| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Research Abstract |
The purpose of this study was to examine the hypothesis that signaling molecules AMPKwould mediate the acute exercise-induced expression of monocarboxylate transporters MCT1and MCT4 in skeletal muscle. The male SD rats were subjected to a bout of high-intensityintermittent swimming (HIS) or low-intensity prolonged swimming exercise (LIS). AMPKphosphorylation was increased in response to LIS and HIS in exercised muscle. MCT1 andMCT4 mRNA were transiently upregulated by HIS and LIS. MCT1 protein was increased afterLIS, but MCT4 protein was increased after HIS, while no changes in MCT1 protein wereobserved. Direct exposure of epitrochlearis to 0.5mM 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR) or 1mM caffeine increased both MCT1 and MCT4 mRNA but notMCT1 and MCT4 protein. When 1mM caffeine-induced pAMPK was inhibited by dantrolene,neither MCT1 nor MCT4 mRNA was increased. The present findings suggest that acute exercisemay upregulate MCT1 and MCT4 mRNA expression thrg-mediated pathway in skeletalmuscle.
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