Enhanced intestinal permeability and intestinal co-morbidities in heat strain: A review and case for autodigestion

Abstract

Enhanced intestinal permeability is a pervasive issue in modern medicine, with implications demonstrably associated with significant health consequences such as sepsis, multiorgan failure, and death. Key issues involve the trigger mechanisms that could compromise intestinal integrity and increase local permeability allowing the passage of larger, potentially dangerous molecules. Heat stress, whether exertional or environmental, may modulate intestinal permeability and begs interesting questions in the context of global climate change, increasing population vulnerabilities, and public health. Emerging evidence indicates that intestinal leakage of digestive enzymes and associated cell dysfunctions--a process referred to as autodigestion--may play a critical role in systemic physiological damage within the body. This increased permeability is exacerbated in the presence of elevated core temperatures. We employed Latent Dirichlet Allocation (LDA) topic modeling methods to analyze the relationship between heat stress and the nascent theory of autodigestion in a systematic, quantifiable, and unbiased manner. From a corpus of 11,233 scientific articles across four relevant scientific journals (Gut, Shock, Temperature, Gastroenterology), it was found that over 1,000 documents expressed a relationship between intestine, enhanced permeability, core temperature, and heat stress. The association has grown stronger in recent years, as heat stress and potential autodigestion are investigated in tandem, yet still by a limited number of specific research studies. Such findings justify the design of future studies to critically test novel interventions against digestive enzymes permeating the intestinal tract, especially the small intestine.

The increase in core body temperature in response to exertional-heat stress can predict exercise-induced gastrointestinal syndrome

“…systemic inflammatory response syndrome and multi-organ failure as a result of sepsis) [ 2 , 3 , 9 , 36 ]. Without discounting and having appreciation for the additional potential for translocation of luminal originating digestive enzymes that has been discussed in relation to endogenous tissue damage and failure [ 57 , 58 ]. It is an important aspect of professional practice to understand how core body temperature impacts key systemic inflammatory cytokines linked with clinical outcomes [ 59 ].…”

No protective benefits of low dose acute L-glutamine supplementation on small intestinal permeability, epithelial injury and bacterial translocation biomarkers in response to subclinical exertional-heat stress: A randomized cross-over trial

“…Whilst direct mortality from exertional heat stroke is largely preventable with provision of rapid (< 1 hour) whole-body cooling (DeMartini et al, 2015), many casualties experience lifelong health complications because of residual organ damage (Wallace et al, 2007). The pathophysiology of EHS has been hypothesised to be at least partially attributable to a systemic inflammatory response triggered by the translocation of pathogenic microbes from the gastrointestinal lumen into the systemic circulation (Lim, 2018;Fung et al, 2021;Walter et al, 2021). Consequently, contemporary research has focussed on evaluating the efficacy of nutritional countermeasures to support intestinal permeability, epithelial injury, and bacterial translocation in response to exertional-heat stress (Costa et al, 2020;Ogden et al, 2020a).…”