Figure 7.

There are two proposed pathophysiological pathways for EHI. The strenuous exercise of racing produces a large amount of metabolic heat, most of which is stored, resulting in hyperthermia. If an individual’s ability to thermoregulate is impaired by high levels of heat and humidity, hyperthermia may reach critical levels. This can trigger the heat toxicity pathway, potentially leading to heat stroke with multi-organ failure. Strenuous exercise also causes a redistribution of cardiac output. Heat and intestinal hypoperfusion combine to cause impairment of the intestinal mucosal barrier, allowing leakage of endotoxin into the central circulation. Limitation of this endotoxemic or ‘heat sepsis’ pathway is dependent on the host’s immune system, which if functioning normally can deactivate endotoxin. If this does not occur, endotoxin can reach a critical level and may activate the systemic inflammatory response syndrome (SIRS), stimulating the production of cytokines, which might actually drive the condition and are thought to mediate many of the adverse consequences of the EHI/HS syndrome.