Mild endotoxemia, NF-κB translocation, and cytokine increase during exertional heat stress in trained and untrained individuals

From National Research Council Canada

Download
  1. (PDF, 851 KB)
DOIResolve DOI: http://doi.org/10.1152/ajpregu.00917.2007
AuthorSearch for: ; Search for: ; Search for: ; Search for:
TypeArticle
Journal titleAJP : Regulatory, Integrative and Comparative Physiology
ISSN0363-6119
1522-1490
Volume295
Issue2
PagesR611–R623
Subjectsplanchnic permeability; immune function; blood volume; cardiovascular/thermoregulatory strain; flow cytometry
Abstract
This study examined endotoxin-mediated cytokinemia during exertional heat stress (EHS). Subjects were divided into trained [TR; n=12, peak aerobic power (VO2peak)=70+/-2 ml.kg lean body mass(-1).min(-1)] and untrained (UT; n=11, VO2peak=50+/-1 ml.kg lean body mass(-1).min(-1)) groups before walking at 4.5 km/h with 2% elevation in a climatic chamber (40 degrees C, 30% relative humidity) wearing protective clothing until exhaustion (Exh). Venous blood samples at baseline and 0.5 degrees C rectal temperature increments (38.0, 38.5, 39.0, 39.5, and 40.0 degrees C/Exh) were analyzed for endotoxin, lipopolysaccharide binding protein, circulating cytokines, and intranuclear NF-kappaB translocation. Baseline and Exh samples were also stimulated with LPS (100 ng/ml) and cultured in vitro in a 37 degrees C water bath for 30 min. Phenotypic determination of natural killer cell frequency was also determined. Enhanced blood (104+/-6 vs. 84+/-3 ml/kg) and plasma volumes (64+/-4 vs. 51+/-2 ml/kg) were observed in TR compared with UT subjects. EHS produced an increased concentration of circulating endotoxin in both TR (8+/-2 pg/ml) and UT subjects (15+/-3 pg/ml) (range: not detected to 32 pg/ml), corresponding with NF-kappaB translocation and cytokine increases in both groups. In addition, circulating levels of tumor necrosis factor-alpha and IL-6 were also elevated combined with concomitant increases in IL-1 receptor antagonist in both groups and IL-10 in TR subjects only. Findings suggest that the threshold for endotoxin leakage and inflammatory activation during EHS occurs at a lower temperature in UT compared with TR subjects and support the endotoxin translocation hypothesis of exertional heat stroke, linking endotoxin tolerance and heat tolerance.
Publication date
PublisherAmerican Physical Society
LanguageEnglish
Peer reviewedYes
NRC publication
This is a non-NRC publication

"Non-NRC publications" are publications authored by NRC employees prior to their employment by NRC.

NPARC number23001234
Export citationExport as RIS
Report a correctionReport a correction
Record identifierb0eac582-8202-4b41-94b3-64ccbd36f3b2
Record created2017-01-09
Record modified2017-01-09
Date modified:
Report a problem on this page