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dc.contributor.authorFiuza-Luces, Carmen
dc.contributor.authorSantos-Lozano, Alejandro
dc.contributor.authorLlavero, Francisco
dc.contributor.authorCampo, Rocío
dc.contributor.authorNogales-Gadea, Gisela
dc.contributor.authorDíez-Bermejo, Jorge
dc.contributor.authorBaladrón, Carlos
dc.contributor.authorGonzález-Murillo, África
dc.contributor.authorArenas, Joaquín
dc.contributor.authorMartín, Miguel A
dc.contributor.authorAndreu, Antoni L
dc.contributor.authorPinós, Tomàs
dc.contributor.authorGálvez, Beatriz G
dc.contributor.authorLopez, Juan Antonio 
dc.contributor.authorVazquez, Jesus 
dc.contributor.authorZugaza, José L
dc.contributor.authorLucia, Alejandro
dc.date.accessioned2018-11-05T08:02:10Z
dc.date.available2018-11-05T08:02:10Z
dc.date.issued2018-03-15
dc.identifier.citationJ Physiol. 2018; 596(6):1035-1061es_ES
dc.identifier.issn0022-3751es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/6565
dc.description.abstractKEY POINTS: Although they are unable to utilize muscle glycogen, McArdle mice adapt favourably to an individualized moderate-intensity endurance exercise training regime. Yet, they fail to reach the performance capacity of healthy mice with normal glycogen availability. There is a remarkable difference in the protein networks involved in muscle tissue adaptations to endurance exercise training in mice with and without glycogen availability. Indeed, endurance exercise training promoted the expression of only three proteins common to both McArdle and wild-type mice: LIMCH1, PARP1 and TIGD4. In turn, trained McArdle mice presented strong expression of mitogen-activated protein kinase 12 (MAPK12). ABSTRACT: McArdle's disease is an inborn disorder of skeletal muscle glycogen metabolism that results in blockade of glycogen breakdown due to mutations in the myophosphorylase gene. We recently developed a mouse model carrying the homozygous p.R50X common human mutation (McArdle mouse), facilitating the study of how glycogen availability affects muscle molecular adaptations to endurance exercise training. Using quantitative differential analysis by liquid chromatography with tandem mass spectrometry, we analysed the quadriceps muscle proteome of 16-week-old McArdle (n = 5) and wild-type (WT) (n = 4) mice previously subjected to 8 weeks' moderate-intensity treadmill training or to an equivalent control (no training) period. Protein networks enriched within the differentially expressed proteins with training in WT and McArdle mice were assessed by hypergeometric enrichment analysis. Whereas endurance exercise training improved the estimated maximal aerobic capacity of both WT and McArdle mice as compared with controls, it was ∼50% lower than normal in McArdle mice before and after training. We found a remarkable difference in the protein networks involved in muscle tissue adaptations induced by endurance exercise training with and without glycogen availability, and training induced the expression of only three proteins common to McArdle and WT mice: LIM and calponin homology domains-containing protein 1 (LIMCH1), poly (ADP-ribose) polymerase 1 (PARP1 - although the training effect was more marked in McArdle mice), and tigger transposable element derived 4 (TIGD4). Trained McArdle mice presented strong expression of mitogen-activated protein kinase 12 (MAPK12). Through an in-depth proteomic analysis, we provide mechanistic insight into how glycogen availability affects muscle protein signalling adaptations to endurance exercise training.es_ES
dc.description.sponsorshipThe CNIC is supported by the Ministry of Economy, Industry and Competitiveness (MEIC) and the Pro CNIC Foundation, and is a Severo Ochoa Centre of Excellence (SEV-2015-0505). This study was funded by grants from Fondo de Investigaciones Sanitarias (PI15/01756, PI15/00558, PI12/00914, and PI14/00903), cofinanced by FEDER. G.N.G. is supported by a Miguel Servet research contract (ISCIII CD14/00032 and FEDER) and C.F.L. by a Sara Borrell post doc contract (CD14/00005). Miguel A. Mart´ın is supported by Fondo de Investigaciones Sanitarias (FIS 15/00432). Tomˆas Pin ´os is supported by Fondo de Investigaciones Sanitarias (FIS PI16/01492).es_ES
dc.language.isoenges_ES
dc.type.hasVersionAMes_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectGlycogenosis type Ves_ES
dc.subjectMcArdle diseasees_ES
dc.subjectExercisees_ES
dc.subjectProteomees_ES
dc.subjectSignalling networkses_ES
dc.subjectTraininges_ES
dc.titleMuscle molecular adaptations to endurance exercise training are conditioned by glycogen availability: a proteomics-based analysis in the McArdle mouse modeles_ES
dc.typejournal articlees_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.identifier.pubmedID29315579es_ES
dc.format.volume596es_ES
dc.format.number6es_ES
dc.format.page1035-1061es_ES
dc.identifier.doi10.1113/JP275292es_ES
dc.contributor.funderMinisterio de Economía, Industria y Competitividad (España) 
dc.contributor.funderFundación ProCNIC 
dc.contributor.funderInstituto de Salud Carlos III 
dc.description.peerreviewedes_ES
dc.identifier.e-issn1469-7793es_ES
dc.relation.publisherversionhttps://doi.org/10.1113/JP275292
dc.identifier.journalThe Journal of physiologyes_ES
dc.repisalud.orgCNICCNIC::Unidades técnicas::Proteómica / Metabolómicaes_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Proteómica cardiovasculares_ES
dc.repisalud.institucionCNICes_ES
dc.rights.accessRightsopen accesses_ES


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Attribution-NonCommercial-NoDerivatives 4.0 Internacional
This item is licensed under a: Attribution-NonCommercial-NoDerivatives 4.0 Internacional