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- W2078491332 abstract "The oxidation of fatty acids is a primary source of energy both at rest and in exercise for both cardiac and skeletal muscle. Previous work in our lab has shown that exercise causes a decline in skeletal muscle function in very-long-chain acyl CoA deficient mice. The affect on cardiac function is not known. PURPOSE The purpose was to determine the effect of prolonged low-intensity exercise on cardiac function in long-chain acyl CoA dehydrogenase (LCAD −/−) and very-long-chain acyl CoA dehydrogenase (VLCAD −/−) deficient mice using transthoracic echocardiography. METHODS Male mice homozygous for VLCAD deficiency along with male mice homozygous for LCAD deficiency and wild type mice were used in this experiment. The mice were randomly assigned to two groups, a sedentary control group and an exercise group. The groups were designated: 1) VLCAD−/−, non-exercised; 2) VLCAD−/−, exercised; 3) LCAD−/−, non-exercised; 4) LCAD−/−, exercised; 5) WT, non-exercised; and 6) WT, exercised. Low-intensity, endurance exercise consisted of running on a treadmill initially at 0% grade and a speed of 30 m min−1 for 20 min. The grade was increased 2% at 20 min and 30 min of exercise. The mice continued to exercise at 30 m min−1 and 4% grade to exhaustion. The mice completed two bouts of exercise 24 h apart. Twenty-four hours after the second bout, the mice were anesthetized using 40 mg Kg−1 sodium pentobarbital (i.p.) for determination of cardiac dimensions, fractional shortening, and ejection fraction using standard echocardiographic short- and long-axis views. Data were analyzed using ANOVA of data in a 2x3 factorial design. All comparisons were made at the 0.05 level of significance. RESULTS Anterior wall diameter was significantly (p <0.05) greater than WT in both LCAD −/− and VLCAD −/− mice both in diastole and systole. During systole, the LCAD −/− left ventricular diameter was significantly (p <0.05) less than the other two groups. Both fractional shortening and the ejection fraction were significantly (p <0.05) depressed in VLCAD −/− mice compared to the other two groups. CONCLUSION The results indicate that VLCAD deficiency causes a reduction in cardiac function independent of the additional stress of exercise. Exercise did not significantly affect the hearts of either VLCAD −/− or LCAD −/− mice. Supported by a grant from the Arkansas Biosciences Institute." @default.
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- W2078491332 date "2005-05-01" @default.
- W2078491332 modified "2023-09-27" @default.
- W2078491332 title "Effect Of Exercise On Cardiac Function In Mice With LCAD And VLCAD Enzyme Deficiency" @default.
- W2078491332 doi "https://doi.org/10.1097/00005768-200505001-00493" @default.
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