The exercise pressor reflex and chemoreflex interaction: cardiovascular implications for the exercising human
Key points Although the exercise pressor reflex (EPR) and the chemoreflex (CR) are recognized for their sympathoexcitatory effect, the cardiovascular implication of their interaction remains elusive. We quantified the individual and interactive cardiovascular consequences of these reflexes during ex...
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| Published in: | The Journal of physiology Vol. 598; no. 12; pp. 2311 - 2321 |
|---|---|
| Main Authors: | , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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England
Wiley Subscription Services, Inc
01.06.2020
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| ISSN: | 0022-3751, 1469-7793, 1469-7793 |
| Online Access: | Get full text |
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| Abstract | Key points
Although the exercise pressor reflex (EPR) and the chemoreflex (CR) are recognized for their sympathoexcitatory effect, the cardiovascular implication of their interaction remains elusive.
We quantified the individual and interactive cardiovascular consequences of these reflexes during exercise and revealed various modes of interaction.
The EPR and hypoxia‐induced CR interaction is hyper‐additive for blood pressure and heart rate (responses during co‐activation of the two reflexes are greater than the summation of the responses evoked by each reflex) and hypo‐additive for peripheral haemodynamics (responses during co‐activation of the reflexes are smaller than the summated responses).
The EPR and hypercapnia‐induced CR interaction results in a simple addition of the individual responses to each reflex (i.e. additive interaction).
Collectively, EPR:CR co‐activation results in significant cardiovascular interactions with restriction in peripheral haemodynamics, resulting from the EPR:CR interaction in hypoxia, likely having the most crucial impact on the functional capacity of an exercising human.
We investigated the interactive effect of the exercise pressor reflex (EPR) and the chemoreflex (CR) on the cardiovascular response to exercise. Eleven healthy participants (5 females) completed a total of six bouts of single‐leg knee‐extension exercise (60% peak work rate, 4 min each) either with or without lumbar intrathecal fentanyl to attenuate group III/IV afferent feedback from lower limbs to modify the EPR, while breathing either ambient air, normocapnic hypoxia (SaO2 ∼79%, PaO2 ∼43 mmHg, PaCO2 ∼33 mmHg, pH ∼7.39), or normoxic hypercapnia (SaO2 ∼98%, PaO2 ∼105 mmHg, PaCO2 ∼50 mmHg, pH ∼7.26) to modify the CR. During co‐activation of the EPR and the hypoxia‐induced CR (O2‐CR), mean arterial pressure and heart rate were significantly greater, whereas leg blood flow and leg vascular conductance were significantly lower than the summation of the responses evoked by each reflex alone. During co‐activation of the EPR and the hypercapnia‐induced CR (CO2‐CR), the haemodynamic responses were not different from the summated responses to each reflex response alone (P ≥ 0.1). Therefore, while the interaction resulting from the EPR:O2‐CR co‐activation is hyper‐additive for blood pressure and heart rate, and hypo‐additive for peripheral haemodynamics, the interaction resulting from the EPR:CO2‐CR co‐activation is simply additive for all cardiovascular parameters. Thus, EPR:CR co‐activation results in significant interactions between cardiovascular reflexes, with the impact differing when the CR activation is achieved by hypoxia or hypercapnia. Since the EPR:CR co‐activation with hypoxia potentiates the pressor response and restricts blood flow to contracting muscles, this interaction entails the most functional impact on an exercising human.
Key points
Although the exercise pressor reflex (EPR) and the chemoreflex (CR) are recognized for their sympathoexcitatory effect, the cardiovascular implication of their interaction remains elusive.
We quantified the individual and interactive cardiovascular consequences of these reflexes during exercise and revealed various modes of interaction.
The EPR and hypoxia‐induced CR interaction is hyper‐additive for blood pressure and heart rate (responses during co‐activation of the two reflexes are greater than the summation of the responses evoked by each reflex) and hypo‐additive for peripheral haemodynamics (responses during co‐activation of the reflexes are smaller than the summated responses).
The EPR and hypercapnia‐induced CR interaction results in a simple addition of the individual responses to each reflex (i.e. additive interaction).
