Document Detail


Central integration of mechanisms in exercise hyperpnea.
MedLine Citation:
PMID:  8183096     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Many hypotheses have been advanced to explain the hyperpnea of exercise and its close relations to the level of metabolic work, expressed as oxygen uptake (VO2) and carbon dioxide production (VCO2). Evidence is presented that a neural central command mechanism from the hypothalamus is important in the driving of both respiration and circulatory adjustments during locomotion or exercise, and that short-term potentiation of neurons in the medulla makes an important contribution. Both are probably augmented by receptors in working muscle and by the effects of increased [K+] acting on the carotid bodies. Feedback from "respiratory" mechanisms, including CO2 and O2 mediated mechanisms and inputs from the lungs, are important in stabilizing ventilation at the level primarily dictated by the major neural mechanisms.
Authors:
F L Eldridge
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Medicine and science in sports and exercise     Volume:  26     ISSN:  0195-9131     ISO Abbreviation:  Med Sci Sports Exerc     Publication Date:  1994 Mar 
Date Detail:
Created Date:  1994-06-15     Completed Date:  1994-06-15     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8005433     Medline TA:  Med Sci Sports Exerc     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  319-27     Citation Subset:  IM; S    
Affiliation:
Department of Medicine, University of North Carolina, Chapel Hill 27599.
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MeSH Terms
Descriptor/Qualifier:
Animals
Exercise / physiology*
Feedback / physiology
Humans
Hypothalamus / physiology*
Neuronal Plasticity / physiology
Respiration / physiology*
Grant Support
ID/Acronym/Agency:
HL-17689/HL/NHLBI NIH HHS

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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