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Updated: Mar 7, 2026

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Differential Intestinal Epithelial Injury Following Passive and Exertional Hyperthermia.

Sharifah Badriyah Alhadad1,2,3, Louisa Si Xian Lim1,2, Jason Kai Wei Lee1,2,3

  • 1Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Block MD9, 2 Medical Drive Level 4, Singapore, 117593, Singapore.

Sports Medicine - Open
|March 6, 2026
PubMed
Summary
This summary is machine-generated.

Exertional hyperthermia, not passive, caused intestinal injury in athletes. This suggests combined thermal, metabolic, and mechanical stress, not just high body temperature, drives gastrointestinal damage.

Keywords:
Core temperatureExertional heat strokeGastrointestinal injuryHeat stressIntestinal fatty acid binding protein

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Area of Science:

  • Exercise Physiology
  • Gastrointestinal Physiology
  • Environmental Physiology

Background:

  • Passive and exertional hyperthermia can impair gastrointestinal (GI) integrity, leading to systemic issues and heat stroke.
  • Intestinal epithelial injury, a key early event, is influenced by thermal, metabolic, and mechanical stressors.
  • This study differentiates the effects of passive (PaH) versus exertional hyperthermia (RUN) on GI injury.

Purpose of the Study:

  • To compare the impact of passive hyperthermia (PaH) and exertional hyperthermia (RUN) on intestinal epithelial injury and endotoxin translocation.
  • To determine the relative contributions of thermal, metabolic, and mechanical stress to GI injury.
  • To explore the effects of prolonged low-intensity exercise (WALK) on GI integrity.

Main Methods:

  • 15 male endurance athletes underwent randomized, counterbalanced conditions: PaH (warm water immersion), WALK (prolonged walking), and RUN (treadmill running).
  • All conditions aimed for a peak core body temperature (Tc) of 39.5°C, volitional exhaustion, or 60 minutes.
  • Measurements included Tc, heart rate, perceptual responses, and concentrations of intestinal fatty acid binding protein (IFABP) and lipopolysaccharides (LPS).

Main Results:

  • Peak Tc was similar between PaH and RUN, but lower in WALK. Cumulative heat load was similar between WALK and RUN, but lower in PaH.
  • Intestinal fatty acid binding protein (IFABP) increased significantly following RUN and WALK, but not PaH.
  • Post-condition IFABP was higher in RUN compared to PaH and WALK. LPS decreased across all conditions.

Conclusions:

  • Exertional hyperthermia, not passive, induced intestinal epithelial injury at matched peak core temperatures.
  • Combined thermal, metabolic, and mechanical stresses, rather than elevated Tc alone, drive GI injury.
  • Prolonged exercise may cause subclinical intestinal injury, necessitating management of exertional load alongside thermal strain.