Collectively, EPR:CR co‐activation results in significant cardiovascular interactions with restriction in peripheral haemodynamics, resulting from the EPR:CR interaction in hypoxia, likely having the most crucial impact on the functional capacity of an exercising human. |
|---|---|
| AbstractList | Although the exercise pressor reflex (EPR) and the chemoreflex (CR) are recognized for their sympathoexcitatory effect, the cardiovascular implication of their interaction remains elusive.
We quantified the individual and interactive cardiovascular consequences of these reflexes during exercise and revealed various modes of interaction.
The EPR and hypoxia‐induced CR interaction is hyper‐additive for blood pressure and heart rate (responses during co‐activation of the two reflexes are greater than the summation of the responses evoked by each reflex) and hypo‐additive for peripheral haemodynamics (responses during co‐activation of the reflexes are smaller than the summated responses).
The EPR and hypercapnia‐induced CR interaction results in a simple addition of the individual responses to each reflex (i.e. additive interaction).
Collectively, EPR:CR co‐activation results in significant cardiovascular interactions with restriction in peripheral haemodynamics, resulting from the EPR:CR interaction in hypoxia, likely having the most crucial impact on the functional capacity of an exercising human. Although the exercise pressor reflex (EPR) and the chemoreflex (CR) are recognized for their sympathoexcitatory effect, the cardiovascular implication of their interaction remains elusive. We quantified the individual and interactive cardiovascular consequences of these reflexes during exercise and revealed various modes of interaction. The EPR and hypoxia-induced CR interaction is hyper-additive for blood pressure and heart rate (responses during co-activation of the two reflexes are greater than the summation of the responses evoked by each reflex) and hypo-additive for peripheral haemodynamics (responses during co-activation of the reflexes are smaller than the summated responses). The EPR and hypercapnia-induced CR interaction results in a simple addition of the individual responses to each reflex (i.e. additive interaction). Collectively, EPR:CR co-activation results in significant cardiovascular interactions with restriction in peripheral haemodynamics, resulting from the EPR:CR interaction in hypoxia, likely having the most crucial impact on the functional capacity of an exercising human. We investigated the interactive effect of the exercise pressor reflex (EPR) and the chemoreflex (CR) on the cardiovascular response to exercise. Eleven healthy participants (5 females) completed a total of six bouts of single-leg knee-extension exercise (60% peak work rate, 4 min each) either with or without lumbar intrathecal fentanyl to attenuate group III/IV afferent feedback from lower limbs to modify the EPR, while breathing either ambient air, normocapnic hypoxia (S O ∼79%, P O ∼43 mmHg, P CO ∼33 mmHg, pH ∼7.39), or normoxic hypercapnia (S O ∼98%, P O ∼105 mmHg, P CO ∼50 mmHg, pH ∼7.26) to modify the CR. During co-activation of the EPR and the hypoxia-induced CR (O -CR), mean arterial pressure and heart rate were significantly greater, whereas leg blood flow and leg vascular conductance were significantly lower than the summation of the responses evoked by each reflex alone. During co-activation of the EPR and the hypercapnia-induced CR (CO -CR), the haemodynamic responses were not different from the summated responses to each reflex response alone (P ≥ 0.1). Therefore, while the interaction resulting from the EPR:O -CR co-activation is hyper-additive for blood pressure and heart rate, and hypo-additive for peripheral haemodynamics, the interaction resulting from the EPR:CO -CR co-activation is simply additive for all cardiovascular parameters. Thus, EPR:CR co-activation results in significant interactions between cardiovascular reflexes, with the impact differing when the CR activation is achieved by hypoxia or hypercapnia. Since the EPR:CR co-activation with hypoxia potentiates the pressor response and restricts blood flow to contracting muscles, this interaction entails the most functional impact on an exercising human. We investigated the interactive effect of the exercise pressor reflex (EPR) and the chemoreflex (CR) on the cardiovascular response to exercise. Eleven healthy participants (5 females) completed a total of six bouts of single‐leg