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dc.contributor.authorMartin-Rincon, Marcos
dc.contributor.authorPérez-López, Antonio
dc.contributor.authorMorales-Alamo, David
dc.contributor.authorPerez-Suarez, Ismael
dc.contributor.authorde Pablos-Velasco, Pedro
dc.contributor.authorPerez-Valera, Mario
dc.contributor.authorPerez-Regalado, Sergio
dc.contributor.authorMartinez-Canton, Miriam
dc.contributor.authorGelabert-Rebato, Miriam
dc.contributor.authorJuan-Habib, Julian William
dc.contributor.authorHolmberg, Hans-Christer
dc.contributor.authorCalbet, Jose Antonio Lopez
dc.date.accessioned2020-05-11T07:06:07Z
dc.date.available2020-05-11T07:06:07Z
dc.date.created2020-03-23T11:33:55Z
dc.date.issued2019
dc.identifier.citationNutrients. 2019, 11(11), 2824.en_US
dc.identifier.issn2072-6643
dc.identifier.urihttps://hdl.handle.net/11250/2653761
dc.descriptionThis article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).en_US
dc.description.abstractThe loss of skeletal muscle mass with energy deficit is thought to be due to protein breakdown by the autophagy-lysosome and the ubiquitin-proteasome systems. We studied the main signaling pathways through which exercise can attenuate the loss of muscle mass during severe energy deficit (5500 kcal/day). Overweight men followed four days of caloric restriction (3.2 kcal/kg body weight day) and prolonged exercise (45 min of one-arm cranking and 8 h walking/day), and three days of control diet and restricted exercise, with an intra-subject design including biopsies from muscles submitted to distinct exercise volumes. Gene expression and signaling data indicate that the main catabolic pathway activated during severe energy deficit in skeletal muscle is the autophagy-lysosome pathway, without apparent activation of the ubiquitin-proteasome pathway. Markers of autophagy induction and flux were reduced by exercise primarily in the muscle submitted to an exceptional exercise volume. Changes in signaling are associated with those in circulating cortisol, testosterone, cortisol/testosterone ratio, insulin, BCAA, and leucine. We conclude that exercise mitigates the loss of muscle mass by attenuating autophagy activation, blunting the phosphorylation of AMPK/ULK1/Beclin1, and leading to p62/SQSTM1 accumulation. This includes the possibility of inhibiting autophagy as a mechanism to counteract muscle loss in humans under severe energy deficit.en_US
dc.language.isoengen_US
dc.subjectautophagy-lysosomeen_US
dc.subjectcaloric restrictionen_US
dc.subjectprotein degradationen_US
dc.subjectskeletal muscleen_US
dc.subjectubiquitin-proteasomeen_US
dc.titleExercise mitigates the loss of muscle mass by attenuating the activation of autophagy during severe energy deficiten_US
dc.typePeer revieweden_US
dc.typeJournal articleen_US
dc.description.versionpublishedVersionen_US
dc.rights.holder© 2019 by the authors.en_US
dc.source.pagenumber1-26en_US
dc.source.volume11en_US
dc.source.journalNutrientsen_US
dc.source.issue11en_US
dc.identifier.doi10.3390/nu11112824
dc.identifier.cristin1802938
dc.description.localcodeSeksjon for fysisk prestasjonsevne / Department of Physical Performanceen_US
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1


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