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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
Pt 2
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pubmed:dateCreated |
2003-7-15
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pubmed:abstractText |
Acute hypoxia increases heart rate (HR) and cardiac output (Qt) at a given oxygen consumption (VO2) during submaximal exercise. It is widely believed that the underlying mechanism involves increased sympathetic activation and circulating catecholamines acting on cardiac beta receptors. Recent evidence indicating a continued role for parasympathetic modulation of HR during moderate exercise suggests that increased parasympathetic withdrawal plays a part in the increase in HR and Qt during hypoxic exercise. To test this, we separately blocked the beta-sympathetic and parasympathetic arms of the autonomic nervous system (ANS) in six healthy subjects (five male, one female; mean +/- S.E.M. age = 31.7+/-1.6 years, normoxic maximal VO2 (VO2,max)=3.1+/-0.3 l min(-1)) during exercise in conditions of normoxia and acute hypoxia (inspired oxygen fraction=0.125) to VO2,max. Data were collected on different days under the following conditions: (1)control, (2) after 8.0 mg propranolol i.v. and (3) after 0.8 mg glycopyrrolate i.v. Qt was measured using open-circuit acetylene uptake. Hypoxia increased venous [adrenaline] and [noradrenaline] but not [dopamine] at a given VO2 (P<0.05, P<0.01 and P=0.2, respectively). HR/VO2 and Qt/VO2 increased during hypoxia in all three conditions (P<0.05). Unexpectedly, the effects of hypoxia on HR and Qt were not significantly different from control with either beta-sympathetic or parasympathetic inhibition. These data suggest that although acute exposure to hypoxia increases circulating [catecholamines], the effects of hypoxia on HR and Qt do not necessarily require intact cardiac muscarinic and beta receptors. It may be that cardiac alpha receptors play a primary role in elevating HR and Qt during hypoxic exercise, or perhaps offer an alternative mechanism when other ANS pathways are blocked.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-10517785,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-10985598,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-11123125,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-11591615,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-11744656,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-12070214,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-12807992,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-13866419,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-1928333,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-2266783,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-235220,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-3023276,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-3311579,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-4151148,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-428052,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-4814308,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-5398888,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-5923231,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-6020242,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-6075748,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-6520045,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-7793415,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-8676580,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-8997321,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-9486244,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12766243-9729588
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0022-3751
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
550
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
605-16
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:12766243-Adrenergic beta-Antagonists,
pubmed-meshheading:12766243-Adult,
pubmed-meshheading:12766243-Anaerobic Threshold,
pubmed-meshheading:12766243-Anoxia,
pubmed-meshheading:12766243-Cardiac Output,
pubmed-meshheading:12766243-Catecholamines,
pubmed-meshheading:12766243-Dopamine,
pubmed-meshheading:12766243-Epinephrine,
pubmed-meshheading:12766243-Exercise,
pubmed-meshheading:12766243-Exercise Test,
pubmed-meshheading:12766243-Female,
pubmed-meshheading:12766243-Glycopyrrolate,
pubmed-meshheading:12766243-Heart Rate,
pubmed-meshheading:12766243-Humans,
pubmed-meshheading:12766243-Male,
pubmed-meshheading:12766243-Norepinephrine,
pubmed-meshheading:12766243-Oxygen Consumption,
pubmed-meshheading:12766243-Parasympatholytics,
pubmed-meshheading:12766243-Propranolol,
pubmed-meshheading:12766243-Respiratory Mechanics,
pubmed-meshheading:12766243-Stroke Volume
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pubmed:year |
2003
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pubmed:articleTitle |
Beta-adrenergic or parasympathetic inhibition, heart rate and cardiac output during normoxic and acute hypoxic exercise in humans.
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pubmed:affiliation |
Department of Medicine, University of California, San Diego, La Jolla, CA 92093, USA. shopkins@ucsd.edu
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pubmed:publicationType |
Journal Article,
Clinical Trial,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
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