GUT MICROBIOTA ADAPTATIONS DURING ISOTHERMIC HEAT ACCLIMATISATION: IMPLICATIONS ON INTESTINAL BARRIER FUNCTION FOLLOWING EXERTIONAL HEAT STRESS

Author(s): NG, N., MICHIKO, N., MANI, R., CHEN, C., MOHAMED, C., LEE, J., LOW, I. , Institution: NATIONAL UNIVERSITY OF SINGAPORE, Country: SINGAPORE, Abstract-ID: 2183

INTRODUCTION:
Isothermal clamping (ITC) based heat acclimatisation maintains a target core temperature during each session and is considered more effective in improving heat tolerance than conventional fixed intensity or duration protocols. Reductions in splanchnic blood flow during exertional heat stress may disrupt the intestinal barrier, allowing microbial products to enter circulation and trigger systemic inflammation, multi-organ failure and potentially death. As the gut microbiota produces metabolites that promote intestinal epithelial function, we profiled gut microbiota changes during ITC to determine if microbiota adaptations were associated with reduced intestinal barrier perturbation following exertional heat stress.
METHODS:
22 participants completed a PRE heat response test (HRT), 10 sessions of training (ITC or control (CON)), followed by a POST HRT. HRT involved a 65-min treadmill walk at 50-70% VO2max (Tdb: 34.1+/-0.1 deg C, RH: 69+/-2%). Blood samples were collected before (BEF) and after (AFT) each HRT to assess markers of intestinal barrier perturbation (Claudin-3 (CLDN3), intestinal fatty acid-binding protein (I-FABP) and lipopolysaccharide-binding protein (LBP)). Participants in ITC (n=10, age: 25+/-5 years, VO2max: 45+/-6 ml/kg/min) performed walk-run cycles to maintain core temperature above 38.5 deg C for 30 min in each training session, while those in CON (n=12, age: 24+/-3 years, VO2max: 44+/-4 ml/kg/min) completed four sets of calisthenic exercises. Seven fecal samples were collected at weekly intervals during the study to profile gut microbiota composition through 16S rRNA sequencing.
RESULTS:
Preliminary results showed that markers of intestinal barrier perturbation did not differ between ITC and CON. BEF-AFT fold-change in CLDN-3 was similar between groups in PRE (ITC: 1.1+/-0.1; CON: 1.2+/-0.2) and POST HRT (ITC: 1.1+/-0.1; CON: 1.2+/-0.2) (p=0.09). Likewise, LBP fold-change did not differ between ITC and CON in PRE (ITC: 1.1+/-0.2; CON: 1.1+/-0.1) and POST HRT (ITC: 1.1+/-0.1; CON: 1.2+/-0.1) (p=0.11). I-FABP fold-change in ITC and CON was also comparable between PRE (ITC: 3.2+/-1.5; CON: 2.9+/-1.9) and POST HRT (ITC: 3.6+/-2.6; CON: 2.9+/-2.2) (p=0.98). Gut microbiota composition did not differ over time between ITC and CON at the phylum or genus level (all p>0.05).
CONCLUSION:
As intestinal barrier perturbation did not differ between ITC and CON at PRE and POST HRT, and gut microbiota composition did not show group-specific changes over time, these results suggest that ITC alone may be insufficient to promote beneficial gut microbiota changes to attenuate intestinal barrier perturbation during exertional heat stress. Hence, combining ITC with nutritional supplementation may be necessary to achieve both thermoregulatory adaptations and enhanced intestinal barrier integrity to mitigate microbial translocation and downstream inflammatory responses during exertional heat stress.