knee‐extension exercise (60% peak work rate, 4 min each) either with or without lumbar intrathecal fentanyl to attenuate group III/IV afferent feedback from lower limbs to modify the EPR, while breathing either ambient air, normocapnic hypoxia (SaO2 ∼79%, PaO2 ∼43 mmHg, PaCO2 ∼33 mmHg, pH ∼7.39), or normoxic hypercapnia (SaO2 ∼98%, PaO2 ∼105 mmHg, PaCO2 ∼50 mmHg, pH ∼7.26) to modify the CR. During co‐activation of the EPR and the hypoxia‐induced CR (O2‐CR), mean arterial pressure and heart rate were significantly greater, whereas leg blood flow and leg vascular conductance were significantly lower than the summation of the responses evoked by each reflex alone. During co‐activation of the EPR and the hypercapnia‐induced CR (CO2‐CR), the haemodynamic responses were not different from the summated responses to each reflex response alone (P ≥ 0.1). Therefore, while the interaction resulting from the EPR:O2‐CR co‐activation is hyper‐additive for blood pressure and heart rate, and hypo‐additive for peripheral haemodynamics, the interaction resulting from the EPR:CO2‐CR co‐activation is simply additive for all cardiovascular parameters. Thus, EPR:CR co‐activation results in significant interactions between cardiovascular reflexes, with the impact differing when the CR activation is achieved by hypoxia or hypercapnia. Since the EPR:CR co‐activation with hypoxia potentiates the pressor response and restricts blood flow to contracting muscles, this interaction entails the most functional impact on an exercising human. We investigated the interactive effect of the exercise pressor reflex (EPR) and the chemoreflex (CR) on the cardiovascular response to exercise. Eleven healthy participants (5 females) completed a total of six bouts of single-leg knee-extension exercise (60% peak work rate, 4 min each) either with or without lumbar intrathecal fentanyl to attenuate group III/IV afferent feedback from lower limbs to modify the EPR, while breathing either ambient air, normocapnic hypoxia (SaO2 ~79%, PaO2 ~43 mmHg, PaCO2 ~33 mmHg, pH ~7.39), or normoxic hypercapnia (SaO2 ~98%, PaO2 ~105 mmHg, PaCO2 ~50 mmHg, pH ~7.26) to modify the CR. During co-activation of the EPR and the hypoxia-induced CR (O2-CR), mean arterial pressure and heart rate were significantly greater, whereas leg blood flow and leg vascular conductance were significantly lower than the summation of the responses evoked by each reflex alone. During co-activation of the EPR and the hypercapnia-induced CR (CO2-CR), the haemodynamic responses were not different from the summated responses to each reflex response alone (P ≥ 0.1). Therefore, while the interaction resulting from the EPR:O2-CR co-activation is hyper-additive for blood pressure and heart rate, and hypo-additive for peripheral haemodynamics, the interaction resulting from the EPR:CO2-CR co-activation is simply additive for all cardiovascular parameters. Thus, EPR:CR co-activation results in significant interactions between cardiovascular reflexes, with the impact differing when the CR activation is achieved by hypoxia or hypercapnia. Since the EPR:CR co-activation with hypoxia potentiates the pressor response and restricts blood flow to contracting muscles, this interaction entails the most functional impact on an exercising human. Although the exercise pressor reflex (EPR) and the chemoreflex (CR) are recognized for their sympathoexcitatory effect, the cardiovascular implication of their interaction remains elusive. We quantified the individual and interactive cardiovascular consequences of these reflexes during exercise and revealed various modes of interaction. The EPR and hypoxia-induced CR interaction is hyper-additive for blood pressure and heart rate (responses during co-activation of the two reflexes are greater than the summation of the responses evoked by each reflex) and hypo-additive for peripheral haemodynamics (responses during co-activation of the reflexes are smaller than the summated responses). The EPR and hypercapnia-induced CR interaction results in a simple addition of the individual responses to each reflex (i.e. additive interaction). Collectively, EPR:CR co-activation results in significant cardiovascular interactions with restriction in peripheral haemodynamics, resulting from the EPR:CR interaction in hypoxia, likely having the most crucial impact on the functional capacity of an exercising human.KEY POINTSAlthough the exercise pressor reflex (EPR) and the chemoreflex (CR) are recognized for their sympathoexcitatory