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dc.contributor.authorHentilä, Jaakko
dc.date.accessioned2020-10-26T13:32:13Z
dc.date.available2020-10-26T13:32:13Z
dc.date.issued2020
dc.identifier.isbn978-951-39-8120-4
dc.identifier.urihttps://jyx.jyu.fi/handle/123456789/72337
dc.description.abstractProteostasis results from an equilibrium between the synthesis of functional and degradation of dysfunctional proteins. It is regulated by biological processes, including unfolded protein response (UPR) and autophagy. UPR tries to relieve endoplasmic reticulum (ER) stress that results from protein misfolding in ER and autophagy degrades cellular organelles and proteins. Autophagy and UPR have a pivotal role for skeletal muscle function, but the current knowledge how they are regulated by different conditions influencing muscle quality is limited. This thesis elucidated the effects of muscle wasting, hypertrophy and exercise on the markers of autophagy and UPR by measuring protein and mRNA expression in skeletal muscle. To elucidate the effects of muscle wasting, mdx and colon carcinoma 26 (C26) tumor-bearing mice were used to study muscular dystrophy and cancer cachexia, respectively. Additionally, the effects of muscle hypertrophy induced by blocking activin receptor ligands in healthy, cancer cachectic and dystrophic mdx mice were examined. Voluntary wheel running was also studied in mdx mice. In addition to experimental animal models, the acute (1 h and 48 h) and long-term effects (21 weeks) of resistance exercise and training (RE and RT, respectively) in young (26 ± 4 years) and older (61 ± 6 years) previously untrained men were elucidated. Furthermore, the effects of 20-week experimental training period (EX), in which strength training was integrated with sprint training, in master sprinter men (40–76 years) were studied. The main results of this thesis were that UPR is induced by muscular dystrophy, as well as by a single RE bout in young and older men. Additionally, muscle hypertrophy induced by activin receptor ligand blocking increased UPR markers in healthy mice, while this increase in UPR markers was not observed in muscle hypertrophy induced by the 21-week RT period in young and older men. Autophagosome content, marked by lipidated LC3 protein (LC3II), was increased in C26 cancer cachexia and by RE and RT in previously untrained young men, as well as in masters sprinters conducting long-term strength training in conjunction with sprint training. These results indicate that, as an adaptation to muscle hypertrophy, wasting and exercise UPR and autophagy are regulated distinctly in skeletal muscle depending on the context. These results may be applied in the future as a scientific basis to develop new strategies to prevent and treat muscle wasting and in offering evidence based exercise recommendations.en
dc.format.mimetypeapplication/pdf
dc.language.isoeng
dc.publisherJyväskylän yliopisto
dc.relation.ispartofseriesJYU dissertations
dc.relation.haspart<b>Artikkeli I:</b> Hulmi, J., Hentilä, J., DeRuisseau, K. C., Oliveira, B. M., Papaioannou, K. G., Autio, R., . . . Atalay, M. (2016). Effects of muscular dystrophy, exercise and blocking activin receptor IIB ligands on the unfolded protein response and oxidative stress. <i>Free Radical Biology and Medicine, 99 (October), 308-322.</i> <a href="https://doi.org/10.1016/j.freeradbiomed.2016.08.017"target="_blank"> DOI: 10.1016/j.freeradbiomed.2016.08.017</a>
dc.relation.haspart<b>Artikkeli II:</b> Hentilä, J., Nissinen, T., Korkmaz, A., Lensu, S., Silvennoinen, M., Pasternack, A., . . . Hulmi, J. (2019). Activin Receptor Ligand Blocking and Cancer Have Distinct Effects on Protein and Redox Homeostasis in Skeletal Muscle and Liver. <i>Frontiers in Physiology, 9, 1917.</i> <a href="https://doi.org/10.3389/fphys.2018.01917"target="_blank"> DOI: 10.3389/fphys.2018.01917</a>
dc.relation.haspart<b>Artikkeli III:</b> Hentilä, J., Ahtiainen, J., Paulsen, G., Raastad, T., Häkkinen, K., Mero, A., & Hulmi, J. (2018). Autophagy is induced by resistance exercise in young men but unfolded protein response is induced regardless of age. <i>Acta Physiologica, 224 (1), e13069.</i> <a href="https://doi.org/10.1111/apha.13069"target="_blank"> DOI: 10.1111/apha.13069</a>
dc.relation.haspart<b>Artikkeli IV:</b> Hentilä J, Hulmi JJ, Laakkonen EK, Ahtiainen JP, Suominen H, Korhonen MT. Sprint and strength training modulates autophagy and proteostasis in aging sprinters. <i>Medicine & Science in Sports & Exercise</i>: September 2020 –Volume 52 – Is-sue 9 – p 1948‐1959. <a href="https://doi.org/10.1249/MSS.0000000000002340"target="_blank">DOI: 10.1249/MSS.0000000000002340</a>
dc.rightsIn Copyright
dc.subjectliikunta
dc.subjectvoimaharjoittelu
dc.subjectlihakset
dc.subjectfysiologia
dc.subjectlihasvoima
dc.subjectlihasmassa
dc.subjectproteiinit
dc.subjectmerkkiaineet
dc.subjectlihaskunto
dc.subjectnuoret
dc.subjectmiehet
dc.subjectikääntyneet
dc.subjectpikajuoksu
dc.subjectsyöpätaudit
dc.subjectproteostaasi
dc.subjectlihaskato
dc.subjectlihaskasvu
dc.subjectautofagia
dc.subjectUPR
dc.subjectlihasdystrofia
dc.subjectkakeksia
dc.subjectaktiivireseptorihoito
dc.subjecthypertrofia
dc.subjectluurankolihas
dc.subjectER-stressi
dc.subjecthapetus-pelkistys-tasapaino
dc.subjectnopeusvoimaharjoittelu
dc.subjectliikuntasuositukset
dc.subjectlihaskatohoitomuodot
dc.subjectunfolded protein response
dc.subjectlaskostumattomien proteiinien vaste
dc.subjectproteiinivaste
dc.subjectskeletal muscle
dc.subjectautophagy
dc.subjectproteostasis
dc.subjecthypertrophy
dc.subjectatrophy
dc.subjectER stress
dc.subjectredox balance
dc.titleMuscle physiology and proteostasis – Effects of changes in muscle size and exercise
dc.typeDiss.
dc.identifier.urnURN:ISBN:978-951-39-8120-4
dc.relation.issn2489-9003
dc.rights.copyright© The Author & University of Jyväskylä
dc.rights.accesslevelopenAccess
dc.type.publicationdoctoralThesis
dc.format.contentfulltext
dc.rights.urlhttp://rightsstatements.org/page/InC/1.0/?language=en
dc.date.digitised


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