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Stretch‐activated signaling is modulated by stretch magnitude and contraction
Author(s) -
Van Dyke Jonathan M.,
Bain James L.W.,
Riley Danny A.
Publication year - 2014
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.23880
Subject(s) - isometric exercise , phosphorylation , contraction (grammar) , kinase , mechanosensitive channels , p38 mitogen activated protein kinases , muscle contraction , chemistry , biophysics , microbiology and biotechnology , biology , mapk/erk pathway , anatomy , endocrinology , medicine , biochemistry , receptor , ion channel
: Stretch therapy is commonly utilized to prevent shortening maladaptation of skeletal muscle. Stretch in combination with isometric contraction prevents shortening, but the signaling mechanisms are not understood. Methods : Using a soleus tenotomy + stretch rat model, the phosphorylation–activation of mechanosensitive kinases (Akt, p70 S6K , p38 MAPK, and ERK1/2) were measured for various stretch magnitudes, set relative to optimal soleus length (Lo). Results : The kinases were not activated by passive stretch until it exceeded the normal physiological range. Stretch + isometric contraction resulted in relatively strong phosphorylation, even at short lengths. Conclusions : Whereas passive stretch results in kinase phosphorylation only during extreme lengthening, isometric contraction generated pronounced phosphorylation of kinases at Lo and Lo + 25%, indicating stimulation of pathways that lead to the preservation or increase of muscle length. Understanding the effects of passive and active stretch with respect to Lo and contraction is essential for predicting therapeutic outcomes and influencing optimal muscle length. Muscle Nerve 49 : 98–107, 2014

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