Abstract
Elevated antigen-stimulated anti-inflammatory cytokine production appears to be a risk factor for upper respiratory tract illness in athletes. The purpose of this study was to determine the effects of prolonged exercise and hydration on antigen-stimulated cytokine production. Twelve healthy males cycled for 120 min at 60% on two occasions, either euhydrated or moderately hypohydrated (induced by fluid restriction for 24 h). Blood samples were collected before and after exercise and following 2 h recovery for determination of cell counts, plasma cortisol, and in vitro antigen-stimulated cytokine production by whole blood culture. Fluid restriction resulted in mean body mass loss of 1.3% and 3.9% before and after exercise, respectively. Exercise elicited a significant leukocytosis and elevated plasma cortisol, with no differences between trials. IL-6 production was significantly reduced 2 h postexercise (P < 0.05), while IL-10 production was elevated postexercise (P < 0.05). IFN-γ and IL-2 production tended to decrease postexercise. No significant effect of hydration status was observed for the measured variables. Prolonged exercise appears to result in augmented anti-inflammatory cytokine release in response to antigen challenge, possibly coupled with acute suppression of proinflammatory cytokine production, corresponding with studies using mitogen or endotoxin as stimulant. Moderate hypohydration does not appear to influence these changes.
Highlights
Prolonged, strenuous exercise has been associated with a temporal depression of host defence, increasing susceptibility to opportunistic infections [1, 2]
Compared to baseline euhydrated body mass, fluid restriction in the dehydrated trial (DH) trial resulted in body mass loss of 1.3 ± 0.7%
Urine osmolality decreased following exercise and was significantly (P < 0.01) higher in DH compared to euhydrated trial (EU) at both time points
Summary
Strenuous exercise has been associated with a temporal depression of host defence, increasing susceptibility to opportunistic infections [1, 2]. Almost certainly, this immunosuppression is multifactorial in origin [3, 4]. Reductions in salivary immunoglobulin A secretion [5,6,7], natural killer cell activity [8], lymphocyte proliferative response [5, 9], and impaired neutrophil phagocytic function [10] following prolonged exercise have been suggested as some of the possible mechanisms and likely explain, at least in part, why elite endurance athletes appear prone to upper respiratory tract infections [11]. Changes in the profile of cytokine production after acute or chronic exercise may influence infection risk and/or the severity and duration of illness symptoms
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