The possible role of intracellular Ca2+ accumulation for the development of immobilization atrophy
Deutscher übersetzter Titel: | Moeglicher Einfluss von intrazellulaerer Ca2+-Anhaeufung auf die Entwicklung von Immobilisationsatrophie |
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Autor: | Soares, J.M.; Duarte, J.A.R.; Carvalho, J.; Appell, Hans-Joachim |
Erschienen in: | International journal of sports medicine |
Veröffentlicht: | 14 (1993), 8, S. 437-439, Lit. |
Format: | Literatur (SPOLIT) |
Publikationstyp: | Zeitschriftenartikel |
Medienart: | Gedruckte Ressource Elektronische Ressource (online) |
Sprache: | Englisch |
ISSN: | 0172-4622, 1439-3964 |
DOI: | 10.1055/s-2007-1021206 |
Schlagworte: | |
Online Zugang: | |
Erfassungsnummer: | PU199408071490 |
Quelle: | BISp |
Abstract des Autors
Little is known about the cellular mechanisms which induce the development of skeletal muscle immobilization atrophy. Initial disturbances in cellular homeostasis seem to occur very early during immobilization. The aim of the study was to investigate whether loss of calcium homeostasis might be of etiological importance for atrophy. Therefore a calcium channel blocker (nifedipine) was administered to mice immobilized for four days, and their soleus muscle was investigated comparatively to immobilized animals without nifedipine. The immobilized muscles showed an atrophy of about 15% which was not the case in nifedipine-treated immobilized muscles. Ultrastructural alterations (lysosomes, mitochondrial damage) were found predominantly in the immobilized muscles, but rarely with nifedipine. It was concluded that nifedipine protected the muscle fibers probably against calcium overload, thereby avoiding an autophagic response and an impairment of mitochondrial respiratory function. Verf.-Referat