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dc.contributor.authorBudiono, Boris P
dc.contributor.authorSee Hoe, Louise E
dc.contributor.authorPeart, Jason N
dc.contributor.authorVider, Jelena
dc.contributor.authorAshton, Kevin J
dc.contributor.authorJacques, Angela
dc.contributor.authorHaseler, Luke J
dc.contributor.authorHeadrick, John P
dc.date.accessioned2021-03-12T03:34:08Z
dc.date.available2021-03-12T03:34:08Z
dc.date.issued2021
dc.identifier.issn0024-3205
dc.identifier.doi10.1016/j.lfs.2021.119253
dc.identifier.urihttp://hdl.handle.net/10072/403111
dc.description.abstractAIM: Exercise is cardioprotective, though optimal interventions are unclear. We assessed duration dependent effects of exercise on myocardial ischemia-reperfusion (I-R) injury, kinase signaling and gene expression. METHODS: Responses to brief (2 day; 2EX), intermediate (7 and 14 day; 7EX and 14EX) and extended (28 day; 28EX) voluntary wheel running (VWR) were studied in male C57Bl/6 mice. Cardiac function, I-R tolerance and survival kinase signaling were assessed in perfused hearts. KEY FINDINGS: Mice progressively increased running distances and intensity, from 2.4 ± 0.2 km/day (0.55 ± 0.04 m/s) at 2-days to 10.6 ± 0.4 km/day (0.72 ± 0.06 m/s) after 28-days. Myocardial mass and contractility were modified at 14-28 days VWR. Cardioprotection was not 'dose-dependent', with I-R tolerance enhanced within 7 days and not further improved with greater VWR duration, volume or intensity. Protection was associated with AKT, ERK1/2 and GSK3β phosphorylation, with phospho-AMPK selectively enhanced with brief VWR. Gene expression was duration-dependent: 7 day VWR up-regulated glycolytic (Pfkm) and down-regulated maladaptive remodeling (Mmp2) genes; 28 day VWR up-regulated caveolar (Cav3), mitochondrial biogenesis (Ppargc1a, Sirt3) and titin (Ttn) genes. Interestingly, I-R tolerance in 2EX/2SED groups improved vs. groups subjected to longer sedentariness, suggesting transient protection on transition to housing with running wheels. SIGNIFICANCE: Cardioprotection is induced with as little as 7 days VWR, yet not enhanced with further or faster running. This protection is linked to survival kinase phospho-regulation (particularly AKT and ERK1/2), with glycolytic, mitochondrial, caveolar and myofibrillar gene changes potentially contributing. Intriguingly, environmental enrichment may also protect via similar kinase regulation.
dc.description.peerreviewedYes
dc.languageeng
dc.publisherElsevier BV
dc.relation.ispartofjournalLife sciences
dc.subject.fieldofresearchBiochemistry and cell biology
dc.subject.fieldofresearchPharmacology and pharmaceutical sciences
dc.subject.fieldofresearchcode3101
dc.subject.fieldofresearchcode3214
dc.subject.keywordsCardioprotection
dc.subject.keywordsExercise
dc.subject.keywordsMyocardial ischemia
dc.subject.keywordsSurvival kinase
dc.subject.keywordsVoluntary activity
dc.titleEffects of voluntary exercise duration on myocardial ischaemic tolerance, kinase signaling and gene expression
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationBudiono, BP; See Hoe, LE; Peart, JN; Vider, J; Ashton, KJ; Jacques, A; Haseler, LJ; Headrick, JP, Effects of voluntary exercise duration on myocardial ischaemic tolerance, kinase signaling and gene expression, Life sciences, 2021
dcterms.dateAccepted2021-02-17
dcterms.licensehttps://creativecommons.org/licenses/by-nc-nd/4.0/
dc.date.updated2021-03-12T02:58:51Z
dc.description.versionAccepted Manuscript (AM)
gro.description.notepublicThis publication has been entered in Griffith Research Online as an advanced online version.
gro.rights.copyright© 2021 Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International Licence (http://creativecommons.org/licenses/by-nc-nd/4.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, providing that the work is properly cited.
gro.hasfulltextFull Text
gro.griffith.authorHeadrick, John P.
gro.griffith.authorPeart, Jason N.


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