Differential effects of metaboreceptor and chemoreceptor activation on sympathetic and cardiac baroreflex control following exercise in hypoxia in human
Muscle metaboreceptors and peripheral chemoreceptors exert differential effects on the cardiorespiratory and autonomic responses following hypoxic exercise. Whether these effects are accompanied by specific changes in sympathetic and cardiac baroreflex control is not known. Sympathetic and cardiac b...
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| Published in | The Journal of physiology Vol. 585; no. 1; pp. 165 - 174 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford, UK
The Physiological Society
15.11.2007
Blackwell Publishing Ltd |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0022-3751 1469-7793 1469-7793 |
| DOI | 10.1113/jphysiol.2007.141002 |
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| Abstract | Muscle metaboreceptors and peripheral chemoreceptors exert differential effects on the cardiorespiratory and autonomic responses
following hypoxic exercise. Whether these effects are accompanied by specific changes in sympathetic and cardiac baroreflex
control is not known. Sympathetic and cardiac baroreflex functions were assessed by intravenous nitroprusside and phenylephrine
boluses in 15 young male subjects. Recordings were performed in random order, under locally circulatory arrested conditions,
during: (1) rest and normoxia (no metaboreflex and no chemoreflex activation); (2) normoxic post-handgrip exercise at 30%
of maximum voluntary contraction (metaboreflex activation without chemoreflex activation); (3) hypoxia without handgrip (10%
O 2 in N 2 , chemoreflex activation without metaboreflex activation); and (4) post-handgrip exercise in hypoxia (chemoreflex and metaboreflex
activation). When compared with normoxic rest (â42 ± 7% muscle sympathetic nerve activity (MSNA) mmHg â1 ), sympathetic baroreflex sensitivity did not change during normoxic post-exercise ischaemia (PEI; â53 ± 9% MSNA mmHg â1 , P = 0.5) and increased during resting hypoxia (â68 ± 5% MSNA mmHg â1 , P < 0.01). Sympathetic baroreflex sensitivity decreased during PEI in hypoxia (â35 ± 6% MSNA mmHg â1 , P < 0.001 versus hypoxia without exercise; P = 0.16 versus normoxic PEI). Conversely, when compared with normoxic rest (11.1 ± 1.7 ms mmHg â1 ), cardiac baroreflex sensitivity did not change during normoxic PEI (8.3 ± 1.3 ms mmHg â1 , P = 0.09), but decreased during resting hypoxia (7.3 ± 0.8 ms mmHg â1 , P < 0.05). Cardiac baroreflex sensitivity was lowest during PEI in hypoxia (4.3 ± 1 ms mmHg â1 , P < 0.01 versus hypoxia without exercise; P < 0.001 versus normoxic exercise). The metaboreceptors and chemoreceptors exert differential effects on sympathetic and cardiac baroreflex
function. Metaboreceptor activation is the major determinant of sympathetic baroreflex sensitivity, when these receptors are
stimulated in the presence of hypoxia. |
|---|---|
| AbstractList | Muscle metaboreceptors and peripheral chemoreceptors exert differential effects on the cardiorespiratory and autonomic responses following hypoxic exercise. Whether these effects are accompanied by specific changes in sympathetic and cardiac baroreflex control is not known. Sympathetic and cardiac baroreflex functions were assessed by intravenous nitroprusside and phenylephrine boluses in 15 young male subjects. Recordings were performed in random order, under locally circulatory arrested conditions, during: (1) rest and normoxia (no metaboreflex and no chemoreflex activation); (2) normoxic post‐handgrip exercise at 30% of maximum voluntary contraction (metaboreflex activation without chemoreflex activation); (3) hypoxia without handgrip (10% O2 in N2, chemoreflex activation without metaboreflex activation); and (4) post‐handgrip exercise in hypoxia (chemoreflex and metaboreflex activation). When compared with normoxic rest (−42 ± 7% muscle sympathetic nerve activity (MSNA) mmHg−1), sympathetic baroreflex sensitivity did not change during