1998 Fiscal Year Final Research Report Summary
Reduction of Preserved Capacity for Skeletal Muscle with Aging and Effect of Exercise
| Project/Area Number |
09680101
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
体育学
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
ISHIHARA Akihiko Fac.Int.Human Stud., Kyoto Univ., Assoc.Prof., 総合人間学部, 助教授 (90184548)
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| Project Period (FY) |
1997 – 1998
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| Keywords | Aging / Exercise Training / Preserved Capacity / Skeletal Muscle |
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| Research Abstract |
Program-1
A voluntary running wheel in which a known load can be added electronically was developed. A voluntary exercise with an additional load resulted in fiber hypertrophy which was proportional to the average running distance. In addition, a recruitment of all motor unit type was induced during loaded-running exercise since fiber hypertrophy was observed in all fiber types in the muscle.
Program-2
The age-related changes in the number and SDH activity of muscle fibers and motoneurons of the tibialis anterior and soleus were studied using 1 0-, 60-, and 120-week-old rats. The number of fast-twitch muscle fibers was decreased at 60 weeks of age, while the number of slow-twitch muscle fibers and alpha motoneurons was decreased at 1 20 weeks of age. In addition, SDH activity of large alpha motoneurons was decreased at 1 20 weeks of age. Therefore, the degenerative process of muscle fibers differs between the fast- and slow-twitch muscles.
Program-3
Forty-week-old rats exercised voluntarily in running wheels with increasing loads for 20 weeks. There were fewer FOG fibers in the soleus muscle, and fewer FG fibers in the tibialis anterior muscle at 60 weeks than at 20 weeks of age. The cross-sectional area of FOG and FG fibers in the tibialis anterior muscle was lower at 60 weeks than at 20 weeks of age. Exercise prevented atrophy of FOG fibers in the tibialis anterior muscle. These findings suggest that exercise can prevent the atrophy of FOG fibers by restoring their decreased metabolic capacity, and by inhibiting the degeneration of neuromuscular junctions.
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