Pathophysiology of exertional heat illness in the Thoroughbred racehorse: Broadening perspective to include an exercise-induced gastrointestinal syndrome in which endotoxaemia and systemic inflammation may contribute to the condition

Abstract

The traditional approach to exertional heat illness (EHI) is based on the premise that external heat is the trigger and sole driver of the condition. During the last few decades, many researchers have suggested that climatic heat alone does not fully explain the pathophysiology of EHI, and a second pathway has been proposed which focuses on the gastrointestinal tract (GIT). The causal agent of EHI in Thoroughbred racehorses is the strenuous exercise of racing. The generation of metabolic heat is prodigious and can cause direct injury to the GIT. The associated redistribution of cardiac output to working muscles is most likely to subject the GIT to substantial hypo-perfusion and if horses race under hot/humid conditions impairing thermoregulation this may exacerbate intestinal hyperthermia. Evidence in human athletes shows that the combination of intestinal hyperthermia and reduced blood flow causes a breakdown in the integrity of the mucosal barrier and leads to increased intestinal permeability, allowing leakage of endotoxin into the central circulation. Normally, protective immune mechanisms clear elevated endotoxin levels, but if there is immune dysfunction and the concentration of endotoxin exceeds a certain threshold, a systemic inflammatory response triggers a cytokine cascade with serious downstream consequences. It is argued that the cytokine inflammatory cascade, rather than core body hyperthermia contributes to the clinical progression of EHI when endotoxaemia is dominant. The authors have presented the current state of knowledge for human subjects and cited studies in racehorses which suggest its relevance. Acknowledgement of the gastrointestinal inflammatory pathway for EHI is important because it provides track veterinarians with a different perspective on prevention and treatment.