normoxic post‐exercise ischaemia (PEI; −53 ± 9% MSNA mmHg−1, P= 0.5) and increased during resting hypoxia (−68 ± 5% MSNA mmHg−1, P < 0.01). Sympathetic baroreflex sensitivity decreased during PEI in hypoxia (−35 ± 6% MSNA mmHg−1, P < 0.001 versus hypoxia without exercise; P= 0.16 versus normoxic PEI). Conversely, when compared with normoxic rest (11.1 ± 1.7 ms mmHg−1), cardiac baroreflex sensitivity did not change during normoxic PEI (8.3 ± 1.3 ms mmHg−1, P= 0.09), but decreased during resting hypoxia (7.3 ± 0.8 ms mmHg−1, P < 0.05). Cardiac baroreflex sensitivity was lowest during PEI in hypoxia (4.3 ± 1 ms mmHg−1, P < 0.01 versus hypoxia without exercise; P < 0.001 versus normoxic exercise). The metaboreceptors and chemoreceptors exert differential effects on sympathetic and cardiac baroreflex function. Metaboreceptor activation is the major determinant of sympathetic baroreflex sensitivity, when these receptors are stimulated in the presence of hypoxia. Muscle metaboreceptors and peripheral chemoreceptors exert differential effects on the cardiorespiratory and autonomic responses following hypoxic exercise. Whether these effects are accompanied by specific changes in sympathetic and cardiac baroreflex control is not known. Sympathetic and cardiac baroreflex functions were assessed by intravenous nitroprusside and phenylephrine boluses in 15 young male subjects. Recordings were performed in random order, under locally circulatory arrested conditions, during: (1) rest and normoxia (no metaboreflex and no chemoreflex activation); (2) normoxic post-handgrip exercise at 30% of maximum voluntary contraction (metaboreflex activation without chemoreflex activation); (3) hypoxia without handgrip (10% O2 in N2, chemoreflex activation without metaboreflex activation); and (4) post-handgrip exercise in hypoxia (chemoreflex and metaboreflex activation). When compared with normoxic rest (-42 +/- 7% muscle sympathetic nerve activity (MSNA) mmHg(-1)), sympathetic baroreflex sensitivity did not change during normoxic post-exercise ischaemia (PEI; -53 +/- 9% MSNA mmHg(-1), P = 0.5) and increased during resting hypoxia (-68 +/- 5% MSNA mmHg(-1), P < 0.01). Sympathetic baroreflex sensitivity decreased during PEI in hypoxia (-35 +/- 6% MSNA mmHg(-1), P < 0.001 versus hypoxia without exercise; P = 0.16 versus normoxic PEI). Conversely, when compared with normoxic rest (11.1 +/- 1.7 ms mmHg(-1)), cardiac baroreflex sensitivity did not change during normoxic PEI (8.3 +/- 1.3 ms mmHg(-1), P = 0.09), but decreased during resting hypoxia (7.3 +/- 0.8 ms mmHg(-1), P < 0.05). Cardiac baroreflex sensitivity was lowest during PEI in hypoxia (4.3 +/- 1 ms mmHg(-1), P < 0.01 versus hypoxia without exercise; P < 0.001 versus normoxic exercise). The metaboreceptors and chemoreceptors exert differential effects on sympathetic and cardiac baroreflex function. Metaboreceptor activation is the major determinant of sympathetic baroreflex sensitivity, when these receptors are stimulated in the presence of hypoxia. Muscle metaboreceptors and peripheral chemoreceptors exert differential effects on the cardiorespiratory and autonomic responses following hypoxic exercise. Whether these effects are accompanied by specific changes in sympathetic and cardiac baroreflex control is not known. Sympathetic and cardiac baroreflex functions were assessed by intravenous nitroprusside and phenylephrine boluses in 15 young male subjects. Recordings were performed in random order, under locally circulatory arrested conditions, during: (1) rest and normoxia (no metaboreflex and no chemoreflex activation); (2) normoxic post-handgrip exercise at 30% of maximum voluntary contraction (metaboreflex activation without chemoreflex activation); (3) hypoxia without handgrip (10% O2 in N2, chemoreflex activation without metaboreflex activation); and (4) post-handgrip exercise in hypoxia (chemoreflex and metaboreflex activation). When compared with normoxic rest (-42 +/- 7% muscle sympathetic nerve activity (MSNA) mmHg(-1)), sympathetic baroreflex sensitivity did not change during normoxic post-exercise ischaemia (PEI; -53 +/- 9% MSNA mmHg(-1), P = 0.5) and increased during resting hypoxia (-68 +/- 5% MSNA mmHg(-1), P < 0.01). Sympathetic baroreflex sensitivity decreased during PEI in hypoxia (-35 +/- 6% MSNA mmHg(-1), P < 0.001 versus hypoxia without exercise; P = 0.16 versus normoxic PEI). Conversely, when compared with normoxic rest (11.1 +/- 1.7 ms mmHg(-1)), cardiac baroreflex sensitivity did not change during normoxic PEI (8.3 +/- 1.3 ms mmHg(-1), P = 0.09), but decreased during resting hypoxia (7.3 +/- 0.8 ms mmHg(-1), P < 0.05). Cardiac baroreflex sensitivity was lowest during PEI in hypoxia (4.3 +/- 1 ms mmHg(-1), P < 0.01 versus hypoxia without exercise; P < 0.001 versus normoxic exercise). The metaboreceptors and chemoreceptors exert differential effects on sympathetic and cardiac baroreflex function. Metaboreceptor activation is the major determinant of sympathetic baroreflex sensitivity, when these receptors are stimulated in the presence of hypoxia.Muscle metaboreceptors and peripheral chemoreceptors exert differential effects on the cardiorespiratory and autonomic responses following hypoxic exercise. Whether these effects are accompanied by specific changes in sympathetic and cardiac baroreflex control is not known. Sympathetic and cardiac baroreflex functions were assessed by intravenous nitroprusside and phenylephrine boluses in 15 young male subjects. Recordings were performed in random order, under locally circulatory arrested conditions, during: (1) rest and normoxia (no metaboreflex and no chemoreflex activation); (2) normoxic post-handgrip exercise at 30% of maximum voluntary contraction (metaboreflex activation without chemoreflex activation); (3) hypoxia without handgrip (10% O2 in N2, chemoreflex activation without metaboreflex activation); and (4) post-handgrip exercise in hypoxia (chemoreflex and metaboreflex activation). When compared with normoxic rest (-42 +/- 7% muscle sympathetic nerve activity (MSNA) mmHg(-1)), sympathetic baroreflex sensitivity did not change during normoxic post-exercise ischaemia (PEI; -53 +/- 9% MSNA mmHg(-1), P = 0.5) and increased during resting hypoxia (-68 +/- 5% MSNA mmHg(-1), P < 0.01). Sympathetic baroreflex sensitivity decreased during PEI in hypoxia (-35 +/- 6% MSNA mmHg(-1), P < 0.001 versus hypoxia without exercise; P = 0.16 versus normoxic PEI). Conversely, when compared with normoxic rest (11.1 +/- 1.7 ms mmHg(-1)), cardiac baroreflex sensitivity did not change during normoxic PEI (8.3 +/- 1.3 ms mmHg(-1), P = 0.09), but decreased during resting hypoxia (7.3 +/- 0.8 ms mmHg(-1), P < 0.05). Cardiac baroreflex sensitivity was lowest during PEI in hypoxia (4.3 +/- 1 ms mmHg(-1), P < 0.01 versus hypoxia without exercise; P < 0.001 versus normoxic exercise). The metaboreceptors and chemoreceptors exert differential effects on sympathetic and cardiac baroreflex function. Metaboreceptor activation is the major determinant of sympathetic baroreflex sensitivity, when these receptors are stimulated in the presence of hypoxia. Muscle metaboreceptors and peripheral chemoreceptors exert differential effects on the cardiorespiratory and autonomic responses following hypoxic exercise. Whether these effects are accompanied by specific changes in sympathetic and cardiac baroreflex control is not known. Sympathetic and cardiac baroreflex functions were assessed by intravenous nitroprusside and phenylephrine boluses in 15 young male subjects. Recordings were performed in random order, under locally circulatory arrested conditions, during: (1) rest and normoxia (no metaboreflex and no chemoreflex activation); (2) normoxic post-handgrip exercise at 30% of maximum voluntary contraction (metaboreflex activation without chemoreflex activation); (3) hypoxia without handgrip (10% O sub(2) in N sub(2), chemoreflex activation without metaboreflex activation); and (4) post-handgrip exercise in hypoxia (chemoreflex and metaboreflex