Document Detail


Exercise training prevents the inflammatory response to hypoxia in cremaster venules.
MedLine Citation:
PMID:  15705731     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Systemic hypoxia produces microvascular inflammation in several tissues, including skeletal muscle. Exercise training (ET) has been shown to reduce the inflammatory component of several diseases. Alternatively, ET could influence hypoxia-induced inflammation by improving tissue oxygenation or increasing mechanical antiadhesive forces at the leukocyte-endothelial interface. The effect of 5 wk of treadmill ET on hypoxia-induced microvascular inflammation was studied in the cremaster microcirculation of rats using intravital microscopy. In untrained rats, hypoxia (arterial Po(2) = 32.3 +/- 2.1 Torr) increased leukocyte-endothelial adherence from 2.3 +/- 0.4 to 10.2 +/- 0.3 leukocytes per 100 microm of venule (P < 0.05) and was accompanied by extravasation of FITC-labeled albumin after 4 h of hypoxia (extra-/intravascular fluorescence intensity ratio = 0.50 +/- 0.07). These responses were attenuated in ET (leukocyte adherence was 1.5 +/- 0.4 during normoxia and 1.8 +/- 0.7 leukocytes per 100 mum venule after 10 min of hypoxia; extra-/intravascular fluorescence intensity ratio = 0.11 +/- 0.02; P < 0.05 vs. untrained) despite similar reductions of arterial (32.4 +/- 1.8 Torr) and microvascular Po(2) (measured with an oxyphor-quenching method) in both groups. Shear rate decreased during hypoxia to similar extents in ET and untrained rats. In addition, circulating blood leukocyte count was similar in ET and untrained rats. The effects of ET on hypoxia-induced leukocyte-endothelial adherence remained up to 4 wk after discontinuing training. Thus ET attenuated hypoxia-induced inflammation despite similar effects of hypoxia on tissue Po(2), venular shear rate, and circulating leukocyte count.
Authors:
Teresa A Orth; Julie A Allen; John G Wood; Norberto C Gonzalez
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.     Date:  2005-02-10
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  98     ISSN:  8750-7587     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2005 Jun 
Date Detail:
Created Date:  2005-05-16     Completed Date:  2005-08-19     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2113-8     Citation Subset:  IM    
Affiliation:
Dept. of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS 66160, USA.
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MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological / immunology
Animals
Anoxia / complications,  immunology*
Exercise Therapy / methods*
Inflammation / etiology,  immunology*,  prevention & control*
Men
Muscle, Skeletal / blood supply,  physiopathology*
Physical Conditioning, Animal / methods*
Rats
Rats, Sprague-Dawley
Vasculitis / etiology,  immunology,  prevention & control
Venules / physiopathology*
Grant Support
ID/Acronym/Agency:
HL 39443/HL/NHLBI NIH HHS; HL 64195/HL/NHLBI NIH HHS

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


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