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dc.contributor.authorWackerhage, Henning
dc.contributor.authorSchoenfeld, Brad J.
dc.contributor.authorHamilton, D. Lee
dc.contributor.authorLehti, Maarit
dc.contributor.authorHulmi, Juha
dc.date.accessioned2019-01-14T11:30:35Z
dc.date.available2020-01-09T22:35:43Z
dc.date.issued2019
dc.identifier.citationWackerhage, H., Schoenfeld, B. J., Hamilton, D. L., Lehti, M., & Hulmi, J. (2019). Stimuli and sensors that initiate skeletal muscle hypertrophy following resistance exercise. <i>Journal of Applied Physiology</i>, <i>126</i>(1), 30-43. <a href="https://doi.org/10.1152/japplphysiol.00685.2018" target="_blank">https://doi.org/10.1152/japplphysiol.00685.2018</a>
dc.identifier.otherCONVID_28670866
dc.identifier.otherTUTKAID_79208
dc.identifier.urihttps://jyx.jyu.fi/handle/123456789/62467
dc.description.abstractOne of the most striking adaptations to exercise is the skeletal muscle hypertrophy that occurs in response to resistance exercise. A large body of work shows that a mammalian target of rapamycin complex 1 (mTORC1)-mediated increase of muscle protein synthesis is the key, but not sole, mechanism by which resistance exercise causes muscle hypertrophy. While much of the hypertrophy signaling cascade has been identified, the initiating, resistance exercise-induced and hypertrophy-stimulating stimuli have remained elusive. For the purpose of this review, we define an initiating, resistance exercise-induced and hypertrophy-stimulating signal as “hypertrophy stimulus,” and the sensor of such a signal as “hypertrophy sensor.” In this review we discuss our current knowledge of specific mechanical stimuli, damage/injury-associated and metabolic stress-associated triggers, as potential hypertrophy stimuli. Mechanical signals are the prime hypertrophy stimuli candidates, and a filamin-C-BAG3-dependent regulation of mTORC1, Hippo, and autophagy signaling is a plausible albeit still incompletely characterized hypertrophy sensor. Other candidate mechanosensing mechanisms are nuclear deformation-initiated signaling or several mechanisms related to costameres, which are the functional equivalents of focal adhesions in other cells. While exercise-induced muscle damage is probably not essential for hypertrophy, it is still unclear whether and how such muscle damage could augment a hypertrophic response. Interventions that combine blood flow restriction and especially low load resistance exercise suggest that resistance exercise-regulated metabolites could be hypertrophy stimuli, but this is based on indirect evidence and metabolite candidates are poorly characterized.fi
dc.format.mimetypeapplication/pdf
dc.language.isoeng
dc.publisherAmerican Physiological Society
dc.relation.ispartofseriesJournal of Applied Physiology
dc.rightsIn Copyright
dc.subject.otherskeletal muscle hypertrophy
dc.subject.othermuscle protein
dc.subject.otherhypertrophy stimulus
dc.subject.otherhypertrophy sensor
dc.titleStimuli and sensors that initiate skeletal muscle hypertrophy following resistance exercise
dc.typearticle
dc.identifier.urnURN:NBN:fi:jyu-201901111165
dc.contributor.laitosLiikuntatieteellinen tiedekuntafi
dc.contributor.laitosFaculty of Sport and Health Sciencesen
dc.contributor.oppiaineLiikuntafysiologiafi
dc.contributor.oppiaineExercise Physiologyen
dc.type.urihttp://purl.org/eprint/type/JournalArticle
dc.date.updated2019-01-11T13:15:15Z
dc.description.reviewstatuspeerReviewed
dc.format.pagerange30-43
dc.relation.issn8750-7587
dc.relation.numberinseries1
dc.relation.volume126
dc.type.versionacceptedVersion
dc.rights.copyright© 2019 the American Physiological Society.
dc.rights.accesslevelopenAccessfi
dc.subject.ysolihakset
dc.subject.ysovoimaharjoittelu
dc.subject.ysolihasmassa
dc.subject.ysoproteiinit
dc.format.contentfulltext
jyx.subject.urihttp://www.yso.fi/onto/yso/p2784
jyx.subject.urihttp://www.yso.fi/onto/yso/p16233
jyx.subject.urihttp://www.yso.fi/onto/yso/p29135
jyx.subject.urihttp://www.yso.fi/onto/yso/p4332
dc.rights.urlhttp://rightsstatements.org/page/InC/1.0/?language=en
dc.relation.doi10.1152/japplphysiol.00685.2018


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