Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/41842
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dc.contributor.authorMartín-Rincon, M. en_US
dc.contributor.authorMorales-Alamo, D.en_US
dc.contributor.authorCalbet, J. A.L.en_US
dc.date.accessioned2018-09-04T17:06:25Z-
dc.date.available2018-09-04T17:06:25Z-
dc.date.issued2018en_US
dc.identifier.issn0905-7188en_US
dc.identifier.urihttp://hdl.handle.net/10553/41842-
dc.description.abstractAlthough exercise exerts multiple beneficial health effects, it may also damage cellular structures. Damaged elements are continuously degraded and its constituents recycled to produce renovated structures through a process called autophagy, which is essential for the adaptation to training. Autophagy is particularly active in skeletal muscle, where it can be evaluated using specific molecular markers of activation (unc-51-like kinase 1 [ULK1] phosphorylation) and specific proteins indicating increased autophagosome content (increased total LC3, LC3-II, LC3-II/LC3-I ratio). Studies in humans are technically limited but have provided evidence suggesting the activation of autophagy in skeletal muscle through AMP-activated protein kinase (AMPK) and its downstream target ULK1. Autophagy activation is more likely when the intensity is elevated and the exercise performed in the fasted state. The autophagy-gene program and autophagosome content are upregulated after ultraendurance running competitions. However, autophagosome content is reduced after endurance exercise at moderate intensities (50% and 70% of VO(2)max) for 60-120minutes. Autophagosome content is decreased within the first few hours after resistance training. The effects of regular endurance and strength training on basal autophagy remain to be established in humans. One study has reported that acute severe hypoxia increases autophagosome content in human skeletal muscle, which is reverted by 20minutes of low-intensity exercise. Experiments with transgenic mice have shown that autophagy is necessary for skeletal muscle adaptation to training. Little is known on how genetic factors, environment, nutrition, drugs and diseases may interact with exercise to modulate autophagy at rest and during exercise in humans.en_US
dc.languageengen_US
dc.relation.ispartofScandinavian Journal of Medicine and Science in Sportsen_US
dc.sourceScandinavian Journal of Medicine and Science in Sports [ISSN 0905-7188], v. 28 (3), p. 772-781en_US
dc.subject241106 Fisiología del ejercicioen_US
dc.subject.otherEndurance trainingen_US
dc.subject.otherNutrient intakeen_US
dc.subject.otherProtein degradationen_US
dc.subject.otherProtein turnoveren_US
dc.subject.otherResistance trainingen_US
dc.subject.otherSignalingen_US
dc.titleExercise-mediated modulation of autophagy in skeletal muscleen_US
dc.typeinfo:eu-repo/semantics/reviewes
dc.typeArticlees
dc.identifier.doi10.1111/sms.12945
dc.identifier.scopus85025835467
dc.identifier.isi000426529300003-
dc.contributor.authorscopusid56841673800
dc.contributor.authorscopusid35148038500
dc.contributor.authorscopusid7004323423
dc.description.lastpage781-
dc.identifier.issue3-
dc.description.firstpage772-
dc.relation.volume28-
dc.investigacionCiencias de la Saluden_US
dc.type2Reseñaen_US
dc.contributor.daisngid3057600
dc.contributor.daisngid1232764
dc.contributor.daisngid90295
dc.contributor.wosstandardWOS:Martin-Rincon, M
dc.contributor.wosstandardWOS:Morales-Alamo, D
dc.contributor.wosstandardWOS:Calbet, JAL
dc.date.coverdateMarzo 2018
dc.identifier.ulpgces
item.grantfulltextnone-
item.fulltextSin texto completo-
crisitem.author.deptRendimiento humano, ejercicio físico y salud-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Educación Física-
crisitem.author.deptRendimiento humano, ejercicio físico y salud-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Educación Física-
crisitem.author.orcid0000-0002-3685-2331-
crisitem.author.orcid0000-0002-9215-6234-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNameMartín Rincón, Marcos-
crisitem.author.fullNameMorales Álamo, David-
crisitem.author.fullNameLópez Calbet, José Antonio-
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