An increasing body of data suggest that strenuous exercise triggers an
inflammatory response having some similarity with those occurring in
sepsis. Indices of this inflammatory response to exercise (IRE) especi
ally include leukocytosis, release of inflammatory mediators and acute
phase reactants, tissue damage, priming of various white blood cell l
ines, production of free radicals; activation of complement, coagulati
on and fibrinolytic cascades. Inflammatory responses to strenuous exer
cise and sepsis could in part be due to the release of endotoxin in bl
ood as common triggering factor, but it seems that tissue damage and/o
r contact system activation are more important triggering mechanisms i
n exercising subjects. While the magnitude and duration of cellular an
d humoral changes associated with IRE are quite different from those o
bserved in sepsis, recent human studies suggested that chronic and/or
excessive IRE could have adverse effects. Among the possible consequen
ces of acute and chronic IRE are delayed onset muscular soreness and l
oss of force, cardiovascular complications, intravascular hemolysis, h
ypoferraemia and increased susceptibility to infection.