Molecular mechanisms of muscular stiffness and their application to human physiology

2014 Fiscal Year Final Research Report

• Project/Area Number: 24300221
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Sports science
• Research Institution: The University of Tokyo
• Principal Investigator: ISHII NAOKATA 東京大学, 総合文化研究科, 教授 (20151326)
• Co-Investigator(Kenkyū-buntansha): NAKAZATO Kouichi 日本体育大学, 保健医療学部, 教授 (00307993) ; SASAKI Kazushige 日本女子大学, 家政学部, 講師 (00451849) ; OCHI Eisuke 岡山大学, 教育学研究科(研究院), 講師 (90468778)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 筋スティフネス / 超音波剪断波 / 長さ－張力関係 / 長さ－スティフネス関係 / 伸張性収縮 / 短縮性収縮 / クロスブリッジ / 筋疲労

Outline of Final Research Achievements

Molecular mechanisms underlying active stiffness (AS) and passive stiffness (PS) of human skeletal muscle were investigated in vivo, by using supersonic shear-wave measurements. In isometric contractions, AS was proportional to both the activation level of muscle and the amount of overlap between thick and thin filaments. In isotonic contractions, the ratio between contractile force and AS (force/AS) was larger under the eccentric condition than under the concentric condition. Muscular fatigue caused changes in the relationship between AS and EMG amplitude apparently in a fiber type dependent fashion. Sustained muscular tone with low activation level caused a slight increase in PS, whereas repeated dynamic contractions caused a transient decrease in PS. These results suggest that muscular stiffness is mainly originated from interactions between actin and myosin and its quantification in vivo is useful to investigate the state of muscle during a variety of human movements.

Free Research Field

筋生理学