effect, the cardiovascular implication of their interaction remains elusive. We quantified the individual and interactive cardiovascular consequences of these reflexes during exercise and revealed various modes of interaction. The EPR and hypoxia-induced CR interaction is hyper-additive for blood pressure and heart rate (responses during co-activation of the two reflexes are greater than the summation of the responses evoked by each reflex) and hypo-additive for peripheral haemodynamics (responses during co-activation of the reflexes are smaller than the summated responses). The EPR and hypercapnia-induced CR interaction results in a simple addition of the individual responses to each reflex (i.e. additive interaction). Collectively, EPR:CR co-activation results in significant cardiovascular interactions with restriction in peripheral haemodynamics, resulting from the EPR:CR interaction in hypoxia, likely having the most crucial impact on the functional capacity of an exercising human.We investigated the interactive effect of the exercise pressor reflex (EPR) and the chemoreflex (CR) on the cardiovascular response to exercise. Eleven healthy participants (5 females) completed a total of six bouts of single-leg knee-extension exercise (60% peak work rate, 4 min each) either with or without lumbar intrathecal fentanyl to attenuate group III/IV afferent feedback from lower limbs to modify the EPR, while breathing either ambient air, normocapnic hypoxia (Sa O2 ∼79%, Pa O2 ∼43 mmHg, Pa CO2 ∼33 mmHg, pH ∼7.39), or normoxic hypercapnia (Sa O2 ∼98%, Pa O2 ∼105 mmHg, Pa CO2 ∼50 mmHg, pH ∼7.26) to modify the CR. During co-activation of the EPR and the hypoxia-induced CR (O2 -CR), mean arterial pressure and heart rate were significantly greater, whereas leg blood flow and leg vascular conductance were significantly lower than the summation of the responses evoked by each reflex alone. During co-activation of the EPR and the hypercapnia-induced CR (CO2 -CR), the haemodynamic responses were not different from the summated responses to each reflex response alone (P ≥ 0.1). Therefore, while the interaction resulting from the EPR:O2 -CR co-activation is hyper-additive for blood pressure and heart rate, and hypo-additive for peripheral haemodynamics, the interaction resulting from the EPR:CO2 -CR co-activation is simply additive for all cardiovascular parameters. Thus, EPR:CR co-activation results in significant interactions between cardiovascular reflexes, with the impact differing when the CR activation is achieved by hypoxia or hypercapnia. Since the EPR:CR co-activation with hypoxia potentiates the pressor response and restricts blood flow to contracting muscles, this interaction entails the most functional impact on an exercising human.ABSTRACTWe investigated the interactive effect of the exercise pressor reflex (EPR) and the chemoreflex (CR) on the cardiovascular response to exercise. Eleven healthy participants (5 females) completed a total of six bouts of single-leg knee-extension exercise (60% peak work rate, 4 min each) either with or without lumbar intrathecal fentanyl to attenuate group III/IV afferent feedback from lower limbs to modify the EPR, while breathing either ambient air, normocapnic hypoxia (Sa O2 ∼79%, Pa O2 ∼43 mmHg, Pa CO2 ∼33 mmHg, pH ∼7.39), or normoxic hypercapnia (Sa O2 ∼98%, Pa O2 ∼105 mmHg, Pa CO2 ∼50 mmHg, pH ∼7.26) to modify the CR. During co-activation of the EPR and the hypoxia-induced CR (O2 -CR), mean arterial pressure and heart rate were significantly greater, whereas leg blood flow and leg vascular conductance were significantly lower than the summation of the responses evoked by each reflex alone. During co-activation of the EPR and the hypercapnia-induced CR (CO2 -CR), the haemodynamic responses were not different from the summated responses to each reflex response alone (P ≥ 0.1). Therefore, while the interaction resulting from the EPR:O2 -CR co-activation is hyper-additive for blood pressure and heart rate, and hypo-additive for peripheral haemodynamics, the interaction resulting from the EPR:CO2 -CR co-activation is simply additive for all cardiovascular parameters. Thus, EPR:CR co-activation results in significant interactions between cardiovascular reflexes, with the impact differing when the CR activation is achieved by hypoxia or hypercapnia. Since the EPR:CR co-activation with hypoxia potentiates the pressor response and restricts blood flow to contracting muscles, this interaction entails the most