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dc.contributor.authorHughes, Michael G.
dc.contributor.authorPotter, Stephen
dc.contributor.authorSims, Craig
dc.contributor.authorButcher, Lee
dc.contributor.authorDavies, Nia
dc.contributor.authorVerheggen, Kenneth
dc.contributor.authorJones, Ken
dc.contributor.authorThomas, Andrew
dc.contributor.authorWebb, Richard
dc.date.accessioned2013-05-28T12:21:02Z
dc.date.available2013-05-28T12:21:02Z
dc.date.issued2010
dc.identifier.citationMoir, H., Hughes, M.G., Potter, S., Sims, C., Butcher, L.R., Davies, N.A., Verheggen, K., Jones, K.P., Thomas, A.W. and Webb, R. (2010) 'Exercise-induced immunosuppression: roles of reactive oxygen species and 5′-AMP-activated protein kinase dephosphorylation within immune cells', Journal of Applied Physiology, 108(5), pp.1284-1292.en_US
dc.identifier.issn8750-7587
dc.identifier.urihttp://hdl.handle.net/10369/4109
dc.description.abstractWe previously proposed 5′-AMP-activated protein kinase (AMPK) dephosphorylation within immune cells as an intracellular mechanism linking exercise and immunosuppression. In this study, AMPK phosphorylation underwent transient (<1 h) decreases (53.8 ± 7.2% basal) immediately after exercise (45 min of cycling at 70% VO2max) in a cohort of 16 adult male participants. Similar effects were seen with running. However, because exercise-induced inactivation of AMPK was previously shown to occur in an AMP-independent manner, the means by which AMPK is inactivated in this context is not yet clear. To investigate the hypothesis that exercise-induced inactivation of AMPK is mediated via signaling mechanisms distinct from changes in cellular AMP-to-ATP ratios, reactive oxygen species (ROS) and intracellular Ca2+ signaling were investigated in mononuclear cells before and after exercise and in cultured monocytic MM6 cells. In in vitro studies, treatment with an antioxidant (ascorbic acid, 4 h, 50 μM) decreased MM6 cell intracellular ROS levels (88.0 ± 5.2% basal) and induced dephosphorylation of AMPK (44.7 ± 17.6% basal). By analogy, the fact that exercise decreased mononuclear cell ROS content (32.8 ± 16.6% basal), possibly due to downregulation (43.4 ± 8.0% basal) of mRNA for NOX2, the catalytic subunit of the cytoplasmic ROS-generating enzyme NADPH oxidase, may provide an explanation for the AMPK-dephosphorylating effect of exercise. In contrast, exercise-induced Ca2+ signaling events did not seem to be coupled to changes in AMPK activity. Thus we propose that the exercise-induced decreases in both intracellular ROS and AMPK phosphorylation seen in this study constitute evidence supporting a role for ROS in controlling AMPK, and hence immune function, in the context of exercise-induced immunosuppression.
dc.language.isoenen_US
dc.publisherAmerican Physiological Society
dc.relation.ispartofseriesJournal of Applied Physiology
dc.titleExercise-induced immunosuppression: roles of reactive oxygen species and 5-AMP-activated protein kinase dephosphorylation within immune cellsen_US
dc.typeArticleen_US
dc.identifier.doihttp://dx.doi.org/10.1152/japplphysiol.00737.2009


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