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Cyclosporin A treatment increases rat soleus muscle oxidative capacities
Author(s) -
Sanchez Hervé,
N'Guessan Benoit,
Ribera Florence,
VenturaClapier Renée,
Bigard Xavier
Publication year - 2003
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.10423
Subject(s) - medicine , endocrinology , oxidative phosphorylation , citrate synthase , soleus muscle , mitochondrion , myosin , oxidative stress , chemistry , biology , biochemistry , skeletal muscle , enzyme
Previous studies suggested that administration of cyclosporin A (CsA), an immunosuppressive agent, contributes to the increased fatigability of heart transplant recipients. The aim of this study was to investigate whether CsA itself, without vehicle, affects the function of mitochondria maintained in situ, in rats treated with CsA (25mg/kg/day) dissolved in ethanol and olive oil. Treatment with CsA induced a 16% decrease in slow myosin heavy chain (MHC) associated with a 225% increase in fast MHCIIa. The proportion of fibers expressing type IIa MHC increased as a result of CsA treatment. Soleus from the CsA‐treated animals showed an increase in both basal (+85%) and maximal (+37%) mitochondrial respiration ( P < 0.001), consistent with a 24% increase in citrate synthase activity, whereas the apparent Km for adenosine diphosphate was unchanged. By itself, CsA has no deleterious effects on muscle oxidative capacity but induces alterations in energy metabolism in accordance with the increased proportion of fast‐twitch oxidative fibers. Muscle Nerve 28: 324–329, 2003