functional impact on an exercising human. Key points Although the exercise pressor reflex (EPR) and the chemoreflex (CR) are recognized for their sympathoexcitatory effect, the cardiovascular implication of their interaction remains elusive. We quantified the individual and interactive cardiovascular consequences of these reflexes during exercise and revealed various modes of interaction. The EPR and hypoxia‐induced CR interaction is hyper‐additive for blood pressure and heart rate (responses during co‐activation of the two reflexes are greater than the summation of the responses evoked by each reflex) and hypo‐additive for peripheral haemodynamics (responses during co‐activation of the reflexes are smaller than the summated responses). The EPR and hypercapnia‐induced CR interaction results in a simple addition of the individual responses to each reflex (i.e. additive interaction). Collectively, EPR:CR co‐activation results in significant cardiovascular interactions with restriction in peripheral haemodynamics, resulting from the EPR:CR interaction in hypoxia, likely having the most crucial impact on the functional capacity of an exercising human. We investigated the interactive effect of the exercise pressor reflex (EPR) and the chemoreflex (CR) on the cardiovascular response to exercise. Eleven healthy participants (5 females) completed a total of six bouts of single‐leg knee‐extension exercise (60% peak work rate, 4 min each) either with or without lumbar intrathecal fentanyl to attenuate group III/IV afferent feedback from lower limbs to modify the EPR, while breathing either ambient air, normocapnic hypoxia (SaO2 ∼79%, PaO2 ∼43 mmHg, PaCO2 ∼33 mmHg, pH ∼7.39), or normoxic hypercapnia (SaO2 ∼98%, PaO2 ∼105 mmHg, PaCO2 ∼50 mmHg, pH ∼7.26) to modify the CR. During co‐activation of the EPR and the hypoxia‐induced CR (O2‐CR), mean arterial pressure and heart rate were significantly greater, whereas leg blood flow and leg vascular conductance were significantly lower than the summation of the responses evoked by each reflex alone. During co‐activation of the EPR and the hypercapnia‐induced CR (CO2‐CR), the haemodynamic responses were not different from the summated responses to each reflex response alone (P ≥ 0.1). Therefore, while the interaction resulting from the EPR:O2‐CR co‐activation is hyper‐additive for blood pressure and heart rate, and hypo‐additive for peripheral haemodynamics, the interaction resulting from the EPR:CO2‐CR co‐activation is simply additive for all cardiovascular parameters. Thus, EPR:CR co‐activation results in significant interactions between cardiovascular reflexes, with the impact differing when the CR activation is achieved by hypoxia or hypercapnia. Since the EPR:CR co‐activation with hypoxia potentiates the pressor response and restricts blood flow to contracting muscles, this interaction entails the most functional impact on an exercising human. Key points Although the exercise pressor reflex (EPR) and the chemoreflex (CR) are recognized for their sympathoexcitatory effect, the cardiovascular implication of their interaction remains elusive. We quantified the individual and interactive cardiovascular consequences of these reflexes during exercise and revealed various modes of interaction. The EPR and hypoxia‐induced CR interaction is hyper‐additive for blood pressure and heart rate (responses during co‐activation of the two reflexes are greater than the summation of the responses evoked by each reflex) and hypo‐additive for peripheral haemodynamics (responses during co‐activation of the reflexes are smaller than the summated responses). The EPR and hypercapnia‐induced CR interaction results in a simple addition of the individual responses to each reflex (i.e. additive interaction). Collectively, EPR:CR co‐activation results in significant cardiovascular interactions with restriction in peripheral haemodynamics, resulting from the EPR:CR interaction in hypoxia, likely having the most crucial impact on the functional capacity of an exercising human. |
| Author | Richardson, Russell S. Buys, Michael J. Weavil, Joshua C. Amann, Markus Georgescu, Vincent P. Thurston, Taylor S. Jessop, Jacob E. Bledsoe, Amber D. Wan, Hsuan‐Yu Hureau, Thomas J. |
| AuthorAffiliation | 2 Geriatric Research, Education, and Clinical Center, Salt Lake City, UT, VAMC, USA 3 Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT, USA 4 Department of Internal Medicine, University of Utah, Salt Lake City, UT, USA 1 Department of Anesthesiology, University of Utah, Salt Lake City, UT, USA |
