INTRODUCTION: Evidence supports an interaction between neuro-endocrine responses to exercise and immune responses to exercise. We hypothesized that prolonged exercise in the heat would evoke a greater stress hormone response and a greater decrease in neutrophil degranulation [lipopolysaccharide (LPS)-stimulated elastase release] than when the same exercise was performed in thermoneutral conditions.

METHODS: In counterbalanced order and separated by 7 d, 13 male cyclists cycled for 2 h at 62 +/- 3% VO2max (mean +/- SEM), with ad libitum water intake, on one occasion with heat (HOT: 30.3 degrees C, 76% RH) and on another occasion without (

CONTROL: 20.4 degrees C, 60% RH). Venous blood samples were collected at pre-, post-, and 2 h post-exercise.

RESULTS: Exercising HR, rating of perceived exertion, rectal temperature, corrected body mass loss, and plasma cortisol at post- and 2 h post-exercise were greater during HOT. A marked neutrophilia was evident at post- and 2 h post-exercise with no difference between trials. LPS-stimulated elastase release per neutrophil decreased post-exercise with no difference between trials (pre-exercise: HOT 189 +/- 20 and CONTROL 210 +/- 32; post-exercise: HOT 127 +/- 18 and CONTROL 136 +/- 29 fg x cell(-1)). There was no effect of exercise or trial on neutrophil CD11b expression (neutrophil activation index) or band cell percentage (neutrophil maturity index).

CONCLUSIONS: Prolonged exercise results in a decrease in neutrophil degranulation that is unaffected by performing the exercise in hot conditions despite the increase in physiological stress. Additionally, these data suggest that the decrease in neutrophil degranulation after prolonged exercise is not associated with a change in neutrophil activation or maturity as previously suggested.