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Cited by 351

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

The influence of immobilization and stretch on protein turnover of rat skeletal muscle.

Open access
Goldspink, D F·1977·The Journal of Physiology

Abstract

1. Changes in muscle size have been studied as a function of time after immobilization and in relation to the functional length of the muscle. 2. When immobilized in a shortened position the soleus and extensor digitorum longus muscles underwent atrophy, showing net losses of tissue protein. This atrophy appears to be caused by decreases in protein synthesis and increases in protein break‐down. Average rates of protein synthesis and degradation were measured in immobilized and unrestrained control muscles by sensitive in vitro methods. 3. When the two muscles were held in a lengthened position they grew compared with internal controls. This rapid growth was primarily due to increased rats of protein synthesis, which possibly arise from a more active involvement of ribosomes in translation. In keeping with these situations of growth, DNA synthesis, DNA and RNA concentrations were found to be higher in the immobilized tissues. 4. Passive stretch and the development of isometric tension via the stretch reflux are suggested as factors stimulating protein synthesis, and hence inducing the growth of muscles held in the lengthened state. Probably neither of these factors will be experienced appreciably in the shortened position of restraint, and the lower level of activity in these immobilized muscles leads to their atrophy.

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Crossref · 10.1113/jphysiol.1977.sp011667

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Metadata

Authors
Goldspink, D. F.
Venue
The Journal of Physiology
Publisher
Wiley
Published
1977-01
Volume
264
Issue
1
Pages
267-282
ISSN
  • 0022-3751 (ISSN-L)
  • 1469-7793
OpenAlex
W2078160543
Cited by
351
References
1
FWCI
4.06
Type
journal article
Language
en
Open access
green

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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