Show simple item record

dc.contributor.authorMoir, Hannah
dc.contributor.authorButcher, Lee
dc.contributor.authorJones, Ken
dc.contributor.authorHughes, Michael G.
dc.contributor.authorNeale, Huw
dc.contributor.authorJia, Huidong
dc.contributor.authorAl-Ismaily, Zuleikha
dc.contributor.authorWebb, Richard
dc.date.accessioned2013-05-28T13:51:20Z
dc.date.available2013-05-28T13:51:20Z
dc.date.issued2008
dc.identifier.citationApplied Physiology, Nutrition and Metabolism, 33(1):75-85.en_US
dc.identifier.issn1715-5312
dc.identifier.urihttp://hdl.handle.net/10369/4114
dc.description.abstractThere is much evidence that prolonged intense exercise suppresses the immune system. However, the intracellular biochemical mechanisms linking exercise and immunosuppression remain obscure. The purpose of this study was to investigate the hypothesis that exercise-induced inactivation of 5’AMP-activated protein kinase (AMPK) disrupts individual immune cell function, and thus may be linked to exercise-induced immunosuppression. To confirm AMPK’s role in immune cells, AMPK activity was assessed in cultured monocytic Mono Mac 6 (MM6) cells. The effects of single bouts of intense exercise (45 min cycling; 70% VO2 max) on several immune parameters including mononuclear cell AMPK phosphorylation were investigated in 10 male volunteers. In vitro, the mitochondrial ATP synthase inhibitor oligomycin brought about transient decreases in cellular [ATP] (0.41 ± 0.04 pmol/cell to 0.31 ± 0.02 pmol/cell), and activation of AMPKa1 (170.7% ± 31.2% basal) and the glycolytic enzyme inducible phosphofructokinase 2 (iPFK-2) (225.0% ± 46.1% basal), with the latter effects coinciding with recovery from ATP depletion. In contrast, exercise-induced transient (~1 h) decreases in AMPKa1 phosphorylation (64.4% ± 17.6% basal). This AMPK inactivation coincided with comparable transient decreases in other immune parameters (salivary IgA levels, serum cytokine levels, monocyte CD36 expression). Although the brief exercise bout employed here is not sufficient to cause full-fledged immunosuppression, exerciseinduced transient decreases in mononuclear cell AMPK activation (as seen in this study) may cause energy depletion within individual immune cells, and therefore have an impact upon their ability to carry out their functions. Thus, we suggest that prolonged, repeated, high-intensity exercise that leads to clinically relevant immunosuppression may do so via AMPK inactivation within immune cells.en_GB
dc.description.abstractThere is much evidence that prolonged intense exercise suppresses the immune system. However, the intracellular biochemical mechanisms linking exercise and immunosuppression remain obscure. The purpose of this study was to investigate the hypothesis that exercise-induced inactivation of 5′AMP-activated protein kinase (AMPK) disrupts individual immune cell function, and thus may be linked to exercise-induced immunosuppression. To confirm AMPK’s role in immune cells, AMPK activity was assessed in cultured monocytic Mono Mac 6 (MM6) cells. The effects of single bouts of intense exercise (45 min cycling; 70% VO2 max) on several immune parameters including mononuclear cell AMPK phosphorylation were investigated in 10 male volunteers. In vitro, the mitochondrial ATP synthase inhibitor oligomycin brought about transient decreases in cellular [ATP] (0.41 ± 0.04 pmol/cell to 0.31 ± 0.02 pmol/cell), and activation of AMPKα1 (170.7% ± 31.2% basal) and the glycolytic enzyme inducible phosphofructokinase 2 (iPFK-2) (225.0% ± 46.1% basal), with the latter effects coinciding with recovery from ATP depletion. In contrast, exercise-induced transient (~1 h) decreases in AMPKα1 phosphorylation (64.4% ± 17.6% basal). This AMPK inactivation coincided with comparable transient decreases in other immune parameters (salivary IgA levels, serum cytokine levels, monocyte CD36 expression). Although the brief exercise bout employed here is not sufficient to cause full-fledged immunosuppression, exercise-induced transient decreases in mononuclear cell AMPK activation (as seen in this study) may cause energy depletion within individual immune cells, and therefore have an impact upon their ability to carry out their functions. Thus, we suggest that prolonged, repeated, high-intensity exercise that leads to clinically relevant immunosuppression may do so via AMPK inactivation within immune cells.
dc.language.isoenen_US
dc.publisherNRC Research Press
dc.relation.ispartofseriesApplied Physiology, Nutrition and Metabolism;
dc.subjectAMPKen_GB
dc.subjectimmunosuppressionen_GB
dc.subjectexerciseen_GB
dc.subjectmononuclear cellsen_GB
dc.subjectcellular energyen_GB
dc.titleAMPK inactivation in mononuclear cells: a potential intracellular mechanism for exercise-induced immunosuppressionen_US
dc.typeArticleen_US
dc.identifier.doihttp://dx.doi.org/10.1139/H07-135


Files in this item

FilesSizeFormatView

There are no files associated with this item.

This item appears in the following collection(s)

Show simple item record