activation). When compared with normoxic rest (-42 plus or minus 7% muscle sympathetic nerve activity (MSNA) mmHg super(-1)), sympathetic baroreflex sensitivity did not change during normoxic post-exercise ischaemia (PEI; -53 plus or minus 9% MSNA mmHg super(-1), P= 0.5) and increased during resting hypoxia (-68 plus or minus 5% MSNA mmHg super(-1), P < 0.01). Sympathetic baroreflex sensitivity decreased during PEI in hypoxia (-35 plus or minus 6% MSNA mmHg super(-1), P < 0.001 versus hypoxia without exercise; P= 0.16 versus normoxic PEI). Conversely, when compared with normoxic rest (11.1 plus or minus 1.7 ms mmHg super(-1)), cardiac baroreflex sensitivity did not change during normoxic PEI (8.3 plus or minus 1.3 ms mmHg super(-1), P= 0.09), but decreased during resting hypoxia (7.3 plus or minus 0.8 ms mmHg super(-1), P < 0.05). Cardiac baroreflex sensitivity was lowest during PEI in hypoxia (4.3 plus or minus 1 ms mmHg super(-1), P < 0.01 versus hypoxia without exercise; P < 0.001 versus normoxic exercise). The metaboreceptors and chemoreceptors exert differential effects on sympathetic and cardiac baroreflex function. Metaboreceptor activation is the major determinant of sympathetic baroreflex sensitivity, when these receptors are stimulated in the presence of hypoxia. Muscle metaboreceptors and peripheral chemoreceptors exert differential effects on the cardiorespiratory and autonomic responses following hypoxic exercise. Whether these effects are accompanied by specific changes in sympathetic and cardiac baroreflex control is not known. Sympathetic and cardiac baroreflex functions were assessed by intravenous nitroprusside and phenylephrine boluses in 15 young male subjects. Recordings were performed in random order, under locally circulatory arrested conditions, during: (1) rest and normoxia (no metaboreflex and no chemoreflex activation); (2) normoxic post-handgrip exercise at 30% of maximum voluntary contraction (metaboreflex activation without chemoreflex activation); (3) hypoxia without handgrip (10% O 2 in N 2 , chemoreflex activation without metaboreflex activation); and (4) post-handgrip exercise in hypoxia (chemoreflex and metaboreflex activation). When compared with normoxic rest (â42 ± 7% muscle sympathetic nerve activity (MSNA) mmHg â1 ), sympathetic baroreflex sensitivity did not change during normoxic post-exercise ischaemia (PEI; â53 ± 9% MSNA mmHg â1 , P = 0.5) and increased during resting hypoxia (â68 ± 5% MSNA mmHg â1 , P < 0.01). Sympathetic baroreflex sensitivity decreased during PEI in hypoxia (â35 ± 6% MSNA mmHg â1 , P < 0.001 versus hypoxia without exercise; P = 0.16 versus normoxic PEI). Conversely, when compared with normoxic rest (11.1 ± 1.7 ms mmHg â1 ), cardiac baroreflex sensitivity did not change during normoxic PEI (8.3 ± 1.3 ms mmHg â1 , P = 0.09), but decreased during resting hypoxia (7.3 ± 0.8 ms mmHg â1 , P < 0.05). Cardiac baroreflex sensitivity was lowest during PEI in hypoxia (4.3 ± 1 ms mmHg â1 , P < 0.01 versus hypoxia without exercise; P < 0.001 versus normoxic exercise). The metaboreceptors and chemoreceptors exert differential effects on sympathetic and cardiac baroreflex function. Metaboreceptor activation is the major determinant of sympathetic baroreflex sensitivity, when these receptors are stimulated in the presence of hypoxia. Muscle metaboreceptors and peripheral chemoreceptors exert differential effects on the cardiorespiratory and autonomic responses following hypoxic exercise. Whether these effects are accompanied by specific changes in sympathetic and cardiac baroreflex control is not known. Sympathetic and cardiac baroreflex functions were assessed by intravenous nitroprusside and phenylephrine boluses in 15 young male subjects. Recordings were performed in random order, under locally circulatory arrested conditions, during: (1) rest and normoxia (no metaboreflex and no chemoreflex activation); (2) normoxic post‐handgrip exercise at 30% of maximum voluntary contraction (metaboreflex activation