2023 Fiscal Year Final Research Report
Does stimulation to stop exercise improve muscle function?
Project/Area Number |
21K19722
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Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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Allocation Type | Multi-year Fund |
Review Section |
Medium-sized Section 59:Sports sciences, physical education, health sciences, and related fields
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Research Institution | Oita University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
伊東 佑太 名古屋学院大学, リハビリテーション学部, 准教授 (30454383)
紀 瑞成 大分大学, 福祉健康科学部, 准教授 (60305034)
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Project Period (FY) |
2021-07-09 – 2024-03-31
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Keywords | 骨格筋 / 筋機能 / オートファジー / マウス |
Outline of Final Research Achievements |
The purpose of this study was to determine the effect of autophagy, which is activated immediately after exercise cessation, on exercise-induced improvement of muscle function. We used muscle atrophy and aging models for this purpose. The exercise load model of our experiments did not show the same results as occur in cultured cells. We conclude that the cause is related to the amount and duration of exercise load. If this phenomenon is clarified in animals, it will lead to the development of new exercise therapies that are effective for patients with muscle atrophy and for the elderly.
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Free Research Field |
基礎理学療法学
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Academic Significance and Societal Importance of the Research Achievements |
筋肥大に至適とされる高強度の運動は,高齢者や疾患を対象とするリハビリテーションにおいては現実的でない.また,実際の臨床現場では,筋肥大が望めない低強度の負荷で運動処方を行うことが多い.この低強度運動において,筋肥大はみられなくとも筋出力は向上するという“不思議”な現象を多くの療法士が経験する.我々が明らかにしたトリ培養筋管細胞の収縮運動で,収縮運動停止直後数時間でおこるオートファジー活性化による筋細胞内のクリアランスがカギとなると考えられる.本現象とメカニズムが明らかになれば,筋萎縮の患者や高齢者に対して有効な,新たな運動療法の開発につながると考える.
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