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Skeletal Muscle Mitochondria in Microembolism‐induced Heart Failure
Author(s) -
Rosca Mariana G,
Stanley William,
Sabbah Hani,
Hoppel Charles
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.600.28
Subject(s) - skeletal muscle , oxidative phosphorylation , mitochondrion , phosphorylation , bioenergetics , heart failure , chemistry , medicine , myopathy , endocrinology , myocyte , biochemistry , biology
Bioenergetic failure is proposed as the primary mechanism responsible for the skeletal muscle myopathy in heart failure (HF). We analyzed the two populations of skeletal muscle mitochondria (subsarcolemmal, SSM, and interfibrillar, IFM) in moderately severe canine coronary microembolization‐induced HF. Activities of the electron transport chain (ETC) complexes, and integrated function (oxidative phosphorylation) in freshly isolated intact mitochondria were measured. The yield of SSM was unchanged while that of IFM was increased in HF. These IFM showed decreased oxidative phosphorylation with complex I substrates while respiratory rates with complexes II, III and IV substrates were normal. The activities of individual ETC complexes, including complex I, were normal. Thus, the content of skeletal muscle IFM is increased by HF, but these mitochondria have a selective defect in oxidative phosphorylation through complex I. We are exploring whether the organization of oxidative phosphorylation in supercomplexes (respirasomes) is disrupted in these skeletal muscle IFM in HF.