without chemoreflex activation); (3) hypoxia without handgrip (10% O 2 in N 2 , chemoreflex activation without metaboreflex activation); and (4) post‐handgrip exercise in hypoxia (chemoreflex and metaboreflex activation). When compared with normoxic rest (−42 ± 7% muscle sympathetic nerve activity (MSNA) mmHg −1 ), sympathetic baroreflex sensitivity did not change during normoxic post‐exercise ischaemia (PEI; −53 ± 9% MSNA mmHg −1 , P = 0.5) and increased during resting hypoxia (−68 ± 5% MSNA mmHg −1 , P < 0.01). Sympathetic baroreflex sensitivity decreased during PEI in hypoxia (−35 ± 6% MSNA mmHg −1 , P < 0.001 versus hypoxia without exercise; P = 0.16 versus normoxic PEI). Conversely, when compared with normoxic rest (11.1 ± 1.7 ms mmHg −1 ), cardiac baroreflex sensitivity did not change during normoxic PEI (8.3 ± 1.3 ms mmHg −1 , P = 0.09), but decreased during resting hypoxia (7.3 ± 0.8 ms mmHg −1 , P < 0.05). Cardiac baroreflex sensitivity was lowest during PEI in hypoxia (4.3 ± 1 ms mmHg −1 , P < 0.01 versus hypoxia without exercise; P < 0.001 versus normoxic exercise). The metaboreceptors and chemoreceptors exert differential effects on sympathetic and cardiac baroreflex function. Metaboreceptor activation is the major determinant of sympathetic baroreflex sensitivity, when these receptors are stimulated in the presence of hypoxia. |
| Author | Jean-François Argacha Olivier Xhaët Sofia Beloka Dionysios Adamopoulos Jean-Luc Elghozi Dominique Laude Anne Houssière Marko Gujic Philippe van de Borne |
| Author_xml | – sequence: 1 givenname: Marko surname: Gujic fullname: Gujic, Marko – sequence: 2 givenname: Dominique surname: Laude fullname: Laude, Dominique – sequence: 3 givenname: Anne surname: Houssière fullname: Houssière, Anne – sequence: 4 givenname: Sofia surname: Beloka fullname: Beloka, Sofia – sequence: 5 givenname: Jean‐François surname: Argacha fullname: Argacha, Jean‐François – sequence: 6 givenname: Dionysios surname: Adamopoulos fullname: Adamopoulos, Dionysios – sequence: 7 givenname: Olivier surname: Xhaët fullname: Xhaët, Olivier – sequence: 8 givenname: Jean‐Luc surname: Elghozi fullname: Elghozi, Jean‐Luc – sequence: 9 givenname: Philippe surname: Van De Borne fullname: Van De Borne, Philippe |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/17884922$$D View this record in MEDLINE/PubMed |
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| PublicationPlace | Oxford, UK |
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| PublicationTitle | The Journal of physiology |
| PublicationTitleAlternate | J Physiol |
| PublicationYear | 2007 |
| Publisher | The Physiological Society Blackwell Publishing Ltd |
| Publisher_xml | – name: The Physiological Society – name: Blackwell Publishing Ltd |
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| Snippet | Muscle metaboreceptors and peripheral chemoreceptors exert differential effects on the cardiorespiratory and autonomic responses
following hypoxic exercise.... Muscle metaboreceptors and peripheral chemoreceptors exert differential effects on the cardiorespiratory and autonomic responses following hypoxic exercise.... |
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| SubjectTerms | Adult Baroreflex - drug effects Baroreflex - physiology Blood Pressure - drug effects Blood Pressure - physiology Cardiovascular Chemoreceptor Cells - drug effects Chemoreceptor Cells - physiology Exercise - physiology Heart - innervation Humans Hypoxia - physiopathology Male Mechanoreceptors - drug effects Mechanoreceptors - physiology Nitroprusside - pharmacology Phenylephrine - pharmacology Rest - physiology Sympathetic Nervous System - physiology Vasoconstrictor Agents - pharmacology Vasodilator Agents - pharmacology |
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| Title | Differential effects of metaboreceptor and chemoreceptor activation on sympathetic and cardiac baroreflex control following exercise in hypoxia in human |
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