Antioxidants attenuate the plasma cytokine response to exercise in humans

Antioxidants attenuate the plasma cytokine response to exercise in humans Abstract Exercise increases plasma TNF-α, IL-1β, and IL-6, yet the stimuli and sources of TNF-α and IL-1β remain largely unknown. We tested the role of oxidative stress and the potential contribution of monocytes in this cytokine (especially IL-1β) response in previously untrained individuals. Six healthy nonathletes performed two 45-min bicycle exercise sessions at 70% ofV˙ o 2 max before and after a combination of antioxidants (vitamins E, A, and C for 60 days; allopurinol for 15 days; and N -acetylcysteine for 3 days). Blood was drawn at baseline, end-exercise, and 30 and 120 min postexercise. Plasma cytokines were determined by ELISA and monocyte intracellular cytokine level by flow cytometry. Before antioxidants, TNF-α increased by 60%, IL-1β by threefold, and IL-6 by sixfold secondary to exercise ( P < 0.05). After antioxidants, plasma IL-1β became undetectable, the TNF-α response to exercise was abolished, and the IL-6 response was significantly blunted ( P < 0.05). Exercise did not increase the percentage of monocytes producing the cytokines or their mean fluorescence intensity. We conclude that in untrained humans oxidative stress is a major stimulus for exercise-induced cytokine production and that monocytes play no role in this process. interleukins flow cytometry oxidative stress ergometry vitamins Footnotes This work was supported by the THORAX Foundation, Athens, Greece. T. Vassilakopoulos was a recipient of a Fellowship from Propondis Foundation. Present address for T. Vassilakopoulos: Critical Care Division, Royal Victoria Hospital, McGill University, 687 Pine Avenue West, Montreal, Canada H3A1A1. Address for reprint requests and other correspondence: T. Vassilakopoulos, Critical Care Dept., Evangelismos Hospital, 45-47 Ipsilandou St., GR-10675 Athens, Greece (E-mail: tvassilakopoulos@yahoo.com ). The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. First published November 27, 2002;10.1152/japplphysiol.00735.2002 Copyright © 2003 the American Physiological Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Applied Physiology The American Physiological Society

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Publisher
The American Physiological Society
Copyright
Copyright © 2011 the American Physiological Society
ISSN
8750-7587
eISSN
1522-1601
D.O.I.
10.1152/japplphysiol.00735.2002
Publisher site
See Article on Publisher Site

Abstract

Abstract Exercise increases plasma TNF-α, IL-1β, and IL-6, yet the stimuli and sources of TNF-α and IL-1β remain largely unknown. We tested the role of oxidative stress and the potential contribution of monocytes in this cytokine (especially IL-1β) response in previously untrained individuals. Six healthy nonathletes performed two 45-min bicycle exercise sessions at 70% ofV˙ o 2 max before and after a combination of antioxidants (vitamins E, A, and C for 60 days; allopurinol for 15 days; and N -acetylcysteine for 3 days). Blood was drawn at baseline, end-exercise, and 30 and 120 min postexercise. Plasma cytokines were determined by ELISA and monocyte intracellular cytokine level by flow cytometry. Before antioxidants, TNF-α increased by 60%, IL-1β by threefold, and IL-6 by sixfold secondary to exercise ( P < 0.05). After antioxidants, plasma IL-1β became undetectable, the TNF-α response to exercise was abolished, and the IL-6 response was significantly blunted ( P < 0.05). Exercise did not increase the percentage of monocytes producing the cytokines or their mean fluorescence intensity. We conclude that in untrained humans oxidative stress is a major stimulus for exercise-induced cytokine production and that monocytes play no role in this process. interleukins flow cytometry oxidative stress ergometry vitamins Footnotes This work was supported by the THORAX Foundation, Athens, Greece. T. Vassilakopoulos was a recipient of a Fellowship from Propondis Foundation. Present address for T. Vassilakopoulos: Critical Care Division, Royal Victoria Hospital, McGill University, 687 Pine Avenue West, Montreal, Canada H3A1A1. Address for reprint requests and other correspondence: T. Vassilakopoulos, Critical Care Dept., Evangelismos Hospital, 45-47 Ipsilandou St., GR-10675 Athens, Greece (E-mail: tvassilakopoulos@yahoo.com ). The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. First published November 27, 2002;10.1152/japplphysiol.00735.2002 Copyright © 2003 the American Physiological Society

Journal

Journal of Applied PhysiologyThe American Physiological Society

Published: Mar 1, 2003

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