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2022 Fiscal Year Final Research Report

Role of hypoxia-sensitive neurons in promoting the exercise effects on bone with metabolic bone disorders

Research Project

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Project/Area Number 20K21764
Research Category

Grant-in-Aid for Challenging Research (Exploratory)

Allocation TypeMulti-year Fund
Review Section Medium-sized Section 59:Sports sciences, physical education, health sciences, and related fields
Research InstitutionNational Institute of Fitness and Sports in Kanoya

Principal Investigator

TAMAKI HIROYUKI  鹿屋体育大学, スポーツ生命科学系, 教授 (40253926)

Co-Investigator(Kenkyū-buntansha) 荻田 太  鹿屋体育大学, スポーツ生命科学系, 教授 (50224134)
Project Period (FY) 2020-07-30 – 2023-03-31
Keywords骨組織 / 神経 / マイクロCT
Outline of Final Research Achievements

Mechanical stimulation such as exercise is effective in maintaining bone mass, but its effect is diminished in bone tissue with metabolic abnormalities and/or in old age. To overcome this dilemma, we examined the osteogenic effects of low-intensity exercise under a hypoxic environment and investigated the role of hypoxia-sensitive neurons innervating bone tissue to maintain bone mass in diabetic aged rats. Low-intensity exercise (swimming) interventions under hypoxic conditions resulted in higher bone mass in the diabetic tibia than that under normoxic conditions. Second, pharmacological inhibition of hypoxia-sensitive neurons caused significant bone loss. Our results suggest that an external environment during exercise (hypoxic environment) that activates the neurons innervating bone tissue, even with low-intensity exercise stimulation, may enhance the effect of exercise on the maintenance of bone mass in metabolic abnormalities.

Free Research Field

体力科学

Academic Significance and Societal Importance of the Research Achievements

本研究は運動する外的環境を調整することでその効果の現れ方を最大限引き出そうとする取り組みであり、得られた結果は、骨代謝異常を有する骨組織において低酸素環境での有効性を示唆した。このことは高齢期や骨代謝異常であっても、力学的強度が低い運動でも骨量維持に有効であり、外的環境を工夫することで骨折リスクが高いケースでの運動処方にも活用できる可能性がある。またこの効果創出に骨内支配する酸素感受性神経が関連している可能性が示されたことは、神経系をターゲットとした新たな療法開発など各分野に波及するポテンシャルを有する。

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Published: 2024-01-30  

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