| AuthorAffiliation_xml | – name: 4 Department of Internal Medicine, University of Utah, Salt Lake City, UT, USA – name: 1 Department of Anesthesiology, University of Utah, Salt Lake City, UT, USA – name: 3 Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT, USA – name: 2 Geriatric Research, Education, and Clinical Center, Salt Lake City, UT, VAMC, USA |
| Author_xml | – sequence: 1 givenname: Hsuan‐Yu orcidid: 0000-0001-8853-8451 surname: Wan fullname: Wan, Hsuan‐Yu email: hsuan-yu.wan@hsc.utah.edu organization: University of Utah – sequence: 2 givenname: Joshua C. orcidid: 0000-0002-2032-8498 surname: Weavil fullname: Weavil, Joshua C. organization: Geriatric Research, Education, and Clinical Center – sequence: 3 givenname: Taylor S. orcidid: 0000-0002-4536-3054 surname: Thurston fullname: Thurston, Taylor S. organization: University of Utah – sequence: 4 givenname: Vincent P. surname: Georgescu fullname: Georgescu, Vincent P. organization: University of Utah – sequence: 5 givenname: Thomas J. orcidid: 0000-0002-6993-5723 surname: Hureau fullname: Hureau, Thomas J. organization: University of Utah – sequence: 6 givenname: Amber D. surname: Bledsoe fullname: Bledsoe, Amber D. organization: University of Utah – sequence: 7 givenname: Michael J. orcidid: 0000-0001-8222-1461 surname: Buys fullname: Buys, Michael J. organization: University of Utah – sequence: 8 givenname: Jacob E. surname: Jessop fullname: Jessop, Jacob E. organization: University of Utah – sequence: 9 givenname: Russell S. surname: Richardson fullname: Richardson, Russell S. organization: University of Utah – sequence: 10 givenname: Markus surname: Amann fullname: Amann, Markus organization: University of Utah |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32170732$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | 2020 The Authors. The Journal of Physiology © 2020 The Physiological Society 2020 The Authors. The Journal of Physiology © 2020 The Physiological Society. Journal compilation © 2020 The Physiological Society |
| Copyright_xml | – notice: 2020 The Authors. The Journal of Physiology © 2020 The Physiological Society – notice: 2020 The Authors. The Journal of Physiology © 2020 The Physiological Society. – notice: Journal compilation © 2020 The Physiological Society |
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| DOI | 10.1113/JP279456 |
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| Keywords | autonomic control hypoxia sympathetic vasoconstriction blood flow hypercapnia |
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| Notes | Linked articles: This article is highlighted in a Perspectives article by Sheel & Peters. To read this article, visit https://doi.org/10.1113/JP279806 Edited by: Harold Schultz & Ken O'Halloran . ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Authors’ contributions H.W. and M.A. contributed to conception and design of the work; H.W., J.C.W., T.S.T., V.P.G., T.J.H., A.D.B., M.J.B., J.E.J., R.S.R. and M.A. contributed to acquisition, analysis or interpretation of data for the work; H.W., R.S.R. and M.A. contributed to drafting the work or revising it critically for important intellectual content. All authors approved the final version of the manuscript and agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All persons designated as authors qualify for authorship, and all those who qualify for authorship are listed. |
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Although the exercise pressor reflex (EPR) and the chemoreflex (CR) are recognized for their sympathoexcitatory effect, the cardiovascular... Although the exercise pressor reflex (EPR) and the chemoreflex (CR) are recognized for their sympathoexcitatory effect, the cardiovascular implication of their... We investigated the interactive effect of the exercise pressor reflex (EPR) and the chemoreflex (CR) on the cardiovascular response to exercise. Eleven healthy... |
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| SubjectTerms | autonomic control Blood flow Blood Pressure Carbon dioxide Chemoreception (internal) Conductance Exercise Female Fentanyl Heart rate Hemodynamics Humans Hypercapnia Hypoxia Leg Muscles pH effects Physical training Reflex Reflexes Sensory neurons sympathetic vasoconstriction |
| Title | The exercise pressor reflex and chemoreflex interaction: cardiovascular implications for the exercising human |
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