Abstract
Exertional heat stroke (EHS) is a life-threatening medical condition involving thermoregulatory failure and is the most severe condition along a continuum of heat-related illnesses. Current EHS policy guidance principally advocates a thermoregulatory management approach, despite growing recognition that gastrointestinal (GI) microbial translocation contributes to disease pathophysiology. Contemporary research has focused to understand the relevance of GI barrier integrity and strategies to maintain it during periods of exertional-heat stress. GI barrier integrity can be assessed non-invasively using a variety of in vivo techniques, including active inert mixed-weight molecular probe recovery tests and passive biomarkers indicative of GI structural integrity loss or microbial translocation. Strenuous exercise is strongly characterised to disrupt GI barrier integrity, and aspects of this response correlate with the corresponding magnitude of thermal strain. The aetiology of GI barrier integrity loss following exertional-heat stress is poorly understood, though may directly relate to localised hyperthermia, splanchnic hypoperfusion-mediated ischemic injury, and neuroendocrine-immune alterations. Nutritional countermeasures to maintain GI barrier integrity following exertional-heat stress provide a promising approach to mitigate EHS. The focus of this review is to evaluate: (1) the GI paradigm of exertional heat stroke; (2) techniques to assess GI barrier integrity; (3) typical GI barrier integrity responses to exertional-heat stress; (4) the aetiology of GI barrier integrity loss following exertional-heat stress; and (5) nutritional countermeasures to maintain GI barrier integrity in response to exertional-heat stress.
Highlights
Exertional heat stroke (EHS) is a life-threatening medical condition involving total thermoregulatory failure, which is the most severe condition along a continuum of heat-related illnesses [1]
Once hyperthermia was above the intensity to evoke heat cytotoxicity, mortality rates were 100% irrespective of pharmaceutical intervention. These findings suggest the GI EHS paradigm to be most relevant in cases when Tcore remains below ~42–43 ◦ C [48]
EHS cases, pro-inflammatory cytokines are produced upon immune activation following binding between microbial translocation (MT) products and toll-like receptors located on cell surface membranes [178]
Summary
Exertional heat stroke (EHS) is a life-threatening medical condition involving total thermoregulatory failure, which is the most severe condition along a continuum of heat-related illnesses [1]. The most popular definitions broadly outline characteristic patient symptoms at time of clinical admission [5] These principally include: (1) a core body temperature (Tcore ) above 40 ◦ C; (2) severe central nervous system disturbance (e.g., delirium, seizures, coma); and (3) multiple organ injury. In consideration of these issues, numerous consensus documents have been published that provide occupational guidance on effective EHS management (e.g., [32,33,34,35]), though predominately take a thermoregulatory approach to disease management (e.g., cooling, heat acclimation). The GI tract is largely effective in preventing GI microbial translocation (MT) into the systemic circulation [40], growing evidence hypothesises a fundamental role of GI MT within the pathophysiology of EHS [36,37]. The aetiology of GI barrier integrity loss; and (5) nutritional countermeasures to support GI barrier integrity during exertional-heat stress
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