THE POSSIBLE ROLE OF INTRACELLULAR CA2+ ACCUMULATION FOR THE DEVELOPMENT OF IMMOBILIZATION ATROPHY

• Type: Article in International Scientific Journal
• Date: 1993

Authors

soares, jmc (Author) Other; duarte, jar (Author) FADEUP; carvalho, j (Author) Other; appell, hj (Author) Other

Journal

Title: International Journal of Sports Medicine

Vol. 14

Pages: 437-439

ISSN: 0172-4622

Publisher: Thieme

Indexing

ISI Web of Knowledge - 22 Citations

Scopus - 25 Citations

Scientific classification

FOS: Medical and Health sciences > Health sciences

Other information

Authenticus ID: P-001-MGJ

DOI: 10.1055/s-2007-1021206

Abstract (EN): 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.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 3