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

From National Research Council Canada

Download	View final version: Mild endotoxemia, NF-κB translocation, and cytokine increase during exertional heat stress in trained and untrained individuals (PDF, 1.0 MiB)
DOI	Resolve DOI: https://doi.org/10.1152/ajpregu.00917.2007
Author	Search for: Selkirk, G. A.; Search for: McLellan, T. M.; Search for: Wright, H. E.; Search for: Rhind, S. G.
Format	Text, Article
Subject	splanchnic 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	2008-08-01
Publisher	American Physical Society
In	AJP : Regulatory, Integrative and Comparative Physiology 295, no. 2: R611–R623.
Language	English
Peer reviewed	Yes
NRC publication	This is a non-NRC publication "Non-NRC publications" are publications authored by NRC employees prior to their employment by NRC.
NPARC number	23001234
Export citation	Export as RIS
Report a correction	Report a correction (opens in a new tab)
Record identifier	b0eac582-8202-4b41-94b3-64ccbd36f3b2
Record created	2017-01-09
Record modified	2020-06-02

Date modified:: 2025-01-15