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Short bouts of stretching increase myo‐D, myostatin and atrogin‐1 in rat soleus muscle
Author(s) -
Peviani Sabrina Messa,
Gomes Anna Raquel Silveira,
Moreira Roberta Fátima Carreira,
Moriscot Anselmo Sigari,
Salvini Tania Fátima
Publication year - 2007
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.20695
Subject(s) - myostatin , soleus muscle , endocrinology , medicine , muscle atrophy , gene expression , flexibility (engineering) , skeletal muscle , isometric exercise , chemistry , gene , biochemistry , statistics , mathematics
Stretching is widely used in rehabilitation and sports activities to improve joint range‐of‐motion and flexibility in humans, but the effect of stretching on the gene expression of skeletal muscle is poorly understood. We evaluated the effect of short bouts of passive stretching of rat soleus muscle on myo‐D, myostatin, and atrogin‐1 gene expressions. Six groups of animals were submitted to a single session of stretching (10 stretches of 1 minute with 30 seconds of rest between them, performed manually) and were evaluated immediately (I), and 8, 24, 48, 72, and 168 hours after the session. To evaluate the effect of repetitive sessions of stretching on the soleus muscle over 1 week, three groups of animals received a single session per day of stretching and the muscle was evaluated immediately after 2, 3, and 7 sessions. The mRNA levels of myo‐D, myostatin, and atrogin‐1 were determined by real‐time polymerase chain reaction. A single session of stretching increased the mRNA levels of myo‐D (after 24 h), myostatin (I, and 168 h later), and atrogin‐1 (after 48 h). Repeated daily session of stretching over 1 week increased myostatin (after 7 sessions) and atrogin‐1 expression (after 2, 3, and 7 sessions). Thus, short bouts of passive stretching are able to increase the gene expression of factors associated with muscle growth (myo‐D), negative regulation of muscle mass (myostatin), and atrophy (atrogin‐1), indicating muscle remodeling through different pathways. Muscle Nerve, 2006