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
Institution
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
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 9:41
Dernière modification de la notice
20/08/2019 15:52