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Heat acclimation reduces gut permeability, endotoxin translocation, and inflammatory/anti‐inflammatory cytokine cascades in humans
Author(s) -
Kuennen Matthew Ryan,
Gillum Trevor,
Christmas Kevin,
Kulovitz Michelle,
Alumbaugh Brent,
Dokladny Karol,
Schneider Suzanne
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.lb644
Subject(s) - lactulose , extracellular , intestinal permeability , acclimatization , core temperature , chemistry , significant difference , cytokine , medicine , immunology , endocrinology , zoology , biochemistry , biology , botany
Purpose To examine human gut barrier responses to a 7‐day heat acclimation (HA) protocol. Methods Five men exercised to a core temperature of 39.20 ± 0.04°C for 7 days to develop HA. Blood drawn pre (Pre) and post (Post) exercise on day 1 and day 7 of HA was assayed for endotoxin, TNF‐a, Il‐6, Il‐10, intracellular (iHSP70) and extracellular HSP70 (eHSP70). Additional measures of gut permeability (lactulose sugar test) were performed at baseline (prior to exercise/heat exposure) and on days 1 and 7 of HA. ResultsHA Day 1 HA Day 7 Pre Post Pre PostEndotoxin (pg/ml) 7.8±1.8 10.7±2.3 * 4.8±0.7 ^ 7.7±2.7 ^ Lactulose (fold Δ from baseline) ‐ 11.1±6.4 * ‐ 6.7±3.3 TNF‐a (pg/ml) 10.9±0.9 13.2±1.5 * 10.4±1.0 10.5±1.1 # Il‐6 (pg/ml) 1.3±0.4 6.8±1.7 * 1.2±0.5 2.9±0.6 * # Il‐10 (pg/ml) 7.5±2.7 20.3±5.3 * 7.5±1.5 10.5±2.4 # eHSP70 (ng/ml) 0.7±0.4 1.5±0.8 * 1.4±0.4 1.3±0.5 iHSP70/actin (pixels) 0.3±0.1 0.6±0.1 * 0.2±0.07 0.9±.04 * #Data are mean ± SE.* difference within conditions, p<.05.# difference between conditions, p<.05.^ difference between conditions, p <.07Conclusions Both direct (endotoxin) and indirect (lactulose sugar test) measures support a reduction in exercise‐induced gut permeability following the 7‐day HA protocol. Reductions in gut permeability were associated with increased exercise HSP70 accumulation and attenuated exercise cytokine responses. This may be a potential mechanism by which HA confers protection against exertional heat illness.