Journal
AMERICAN JOURNAL OF PATHOLOGY
Volume 170, Issue 2, Pages 599-608Publisher
ELSEVIER SCIENCE INC
DOI: 10.2353/ajpath.2007.060505
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The fiber specificity of skeletal muscle abnormalities in chronic heart failure (CHF) has not been defined. We show here that transgenic mice (8 weeks old) with cardiac-specific overexpression of calsequestrin developed CRF (50.9% decrease in fractional shortening and 56.4% increase hi lung weight, P < 0.001), cachexia (37.8% decrease in body weight, P < 0.001), and exercise intolerance (69.3% decrease in running distance to exhaustion, P < 0.001) without a significant change in muscle fiber-type composition. Slow oxidative soleus muscle maintained muscle mass, whereas fast glycolytic tibialis anterior and plantaris muscles underwent atrophy (11.6 and 13.3%, respectively; P < 0.05). in plantaris muscle, glycolytic type IId/x and IIb, but not oxidative type I and IIa, fibers displayed significant decreases in cross-sectional area (20.3%, P < 0.05). Fast glycolytic white vastus lateralis muscle. showed sarcomere degeneration and decreased cytochrome c oxidase IV (39.5%, P < 0.01) and peroxisome proliferator-activated receptory coactivator 1 alpha protein expression (30.3%, P < 0.01) along with a dramatic induction of the MAFbx/Atrogin-1 mRNA. These findings suggest that exercise intolerance can occur in CHF without fiber type switching in skeletal muscle and that oxidative phenotype renders myofibers resistant to pathological insults induced by CHF.
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