Document Detail


Beta-adrenergic or parasympathetic inhibition, heart rate and cardiac output during normoxic and acute hypoxic exercise in humans.
MedLine Citation:
PMID:  12766243     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Susan R Hopkins; Harm J Bogaard; Kyuichi Niizeki; Yoshiki Yamaya; Michael G Ziegler; Peter D Wagner
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Publication Detail:
Type:  Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.     Date:  2003-05-23
Journal Detail:
Title:  The Journal of physiology     Volume:  550     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2003 Jul 
Date Detail:
Created Date:  2003-07-15     Completed Date:  2004-03-08     Revised Date:  2013-06-09    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  605-16     Citation Subset:  IM    
Affiliation:
Department of Medicine, University of California, San Diego, La Jolla, CA 92093, USA. shopkins@ucsd.edu
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MeSH Terms
Descriptor/Qualifier:
Adrenergic beta-Antagonists / pharmacology*
Adult
Anaerobic Threshold / physiology
Anoxia / physiopathology*
Cardiac Output / drug effects*,  physiology*
Catecholamines / blood
Dopamine / blood
Epinephrine / blood
Exercise / physiology*
Exercise Test
Female
Glycopyrrolate / pharmacology
Heart Rate / drug effects*,  physiology*
Humans
Male
Norepinephrine / blood
Oxygen Consumption / physiology
Parasympatholytics / pharmacology*
Propranolol / pharmacology
Respiratory Mechanics / physiology
Stroke Volume / drug effects,  physiology
Grant Support
ID/Acronym/Agency:
HL17731/HL/NHLBI NIH HHS; M01RR00827/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Adrenergic beta-Antagonists; 0/Catecholamines; 0/Parasympatholytics; 51-41-2/Norepinephrine; 51-43-4/Epinephrine; 525-66-6/Propranolol; 596-51-0/Glycopyrrolate
Comments/Corrections
Comment In:
J Physiol. 2003 Jul 15;550(Pt 2):335   [PMID:  12807992 ]

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