Abstract
Reduced splanchnic blood flow and hyperthermia during exercise-heat stress can produce gastrointestinal barrier dysfunction and increased gastrointestinal permeability. This may allow endotoxin to enter the internal environment, causing local and systemic immune responses. These responses may be involved in the cause and outcome of exertional heatstroke. Countermeasures may reduce gastrointestinal permeability and possibly exertional heatstroke occurrence and outcome.