Reactive oxygen species and fatigue-induced prolonged low-frequency force depression in skeletal muscle fibres of rats, mice and SOD2 overexpressing mice.

Détails

ID Serval
serval:BIB_8E0EA64CCCF9
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Reactive oxygen species and fatigue-induced prolonged low-frequency force depression in skeletal muscle fibres of rats, mice and SOD2 overexpressing mice.
Périodique
Journal of Physiology
Auteur(s)
Bruton J.D., Place N., Yamada T., Silva J.P., Andrade F.H., Dahlstedt A.J., Zhang S.J., Katz A., Larsson N.G., Westerblad H.
ISSN
0022-3751 (Print)
ISSN-L
0022-3751
Statut éditorial
Publié
Date de publication
2008
Volume
586
Numéro
1
Pages
175-184
Langue
anglais
Résumé
Skeletal muscle often shows a delayed force recovery after fatiguing stimulation, especially at low stimulation frequencies. In this study we focus on the role of reactive oxygen species (ROS) in this fatigue-induced prolonged low-frequency force depression. Intact, single muscle fibres were dissected from flexor digitorum brevis (FDB) muscles of rats and wild-type and superoxide dismutase 2 (SOD2) overexpressing mice. Force and myoplasmic free [Ca(2+)] ([Ca(2+)](i)) were measured. Fibres were stimulated at different frequencies before and 30 min after fatigue induced by repeated tetani. The results show a marked force decrease at low stimulation frequencies 30 min after fatiguing stimulation in all fibres. This decrease was associated with reduced tetanic [Ca(2+)](i) in wild-type mouse fibres, whereas rat fibres and mouse SOD2 overexpressing fibres instead displayed a decreased myofibrillar Ca(2+) sensitivity. The SOD activity was approximately 50% lower in wild-type mouse than in rat FDB muscles. Myoplasmic ROS increased during repeated tetanic stimulation in rat fibres but not in wild-type mouse fibres. The decreased Ca(2+) sensitivity in rat fibres could be partially reversed by application of the reducing agent dithiothreitol, whereas the decrease in tetanic [Ca(2+)](i) in wild-type mouse fibres was not affected by dithiothreitol or the antioxidant N-acetylcysteine. In conclusion, we describe two different causes of fatigue-induced prolonged low-frequency force depression, which correlate to differences in SOD activity and ROS metabolism. These findings may have clinical implications since ROS-mediated impairments in myofibrillar function can be counteracted by reductants and antioxidants, whereas changes in SR Ca(2+) handling appear more resistant to interventions.
Mots-clé
Acetylcysteine/pharmacology, Animals, Antioxidants/pharmacology, Calcium/metabolism, Dithiothreitol/pharmacology, Gene Expression Regulation, Enzymologic, Male, Mice, Mice, Inbred Strains, Muscle Contraction/drug effects, Muscle Contraction/physiology, Muscle Fatigue/physiology, Muscle, Skeletal/metabolism, Rats, Reactive Oxygen Species/metabolism, Sarcoplasmic Reticulum/metabolism, Superoxide Dismutase/genetics, Superoxide Dismutase/metabolism
Pubmed
Web of science
Open Access
Oui
Création de la notice
20/09/2013 8:41
Dernière modification de la notice
20/08/2019 14:52
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