Abstract

Hyperthermia and exertional heat illness increase gastrointestinal (GI) permeability, although whether the latter is only via hyperthermia is unclear. The aim of this pilot study was to determine whether different changes in GI permeability, characterized by an increased plasma lactulose:rhamnose concentration ratio ([L:R]), occurred in exercise hyperthermia in comparison to equivalent passive hyperthermia. Six healthy adult male participants (age 25 ± 5 years, mass 77.0 ± 6.7 kg, height 181 ± 6 cm, peak oxygen uptake [V·O2peak] 48 ± 8 ml.kg−1.min−1) underwent exercise under hot conditions (Ex‐Heat) and passive heating during hot water immersion (HWI). Heart rate (HR), rectal temperature (TCORE), rating of perceived exertion (RPE), and whole‐body sweat loss (WBSL) were recorded throughout the trials. The L:R ratio, peak HR, change in HR, and change in RPE were higher in Ex‐Heat than HWI, despite no differences in trial duration, peak core temperature or WBSL. L:R was strongly correlated (p < 0.05) with HR peak (r = 0.626) and change in HR (r = 0.615) but no other variable. The greater L:R in Ex‐Heat, despite equal TCORE responses to HWI, indicates that increased cardiovascular strain occurred during exercise, and exacerbates hyperthermia‐induced GI permeability at the same absolute temperature.

Highlights

  • Heat illness, whether due to exertional activity or passive heat gain, for example, in heatwaves, carries a significant risk of morbidity and mortality

  • A difference over time was identified for core body temperature (TCORE) (f = 1768.8, p < 0.001), Heart rate (HR) (f = 1375.5, p < 0.001), rating of perceived exertion (RPE) (f = 38.3, p = 0.002), thermal sensation (TS) (f = 141.8, p < 0.001), and thermal comfort (TC) (f = 489.6, p < 0.001), with no difference in gut permeability symptom scale (GPSS) (f = 4.153, p = 0.097)

  • An interaction effect was identified for HR (f = 96.6, p < 0.001) and RPE (f = 17.4, p = 0.009) only

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Summary

Introduction

Whether due to exertional activity (exertional heat illness [EHI]) or passive heat gain, for example, in heatwaves, carries a significant risk of morbidity and mortality. Hyperthermia increases GI permeability, though it remains equivocal whether this is a result of the direct effect of temperature on the intestinal epithelium, or whether competing demands for finite cardiac output increases between central and peripheral circulation creates local ischemia, which, in turn, reduces paracellular resistance to heat stress (Hall et al, 2001). Both exercise (March et al, 2017; Smetanka et al, 1999) and heat strain in vitro (Dokladny et al, 2006; Hall et al, 2001; Koch et al, 2019) damage gut wall integrity. Determining the independent and combined effects of heat stress and exercise on GI permeability may further our understanding of the pathophysiology of EHI, in particular, the subsequent endotoxemia and inflammatory response, which may support the development of preventative and/ or therapeutic interventions

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