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1 Department of Pulmonary
Diseases,
Animal and clinical studies have shown
respiratory muscle dysfunction caused by treatment with
glucocorticoids. The present study was designed to investigate whether
anabolic steroids are able to antagonize the loss of diaphragm force
induced by long-term low-dose methylprednisolone (MP) administration.
Male adult rats were randomized to receive saline or MP (0.2 mg · kg
1 · day
1
sc) during 9 mo, with or without nandrolone decanoate (ND; 1 mg · kg
1 · wk
1
im) during the last 3 mo. The ~10% reduction in force generation of
isolated diaphragm bundles induced by MP was completely abolished by
addition of ND. The MP-induced decrease in number of fibers expressing
type IIb myosin heavy chains was not reversed by ND. MP slightly
reduced type I, IIa, and IIx fiber cross-sectional areas
(CSA), but not type IIb fiber CSA. Addition of ND abolished the
reduction in IIa and IIx fiber CSA. The MP-induced alterations in
glycogenolytic activity and fatty acid oxidation capacity were not
reversed by ND. In conclusion, the marked reduction in diaphragm force
caused by long-term low-dose MP was completely abolished by addition of
ND. ND in part also antagonized the effects of MP on diaphragm
morphology but showed no beneficial effects on biochemical changes.
glucocorticoids; contractile properties; myosin heavy chains; biochemistry
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