Author(s): GIBSON, O., LAITANO, O., WATANABE, K., GONZÁLEZ-ALONSO, J., Institution: BRUNEL UNIVERSITY LONDON, Country: UNITED KINGDOM, Abstract-ID: 2325

INTRODUCTION:
Hyperthermia, whether passive or exertional, can cause small intestine epithelial injury. Epithelial injury can elevate gastrointestinal permeability, facilitate endotoxin translocation and an inflammatory cytokine/chemokine response which are contributory factors in heat illness (Garcia et al., 2022). Exercise-heat stress causes epithelial injury as quantified by changes in intestinal fatty acid binding protein (iFABP) (Walter, et al., 2021a), and a greater inflammatory response relative to normothermic exercise (Garcia et al., 2022). Responses during passive hyperthermia of equivalent magnitudes to exercise-heat stress have yet to be clearly described (Walter et al., 2021b). This experiment aimed to quantify the changes in iFABP, and cytokine/chemokine responses during prolonged passive hyperthermia. It was hypothesised that passive hyperthermia would increase iFABP and cytokine/chemokine concentrations.
METHODS:
In a counterbalanced order, eight young, healthy males visited the lab on four occasions to undertake 3 h of rest (CON); 3 h of one leg heating (OLH); 3 h of two legs heating (TLH); and 2.5 h of whole-body heating (WBH). Heating was applied via a water perfused garment circulating 50°C water. Core (Tcore) and thigh muscle temperature (Tm) were measured continuously, with the concentration of iFABP and selected cytokines and chemokines (EGF, Eotaxin, FGF-2, FLT-3L, Fractalkine, G-CSF, GM-CSF, GRO, IFN-α2, IFN-γ, IL-6, IL-10, IL-12p40, MCP-3, MDC, sCD40L, TGF-α, TNFα, VEGFα) quantified periodically. Regional (Leg, arm and head) and systemic haemodynamics (cardiac output) were measured by echocardiography and Doppler ultrasound to quantify torso blood flow.
RESULTS:
Tcore and Tm increased from baseline in OLH (+0.4 ± 0.2°C, +3.4 ± 1.2°C), TLH (+0.7 ± 0.2°C, +3.4 ± 1.3°C) and WBH (+2.3 ± 0.4°C, +6.0 ± 1.7°C) respectively (p < 0.05), but were unchanged in CON. Torso blood flow increased (p < 0.05) from baseline in OLH (+0.26 ± 0.51 L.min-1), TLH (+0.47 ± 0.60 L.min-1) and WBH (+3.24 ± 1.43 L.min-1), but was also unchanged in CON. Cardiac output increased in OLH (+2.1 ± 0.6 L.min-1), TLH (+3.4 ± 0.7 L.min-1), and WBH (+7.3 ± 1.0 L.min-1) vs CON respectively (p < 0.05). Circulating iFABP, and all chemokine/cytokines were unchanged from baseline (p > 0.05) in CON, OLH, TLH or WBH.
CONCLUSION:
These data identify that iFABP and circulating cytokine and chemokine concentrations do not significantly increase during prolonged local and systemic passive heating. This finding questions the independent effect of hyperthermia on circulating markers of gastrointestinal permeability and subsequent inflammation in healthy humans.

References
Garcia, C. K., et al., (2022). Exertional heat stroke: pathophysiology and risk factors. BMJ medicine, 1(1):e000239
Walter, E., (2021a). Eur. J. Appl. Physiol., 121(4), 1179-1187
Walter, E., (2021b). Physiol. Rep., 9(16), e14945