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dc.contributor.authorHentilä, Jaakko
dc.contributor.authorHulmi, Juha J.
dc.contributor.authorLaakkonen, Eija K.
dc.contributor.authorAhtiainen, Juha P.
dc.contributor.authorSuominen, Harri
dc.contributor.authorKorhonen, Marko T.
dc.date.accessioned2020-03-24T09:27:48Z
dc.date.available2020-03-24T09:27:48Z
dc.date.issued2020
dc.identifier.citationHentilä, J., Hulmi, J. J., Laakkonen, E. K., Ahtiainen, J. P., Suominen, H., & Korhonen, M. T. (2020). Sprint and Strength Training Modulates Autophagy and Proteostasis in Aging Sprinters. <i>Medicine and Science in Sports and Exercise</i>, <i>52</i>(9), 1948-1959. <a href="https://doi.org/10.1249/MSS.0000000000002340" target="_blank">https://doi.org/10.1249/MSS.0000000000002340</a>
dc.identifier.otherCONVID_35097308
dc.identifier.urihttps://jyx.jyu.fi/handle/123456789/68298
dc.description.abstractPurpose Exercise and aging may modulate muscle protein homeostasis and autophagy, but few studies examine highly-trained middle-aged or older individuals. This study elucidated the effects of a new long-term training stimulus on markers of muscle autophagy and unfolded protein response (UPR) and on sprint running performance in masters sprinters. Methods Thirty-two male competitive sprinters (aged 40–76 years) were randomly divided into experimental (EX) and control (CTRL) groups. The EX training program was a combination of heavy and explosive strength and sprint exercises aimed at improving sprint performance. Fifteen and thirteen participants completed the 20-week intervention period in EX and CTRL, respectively. The latter were told to continue their routine exercises. Key protein markers were analyzed by western blotting from vastus lateralis (VL) muscle biopsies. Muscle thickness of VL was analyzed by ultrasonography and sprint performance by a 60-meter running test. Results EX induced improvement in 60-meter sprint performance when compared to controls (time x group, P = 0.003) without changes in VL muscle thickness. Content of lipidated microtubule-associated protein 1A/1B-light chain 3 (LC3-II) increased in EX (P = 0.022) suggesting increased autophagosome content. Additionally, an autophagosome clearance marker sequestosome 1 (p62) decreased in EX (P = 0.006). Markers of UPR selectively modulated with decreases (e.g. ATF4, P = 0.003) and increases (e.g. EIF2α, P = 0.019) observed in EX. Conclusions These findings suggest that a new intensive training stimulus that combines strength training with sprint training may increase muscle autophagosome content in a basal state without any evidence of impaired autophagosome clearance in masters sprinters. Simultaneously, the combined training may have a selective effect on the content of UPR signaling components.en
dc.format.mimetypeapplication/pdf
dc.languageeng
dc.language.isoeng
dc.publisherLippincott Williams & Wilkins
dc.relation.ispartofseriesMedicine and Science in Sports and Exercise
dc.rightsIn Copyright
dc.subject.othermasters athlete
dc.subject.otherskeletal muscle
dc.subject.otherunfolded protein response
dc.titleSprint and Strength Training Modulates Autophagy and Proteostasis in Aging Sprinters
dc.typearticle
dc.identifier.urnURN:NBN:fi:jyu-202003242519
dc.contributor.laitosLiikuntatieteellinen tiedekuntafi
dc.contributor.laitosFaculty of Sport and Health Sciencesen
dc.contributor.oppiaineValmennus- ja testausoppifi
dc.contributor.oppiaineBiomekaniikkafi
dc.contributor.oppiaineLiikuntafysiologiafi
dc.contributor.oppiaineGerontologia ja kansanterveysfi
dc.contributor.oppiaineGerontologian tutkimuskeskusfi
dc.contributor.oppiaineHyvinvoinnin tutkimuksen yhteisöfi
dc.contributor.oppiaineScience of Sport Coaching and Fitness Testingen
dc.contributor.oppiaineBiomechanicsen
dc.contributor.oppiaineExercise Physiologyen
dc.contributor.oppiaineGerontology and Public Healthen
dc.contributor.oppiaineGerontology Research Centeren
dc.contributor.oppiaineSchool of Wellbeingen
dc.type.urihttp://purl.org/eprint/type/JournalArticle
dc.type.coarhttp://purl.org/coar/resource_type/c_2df8fbb1
dc.description.reviewstatuspeerReviewed
dc.format.pagerange1948-1959
dc.relation.issn0195-9131
dc.relation.numberinseries9
dc.relation.volume52
dc.type.versionacceptedVersion
dc.rights.copyright© 2020 by the American College of Sports Medicine
dc.rights.accesslevelopenAccessfi
dc.relation.grantnumber275922
dc.subject.ysolihakset
dc.subject.ysoproteiinit
dc.subject.ysoikääntyminen
dc.subject.ysosolufysiologia
dc.subject.ysourheilijat
dc.format.contentfulltext
jyx.subject.urihttp://www.yso.fi/onto/yso/p2784
jyx.subject.urihttp://www.yso.fi/onto/yso/p4332
jyx.subject.urihttp://www.yso.fi/onto/yso/p5056
jyx.subject.urihttp://www.yso.fi/onto/yso/p25367
jyx.subject.urihttp://www.yso.fi/onto/yso/p3315
dc.rights.urlhttp://rightsstatements.org/page/InC/1.0/?language=en
dc.relation.doi10.1249/MSS.0000000000002340
dc.relation.funderResearch Council of Finlanden
dc.relation.funderSuomen Akatemiafi
jyx.fundingprogramAcademy Research Fellow, AoFen
jyx.fundingprogramAkatemiatutkija, SAfi
jyx.fundinginformationThis study was supported by the grants from the Academy of Finland (275922) to J.J.H., the Finnish Ministry of Education and Culture, the Finnish Cultural Foundation, Peurunka-Medical Rehabilitation Foundation, Ellen and Artturi Nyyssönen Foundation, Academy of Finland (250683) and Juho Vainio Foundation to M.T.K. and H.S., and the Finnish Cultural Foundation to J.H.
dc.type.okmA1


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