735-1097(96)00323-3
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
