Muscle residual force enhancement: a brief review
Autor(a) principal: | |
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Data de Publicação: | 2013 |
Outros Autores: | |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Clinics |
Texto Completo: | https://www.revistas.usp.br/clinics/article/view/53169 |
Resumo: | Muscle residual force enhancement has been observed in different muscle preparations for more than half a century. Nonetheless, its mechanism remains unclear; to date, there are three generally accepted hypotheses: 1) sarcomere length non-uniformity, 2) engagement of passive elements, and 3) an increased number of cross-bridges. The first hypothesis uses sarcomere non-homogeneity and instability to explain how "weak" sarcomeres would convey the higher tension generated by an enhanced overlap from "stronger" sarcomeres, allowing the whole system to produce higher forces than predicted by the force-length relationship; non-uniformity provides theoretical support for a large amount of the experimental data. The second hypothesis suggests that passive elements within the sarcomeres (i.e., titin) could gain strain upon calcium activation followed by stretch. Finally, the third hypothesis suggests that muscle stretch after activation would alter cross-bridge kinetics to increase the number of attached cross-bridges. Presently, we cannot completely rule out any of the three hypotheses. Different experimental results suggest that the mechanisms on which these three hypotheses are based could all coexist. |
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Clinics |
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Muscle residual force enhancement: a brief review Force EnhancementStretchMuscleFibersMyofibrils Muscle residual force enhancement has been observed in different muscle preparations for more than half a century. Nonetheless, its mechanism remains unclear; to date, there are three generally accepted hypotheses: 1) sarcomere length non-uniformity, 2) engagement of passive elements, and 3) an increased number of cross-bridges. The first hypothesis uses sarcomere non-homogeneity and instability to explain how "weak" sarcomeres would convey the higher tension generated by an enhanced overlap from "stronger" sarcomeres, allowing the whole system to produce higher forces than predicted by the force-length relationship; non-uniformity provides theoretical support for a large amount of the experimental data. The second hypothesis suggests that passive elements within the sarcomeres (i.e., titin) could gain strain upon calcium activation followed by stretch. Finally, the third hypothesis suggests that muscle stretch after activation would alter cross-bridge kinetics to increase the number of attached cross-bridges. Presently, we cannot completely rule out any of the three hypotheses. Different experimental results suggest that the mechanisms on which these three hypotheses are based could all coexist. Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo2013-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://www.revistas.usp.br/clinics/article/view/5316910.6061/CLINICS/2013(02)R01Clinics; v. 68 n. 2 (2013); 269-274 Clinics; Vol. 68 Núm. 2 (2013); 269-274 Clinics; Vol. 68 No. 2 (2013); 269-274 1980-53221807-5932reponame:Clinicsinstname:Universidade de São Paulo (USP)instacron:USPenghttps://www.revistas.usp.br/clinics/article/view/53169/57230Minozzo, Fábio CarderelliLira, Claudio Andre Barbosa deinfo:eu-repo/semantics/openAccess2013-04-08T20:40:37Zoai:revistas.usp.br:article/53169Revistahttps://www.revistas.usp.br/clinicsPUBhttps://www.revistas.usp.br/clinics/oai||clinics@hc.fm.usp.br1980-53221807-5932opendoar:2013-04-08T20:40:37Clinics - Universidade de São Paulo (USP)false |
dc.title.none.fl_str_mv |
Muscle residual force enhancement: a brief review |
title |
Muscle residual force enhancement: a brief review |
spellingShingle |
Muscle residual force enhancement: a brief review Minozzo, Fábio Carderelli Force Enhancement Stretch Muscle Fibers Myofibrils |
title_short |
Muscle residual force enhancement: a brief review |
title_full |
Muscle residual force enhancement: a brief review |
title_fullStr |
Muscle residual force enhancement: a brief review |
title_full_unstemmed |
Muscle residual force enhancement: a brief review |
title_sort |
Muscle residual force enhancement: a brief review |
author |
Minozzo, Fábio Carderelli |
author_facet |
Minozzo, Fábio Carderelli Lira, Claudio Andre Barbosa de |
author_role |
author |
author2 |
Lira, Claudio Andre Barbosa de |
author2_role |
author |
dc.contributor.author.fl_str_mv |
Minozzo, Fábio Carderelli Lira, Claudio Andre Barbosa de |
dc.subject.por.fl_str_mv |
Force Enhancement Stretch Muscle Fibers Myofibrils |
topic |
Force Enhancement Stretch Muscle Fibers Myofibrils |
description |
Muscle residual force enhancement has been observed in different muscle preparations for more than half a century. Nonetheless, its mechanism remains unclear; to date, there are three generally accepted hypotheses: 1) sarcomere length non-uniformity, 2) engagement of passive elements, and 3) an increased number of cross-bridges. The first hypothesis uses sarcomere non-homogeneity and instability to explain how "weak" sarcomeres would convey the higher tension generated by an enhanced overlap from "stronger" sarcomeres, allowing the whole system to produce higher forces than predicted by the force-length relationship; non-uniformity provides theoretical support for a large amount of the experimental data. The second hypothesis suggests that passive elements within the sarcomeres (i.e., titin) could gain strain upon calcium activation followed by stretch. Finally, the third hypothesis suggests that muscle stretch after activation would alter cross-bridge kinetics to increase the number of attached cross-bridges. Presently, we cannot completely rule out any of the three hypotheses. Different experimental results suggest that the mechanisms on which these three hypotheses are based could all coexist. |
publishDate |
2013 |
dc.date.none.fl_str_mv |
2013-01-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
https://www.revistas.usp.br/clinics/article/view/53169 10.6061/CLINICS/2013(02)R01 |
url |
https://www.revistas.usp.br/clinics/article/view/53169 |
identifier_str_mv |
10.6061/CLINICS/2013(02)R01 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
https://www.revistas.usp.br/clinics/article/view/53169/57230 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
application/pdf |
dc.publisher.none.fl_str_mv |
Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo |
publisher.none.fl_str_mv |
Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo |
dc.source.none.fl_str_mv |
Clinics; v. 68 n. 2 (2013); 269-274 Clinics; Vol. 68 Núm. 2 (2013); 269-274 Clinics; Vol. 68 No. 2 (2013); 269-274 1980-5322 1807-5932 reponame:Clinics instname:Universidade de São Paulo (USP) instacron:USP |
instname_str |
Universidade de São Paulo (USP) |
instacron_str |
USP |
institution |
USP |
reponame_str |
Clinics |
collection |
Clinics |
repository.name.fl_str_mv |
Clinics - Universidade de São Paulo (USP) |
repository.mail.fl_str_mv |
||clinics@hc.fm.usp.br |
_version_ |
1787713176145494016 |