The underlying mechanisms of delayed force recovery from fatigue are dependent on reactive oxygen species metabolism in skeletal muscle fibres.
Détails
ID Serval
serval:BIB_ABD558D0AEBF
Type
Actes de conférence (partie): contribution originale à la littérature scientifique, publiée à l'occasion de conférences scientifiques, dans un ouvrage de compte-rendu (proceedings), ou dans l'édition spéciale d'un journal reconnu (conference proceedings).
Sous-type
Abstract (résumé de présentation): article court qui reprend les éléments essentiels présentés à l'occasion d'une conférence scientifique dans un poster ou lors d'une intervention orale.
Collection
Publications
Institution
Titre
The underlying mechanisms of delayed force recovery from fatigue are dependent on reactive oxygen species metabolism in skeletal muscle fibres.
Titre de la conférence
Federation of European Physiological Societies Meeting. Bratislava (Slovakia)
ISBN
1748-1716
Statut éditorial
Publié
Date de publication
2007
Volume
191
Série
Acta Physiologica
Pages
PTH09-70
Langue
anglais
Notes
Joint Meeting of The Slovak Physiological Society, The Physiological Society and The Federation of European Physiological Societies 11/09/2007-14/09/2007 Bratislava, Slovakia
Résumé
Aims:
The present study was conducted in order to test the hypothesis that differences in reactive oxygen species (ROS) metabolism are responsible for different causes of decreased force at low frequencies (i.e. decreased SR Ca2+release vs. reduced myofibrillar Ca2+sensitivity). Methods:
Intact, single muscle fibres were dissected from flexor digitorum brevis muscles of rats and mice (wildtype and superoxide dismutase (SOD2) overexpressing). Force and myoplasmic free [Ca2+] ([Ca2+]i) were measured. Fibres were stimulated at frequencies varying from 15 to 100 Hz before and 30 min after fatigue induced by repeated tetani (70 Hz, 350 ms). Results:
Force was markedly decreased (~60-70%, P < 0.05) at low stimulation frequencies 30 min after fatiguing stimulation in all fibres. This reduction was associated with reduced tetanic [Ca2+]i in wildtype mouse fibres (to 64 ± 11% of the original, P < 0.05), which can not be reversed by application of the reducing agent dithiothreitol or the antioxidant N-acetylcysteine. In contrast, rat fibres and mouse SOD2 overexpressing fibres showed a significant (P < 0.05) decreased myofibrillar Ca2+sensitivity (assessed by measuring the [Ca2+]i required to produce 50% of the maximal tetanic force), which can be partially reversed by application of the reducing agent dithiothreitol.
Conclusion:
In conclusion, the origin of the delayed force recovery seems to depend on the 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 Ca2+handling appear more robust.
The present study was conducted in order to test the hypothesis that differences in reactive oxygen species (ROS) metabolism are responsible for different causes of decreased force at low frequencies (i.e. decreased SR Ca2+release vs. reduced myofibrillar Ca2+sensitivity). Methods:
Intact, single muscle fibres were dissected from flexor digitorum brevis muscles of rats and mice (wildtype and superoxide dismutase (SOD2) overexpressing). Force and myoplasmic free [Ca2+] ([Ca2+]i) were measured. Fibres were stimulated at frequencies varying from 15 to 100 Hz before and 30 min after fatigue induced by repeated tetani (70 Hz, 350 ms). Results:
Force was markedly decreased (~60-70%, P < 0.05) at low stimulation frequencies 30 min after fatiguing stimulation in all fibres. This reduction was associated with reduced tetanic [Ca2+]i in wildtype mouse fibres (to 64 ± 11% of the original, P < 0.05), which can not be reversed by application of the reducing agent dithiothreitol or the antioxidant N-acetylcysteine. In contrast, rat fibres and mouse SOD2 overexpressing fibres showed a significant (P < 0.05) decreased myofibrillar Ca2+sensitivity (assessed by measuring the [Ca2+]i required to produce 50% of the maximal tetanic force), which can be partially reversed by application of the reducing agent dithiothreitol.
Conclusion:
In conclusion, the origin of the delayed force recovery seems to depend on the 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 Ca2+handling appear more robust.
Création de la notice
20/09/2013 10:43
Dernière modification de la notice
20/08/2019 16:15
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