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Costamere remodeling with muscle loading and unloading in healthy young men
Author(s) -
Li Ruowei,
Narici Marco V.,
Erskine Robert M.,
Seynnes Olivier R.,
Rittweger Jörn,
Pišot Rado,
Šimunič Boštjan,
Flück Martin
Publication year - 2013
Publication title -
journal of anatomy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 118
eISSN - 1469-7580
pISSN - 0021-8782
DOI - 10.1111/joa.12101
Subject(s) - vinculin , focal adhesion , myosin , myofibril , sarcolemma , isometric exercise , integrin , medicine , microbiology and biotechnology , myocyte , chemistry , biology , endocrinology , anatomy , signal transduction , receptor
Abstract Costameres are mechano‐sensory sites of focal adhesion in the sarcolemma that provide a structural anchor for myofibrils. Their turnover is regulated by integrin‐associated focal adhesion kinase ( FAK ). We hypothesized that changes in content of costamere components (beta 1 integrin, FAK , meta‐vinculin, gamma‐vinculin) with increased and reduced loading of human anti‐gravity muscle would: (i) relate to changes in muscle size and molecular parameters of muscle size regulation [p70 S 6 K , myosin heavy chain ( MHC )1 and MHC II A ]; (ii) correspond to adjustments in activity and expression of FAK , and its negative regulator, FRNK ; and (iii) reflect the temporal response to reduced and increased loading. Unloading induced a progressive decline in thickness of human vastus lateralis muscle after 8 and 34 days of bedrest (−4% and −14%, respectively; n  = 9), contrasting the increase in muscle thickness after 10 and 27 days of resistance training (+5% and +13%; n  = 6). Changes in muscle thickness were correlated with changes in cross‐sectional area of type I muscle fibers ( r  = 0.66) and beta 1 integrin content ( r  = 0.76) at the mid‐point of altered loading. Changes in meta‐vinculin and FAK ‐p Y 397 content were correlated ( r  = 0.85) and differed, together with the changes of beta 1 integrin, MHCI , MHCII and p70 S 6 K , between the mid‐ and end‐point of resistance training. By contrast, costamere protein level changes did not differ between time points of bedrest. The findings emphasize the role of FAK ‐regulated costamere turnover in the load‐dependent addition and removal of myofibrils, and argue for two phases of muscle remodeling with resistance training, which do not manifest at the macroscopic level.

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