3.8 Article

Effects of oat β-glucan on innate immunity and infection after exercise stress

Journal

MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
Volume 36, Issue 8, Pages 1321-1327

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1249/01.MSS.0000135790.68893.6D

Keywords

macrophage; nutrition; natural killer cell; HSV-1; morbidity; mortality

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Exhaustive exercise has been associated with an increased risk for URTI. Oat beta-glucan is a mild immune system enhancer and may offset immune suppression associated with exercise stress. Purpose: To test the effects of oat beta-glucan (ObetaG) on respiratory infection, macrophage antiviral resistance, and NK cytotoxicity. Methods: Mice were randomly assigned to one of four groups: Ex-H2O, Ex-ObetaG, Con-H2O, or Con-ObetaG. ObetaG was fed in the drinking water for 10 d before intranasal inoculation of HSV-1 or sacrifice. Exercise consisted of treadmill running to volitional fatigue (similar to140 min) for three consecutive days. Fifteen minutes after the last bout of exercise or rest, mice (N = 24) were intranasally inoculated with a standardized dose of HSV-1. Mice were monitored twice daily for morbidity and mortality. Additional mice were sacrificed after exercise, peritoneal macrophages were obtained via i.p. lavage and assayed for antiviral resistance to HSV-1 (N = 18), and spleens were harvested and assayed for NK cell cytotoxicity (N = 12). Results: Exercise stress was associated with a 28% increase in morbidity (P = 0.036) and 18% increase in mortality (P = 0.15). Ingestion of ObetaG before infection prevented this increase in morbidity (P = 0.048) and mortality (P = 0.05). Exercise stress was associated with a decrease in macrophage antiviral resistance (P = 0.007), which was blocked by ingestion of ObetaG (P < 0.001). There were no effects of exercise or ObetaG on NK cytotoxicity. Conclusion: These data suggest that daily ingestion of ObetaG may offset the increased risk of URTI associated with exercise stress, which may be mediated, at least in part, by an increase in macrophage antiviral resistance.

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