Contribution of Peripheral Chemoreceptors to Exercise Intolerance in Heart Failure

Peripheral chemoreceptors (PChRs), because of their strategic localization at the bifurcation of the common carotid artery and along the aortic arch, play an important protective role against hypoxia. Stimulation of PChRs evokes hyperventilation and hypertension to maintain adequate oxygenation of c...

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Main Authors: Katarzyna Kulej-Lyko, Piotr Niewinski, Stanislaw Tubek, Piotr Ponikowski
Format: Article
Language:English
Published: Frontiers Media S.A. 2022-04-01
Series:Frontiers in Physiology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fphys.2022.878363/full
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author Katarzyna Kulej-Lyko
Katarzyna Kulej-Lyko
Piotr Niewinski
Piotr Niewinski
Stanislaw Tubek
Stanislaw Tubek
Piotr Ponikowski
Piotr Ponikowski
author_facet Katarzyna Kulej-Lyko
Katarzyna Kulej-Lyko
Piotr Niewinski
Piotr Niewinski
Stanislaw Tubek
Stanislaw Tubek
Piotr Ponikowski
Piotr Ponikowski
author_sort Katarzyna Kulej-Lyko
collection DOAJ
description Peripheral chemoreceptors (PChRs), because of their strategic localization at the bifurcation of the common carotid artery and along the aortic arch, play an important protective role against hypoxia. Stimulation of PChRs evokes hyperventilation and hypertension to maintain adequate oxygenation of critical organs. A relationship between increased sensitivity of PChRs (hyperreflexia) and exercise intolerance (ExIn) in patients with heart failure (HF) has been previously reported. Moreover, some studies employing an acute blockade of PChRs (e.g., using oxygen or opioids) demonstrated improvement in exercise capacity, suggesting that hypertonicity is also involved in the development of ExIn in HF. Nonetheless, the precise mechanisms linking dysfunctional PChRs to ExIn remain unclear. From the clinical perspective, there are two main factors limiting exercise capacity in HF patients: subjective perception of dyspnoea and muscle fatigue. Both have many determinants that might be influenced by abnormal signalling from PChRs, including: exertional hyperventilation, oscillatory ventilation, ergoreceptor oversensitivity, and augmented sympathetic tone. The latter results in reduced muscle perfusion and altered muscle structure. In this review, we intend to present the milieu of abnormalities tied to malfunctioning PChRs and discuss their role in the complex relationships leading, ultimately, to ExIn.
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spelling doaj.art-45e797af29714f1dbaa7681f6a50f9952022-12-22T00:10:26ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2022-04-011310.3389/fphys.2022.878363878363Contribution of Peripheral Chemoreceptors to Exercise Intolerance in Heart FailureKatarzyna Kulej-Lyko0Katarzyna Kulej-Lyko1Piotr Niewinski2Piotr Niewinski3Stanislaw Tubek4Stanislaw Tubek5Piotr Ponikowski6Piotr Ponikowski7Institute of Heart Diseases, Wroclaw Medical University, Wroclaw, PolandDepartment of Cardiology, University Clinical Hospital, Wroclaw, PolandInstitute of Heart Diseases, Wroclaw Medical University, Wroclaw, PolandDepartment of Cardiology, University Clinical Hospital, Wroclaw, PolandInstitute of Heart Diseases, Wroclaw Medical University, Wroclaw, PolandDepartment of Cardiology, University Clinical Hospital, Wroclaw, PolandInstitute of Heart Diseases, Wroclaw Medical University, Wroclaw, PolandDepartment of Cardiology, University Clinical Hospital, Wroclaw, PolandPeripheral chemoreceptors (PChRs), because of their strategic localization at the bifurcation of the common carotid artery and along the aortic arch, play an important protective role against hypoxia. Stimulation of PChRs evokes hyperventilation and hypertension to maintain adequate oxygenation of critical organs. A relationship between increased sensitivity of PChRs (hyperreflexia) and exercise intolerance (ExIn) in patients with heart failure (HF) has been previously reported. Moreover, some studies employing an acute blockade of PChRs (e.g., using oxygen or opioids) demonstrated improvement in exercise capacity, suggesting that hypertonicity is also involved in the development of ExIn in HF. Nonetheless, the precise mechanisms linking dysfunctional PChRs to ExIn remain unclear. From the clinical perspective, there are two main factors limiting exercise capacity in HF patients: subjective perception of dyspnoea and muscle fatigue. Both have many determinants that might be influenced by abnormal signalling from PChRs, including: exertional hyperventilation, oscillatory ventilation, ergoreceptor oversensitivity, and augmented sympathetic tone. The latter results in reduced muscle perfusion and altered muscle structure. In this review, we intend to present the milieu of abnormalities tied to malfunctioning PChRs and discuss their role in the complex relationships leading, ultimately, to ExIn.https://www.frontiersin.org/articles/10.3389/fphys.2022.878363/fullperipheral chemoreceptorscarotid bodiesheart failureexercise intolerancedyspnoeamuscle fatigue
spellingShingle Katarzyna Kulej-Lyko
Katarzyna Kulej-Lyko
Piotr Niewinski
Piotr Niewinski
Stanislaw Tubek
Stanislaw Tubek
Piotr Ponikowski
Piotr Ponikowski
Contribution of Peripheral Chemoreceptors to Exercise Intolerance in Heart Failure
Frontiers in Physiology
peripheral chemoreceptors
carotid bodies
heart failure
exercise intolerance
dyspnoea
muscle fatigue
title Contribution of Peripheral Chemoreceptors to Exercise Intolerance in Heart Failure
title_full Contribution of Peripheral Chemoreceptors to Exercise Intolerance in Heart Failure
title_fullStr Contribution of Peripheral Chemoreceptors to Exercise Intolerance in Heart Failure
title_full_unstemmed Contribution of Peripheral Chemoreceptors to Exercise Intolerance in Heart Failure
title_short Contribution of Peripheral Chemoreceptors to Exercise Intolerance in Heart Failure
title_sort contribution of peripheral chemoreceptors to exercise intolerance in heart failure
topic peripheral chemoreceptors
carotid bodies
heart failure
exercise intolerance
dyspnoea
muscle fatigue
url https://www.frontiersin.org/articles/10.3389/fphys.2022.878363/full
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