| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2003: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2002: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Research Abstract |
The purpose of this study was to elucidate the mechanisms underlying low-intensity-exercise-induced peroxisome proliferator-activated receptor γ coactivator-1 α (PGC-1 α) protein expression in rat skeletal muscles. Rats (5-6-week-old) swam without a load and ran on the treadmill at a speed of 13 m/min, respectively, in two 3-h sessions separated by 45 min of rest. PGC-1 α content in epitrochlearis muscle (EPI) was increased by 75 % and 95 %, immediately and 6-h post-swimming, respectively, with no increase in PGC-1 α content in the soleus (SOL). After running, PGC-1 α content in EPI was unchanged, while a 107 % increase in PGC- 1 α content was observed in SOL 6-h post-running. Furthermore, in EPI and SOL as well as other muscles (triceps, plantaris, red and white gastrocnemius), PGC-1 α expression was enhanced concomitant with reduced glycogen post-exercise, suggesting that expression of PGC-1 α occurs in skeletal muscle recruited during exercise.
Six-hour after in vitro electrical stimulation, mRNA of PGC-1 α increased in epitrochlearis muscle dissected from sedentary rat. PGC-1 α content in EPI was increased after 18-h in vitro incubation with 0.5 mM 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) and 4 mM caffeine. However, AICAR incubation did not affect PGC-1 α content in the SOL, while PGC-1 α content in the SOL was increased after caffeine incubation. These results suggest that exercise-induced PGC-1 α expression in skeletal muscle may mediated by at least two exercise-induced signaling factors : AMPK activation and Ca2+ elevation. The number of factors involved (both AMPK and Ca2+, or Ca2+ only) in exercise-induced PGC-1 α expression may differ among muscles.
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