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

Details

Serval ID
serval:BIB_8E0EA64CCCF9
Type
Article: article from journal or magazin.
Collection
Publications
Title
Reactive oxygen species and fatigue-induced prolonged low-frequency force depression in skeletal muscle fibres of rats, mice and SOD2 overexpressing mice.
Journal
Journal of Physiology
Author(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
Publication state
Published
Issued date
2008
Volume
586
Number
1
Pages
175-184
Language
english
Abstract
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.
Keywords
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
Yes
Create date
20/09/2013 8:41
Last modification date
20/08/2019 14:52
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