Please use this identifier to cite or link to this item: http://hdl.handle.net/1893/22908
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dc.contributor.authorApro, William-
dc.contributor.authorMoberg, Marcus-
dc.contributor.authorHamilton, David Lee-
dc.contributor.authorEkblom, Bjorn-
dc.contributor.authorvan, Hall Gerrit-
dc.contributor.authorHolmberg, Hans-Christer-
dc.contributor.authorBlomstrand, Eva-
dc.date.accessioned2016-09-10T00:19:48Z-
dc.date.issued2015-03-15-
dc.identifier.urihttp://hdl.handle.net/1893/22908-
dc.description.abstractCombining endurance and strength training in the same session has been reported to reduce the anabolic response to the latter form of exercise. The underlying mechanism, based primarily on results from rodent muscle, is proposed to involve AMPK-dependent inhibition of mTORC1 signaling. This hypothesis was tested in eight trained male subjects who in randomized order performed either resistance exercise only (R) or interval cycling followed by resistance exercise (ER). Biopsies taken from the vastus lateralis before and after endurance exercise and repeatedly after resistance exercise were assessed for glycogen content, kinase activity, protein phosphorylation, and gene expression. Mixed muscle fractional synthetic rate was measured at rest and during 3 h of recovery using the stable isotope technique. In ER, AMPK activity was elevated immediately after both endurance and resistance exercise (∼90%,P< 0.05) but was unchanged in R. Thr389phosphorylation of S6K1 was increased severalfold immediately after exercise (P< 0.05) in both trials and increased further throughout recovery. After 90 and 180 min recovery, S6K1 activity was elevated (∼55 and ∼110%, respectively,P< 0.05) and eukaryotic elongation factor 2 phosphorylation was reduced (∼55%,P< 0.05) with no difference between trials. In contrast, markers for protein catabolism were differently influenced by the two modes of exercise; ER induced a significant increase in gene and protein expression of MuRF1 (P< 0.05), which was not observed following R exercise only. In conclusion, cycling-induced elevation in AMPK activity does not inhibit mTOR complex 1 signaling after subsequent resistance exercise but may instead interfere with the hypertrophic response by influencing key components in protein breakdown.en_UK
dc.language.isoen-
dc.publisherAmerican Physiological Society-
dc.relationApro W, Moberg M, Hamilton DL, Ekblom B, van Hall G, Holmberg H & Blomstrand E (2015) Resistance exercise-induced S6K1 kinase activity is not inhibited in human skeletal muscle despite prior activation of AMPK by high-intensity interval cycling, American Journal of Physiology - Endocrinology and Metabolism, 308 (6), pp. E470-E481.-
dc.rightsThe publisher does not allow this work to be made publicly available in this Repository. Please use the Request a Copy feature at the foot of the Repository record to request a copy directly from the author. You can only request a copy if you wish to use this work for your own research or private study.-
dc.subjectAMPKen_UK
dc.subjectconcurrent exerciseen_UK
dc.subjectS6K1en_UK
dc.subjectmTORC1en_UK
dc.titleResistance exercise-induced S6K1 kinase activity is not inhibited in human skeletal muscle despite prior activation of AMPK by high-intensity interval cyclingen_UK
dc.typeJournal Articleen_UK
dc.rights.embargodate2999-12-31T00:00:00Z-
dc.rights.embargoreasonThe publisher does not allow this work to be made publicly available in this Repository therefore there is an embargo on the full text of the work.-
dc.identifier.doihttp://dx.doi.org/10.1152/ajpendo.00486.2014-
dc.identifier.pmid25605643-
dc.citation.jtitleAmerican Journal of Physiology - Endocrinology and Metabolism-
dc.citation.issn0193-1849-
dc.citation.volume308-
dc.citation.issue6-
dc.citation.spageE470-
dc.citation.epageE481-
dc.citation.publicationstatusPublished-
dc.citation.peerreviewedRefereed-
dc.type.statusPublisher version (final published refereed version)-
dc.author.emaild.l.hamilton@stir.ac.uk-
dc.citation.date15/03/2015-
dc.contributor.affiliationSwedish School of Sport and Health Sciences (GIH)-
dc.contributor.affiliationSwedish School of Sport and Health Sciences (GIH)-
dc.contributor.affiliationSport-
dc.contributor.affiliationSwedish School of Sport and Health Sciences (GIH)-
dc.contributor.affiliationUniversity of Copenhagen-
dc.contributor.affiliationMid Sweden University, Sweden-
dc.contributor.affiliationSwedish School of Sport and Health Sciences (GIH)-
dc.rights.embargoterms2999-12-31-
dc.rights.embargoliftdate2999-12-31-
dc.identifier.isi000351062500004-
Appears in Collections:Faculty of Health Sciences and Sport Journal Articles

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