| Project/Area Number |
24800074
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Sports science
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| Research Institution | Doshisha University |
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Principal Investigator |
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| Project Period (FY) |
2010 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 持久的トレーニング / ミオグロビン / 転写因子 / 筋組織 / ミトコンドリア / 持久性トレーニング / 骨格筋 / シグナル伝達 |
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| Research Abstract |
Endurance exercise training (eTR) improves muscle oxidative capacity via an increase in both mitochondrial protein and myoglobin (Mb). Overexpression of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) increases Mb expression in skeletal muscle. Knockout of PGC-1α, however, does not attenuate eTR-induced increase in Mb expression. Therefore, it is controversial how PGC-1α is involved in eTR-induced increase in Mb expression in skeletal muscle. The purpose of this study was to verify whether an increase in PGC-1α expression in skeletal muscle is required for the eTR-induced increase in Mb expression. Timing of increase in Mb expression due to eTR was different from that of mitochondria protein (COX IV). PGC-1α expression did not show any significant differences during the training protocol in this study. Moreover, the PGC-1α mRNA knockdown by siRNA transfection did not attenuate Mb mRNA expression in C2C12 cells. In conclusion, PGC-1α is not essential for the eTR-induced increase in Mb expression in skeletal muscle.
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