Abstract
Heat stroke (HS) is an ancient illness dating back more than 2000 years and continues to be a health threat and to cause fatality during physical exertion, especially in military personnel, fire-fighters, athletes, and outdoor laborers. The current paradigm in the pathophysiology and prevention of HS focuses predominantly on heat as the primary trigger and driver of HS, which has not changed significantly for centuries. However, pathological and clinical reports from HS victims and research evidence from animal and human studies support the notion that heat alone does not fully explain the pathophysiology of HS and that HS may also be triggered and driven by heat- and exercise-induced endotoxemia. Exposure to heat and exercise stresses independently promote the translocation of lipopolysaccharides (LPS) from gram-negative bacteria in the gut to blood in the circulatory system. Blood concentration of LPS can increase to a threshold that triggers the systemic inflammatory response, leading to the downstream ramifications of cellular and organ damage with sepsis as the end point i.e., heat sepsis. The dual pathway model (DPM) of HS proposed that HS is triggered by two independent pathways sequentially along the core temperature continuum of >40 °C. HS is triggered by heat sepsis at Tc < 42 °C and by the heat toxicity at Tc > 42 °C, where the direct effects of heat alone can cause cellular and organ damage. Therefore, heat sepsis precedes heat toxicity in the pathophysiology of HS.
Highlights
Heat stroke (HS) is the fatal form of heat injury that dates back more than 2000 years
These results suggest that bovine colostrum may offer protection against heat sepsis by contributing to LPS removal during exercise and heat exposure
These results suggest that the endocrine system may play important roles in protecting the major organs from the effects of heat sepsis and toxicity after the onset of HS
Summary
Heat stroke (HS) is the fatal form of heat injury that dates back more than 2000 years. Public health institutions and consensus statements from professional organizations such as the American College of Sports Medicine [24] and the National Athlete Trainer Association [25] promote a heat-centered approach to prevent HS These preventive measures are centered on avoiding a high body temperature during physical exertion by performing physical work within a permissible environmental temperature, including adequate fluid intake, wearing breathable clothing, and undergoing heat acclimatization [21,22,24,25]. The rectal temperature of runners measured at intervals and at the end of marathon races reached 41.1 to 41.9 ◦ C without any symptoms of heat injury [41,42] These data indicate that having a high Tc alone, up to about 42 ◦ C, is physiologically tolerable and is not predictive of HS in trained and healthy individuals. This review will use the term “heat stroke” to refer to HS in general without differentiating between the forms of HS
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