Single muscle fibre contractile function with ageing.
Single muscle fibre contractile function with ageing.
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DOI：
10.1113/jp282298
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发表时间：
2022-12
影响因子：
5.5
通讯作者：
Sundberg, Christopher W.
中科院分区：
文献类型：
--
作者：
Grosicki, Gregory J.;Zepeda, Carlos S.;Sundberg, Christopher W.
Ageing is accompanied by decrements in the size and function of skeletal muscle that compromises independence and quality of life in older adults. Developing therapeutic strategies to ameliorate these changes is critical but requires an in-depth mechanistic understanding of the underlying physiology. Over the past 25 years, studies on the contractile mechanics of isolated human muscle fibres have been instrumental in facilitating our understanding of the cellular mechanisms contributing to age-related skeletal muscle dysfunction. The purpose of this review is to characterize the changes that occur in single muscle fibre size and contractile function with ageing and identify key areas for future research. Surprisingly, most studies observe that the size and contractile function of fibres expressing slow myosin heavy chain (MHC) I are well-preserved with ageing. In contrast, there are profound age-related decrements in the size and contractile function of the fibres expressing the MHC II isoforms. Notably, lifelong aerobic exercise training is unable to prevent most of the decrements in fast fibre contractile function, which have been implicated as a primary mechanism for the age-related loss in whole-muscle power output. These findings reveal a critical need to investigate the effectiveness of other nutritional, pharmaceutical, or exercise strategies, such as lifelong resistance training, to preserve fast fibre size and function with ageing. Moreover, integrating single fibre contractile mechanics with the molecular profile and other parameters important to contractile function (e.g., phosphorylation of regulatory proteins, innervation status, mitochondrial function, fibre economy) is necessary to comprehensively understand the ageing skeletal muscle phenotype. Advancing age is accompanied by decrements in whole-muscle strength and power that exceed the losses in muscle mass. The single fibre preparation has been instrumental in facilitating our understanding of the cellular mechanisms contributing to this phenomenon. Surprisingly, and at odds with some of the earlier findings, both size and contractile function (force, power, shortening velocity, Ca2+ sensitivity, and rates of force development [RFD]) of the MHC I fibres appear well-preserved with ageing. In contrast, several studies observe profound age-related decrements in function – namely force and power – of the MHC II fibres. The decrements in MHC II fibre function are primarily attributable to fibre atrophy, rather than age-related alterations in the intrinsic contractile mechanics, per se. Since MHC II fibres can generate greater force and power than MHC I fibres, these findings implicate fast fibre atrophy as an important therapeutic target for attenuating age-related decrements in whole-muscle strength and power.
Ageing is accompanied by decrements in the size and function of skeletal muscle that compromises independence and quality of life in older adults. Developing therapeutic strategies to ameliorate these changes is critical but requires an in-depth mechanistic understanding of the underlying physiology. Over the past 25 years, studies on the contractile mechanics of isolated human muscle fibres have been instrumental in facilitating our understanding of the cellular mechanisms contributing to age-related skeletal muscle dysfunction. The purpose of this review is to characterize the changes that occur in single muscle fibre size and contractile function with ageing and identify key areas for future research. Surprisingly, most studies observe that the size and contractile function of fibres expressing slow myosin heavy chain (MHC) I are well-preserved with ageing. In contrast, there are profound age-related decrements in the size and contractile function of the fibres expressing the MHC II isoforms. Notably, lifelong aerobic exercise training is unable to prevent most of the decrements in fast fibre contractile function, which have been implicated as a primary mechanism for the age-related loss in whole-muscle power output. These findings reveal a critical need to investigate the effectiveness of other nutritional, pharmaceutical, or exercise strategies, such as lifelong resistance training, to preserve fast fibre size and function with ageing. Moreover, integrating single fibre contractile mechanics with the molecular profile and other parameters important to contractile function (e.g., phosphorylation of regulatory proteins, innervation status, mitochondrial function, fibre economy) is necessary to comprehensively understand the ageing skeletal muscle phenotype. Advancing age is accompanied by decrements in whole-muscle strength and power that exceed the losses in muscle mass. The single fibre preparation has been instrumental in facilitating our understanding of the cellular mechanisms contributing to this phenomenon. Surprisingly, and at odds with some of the earlier findings, both size and contractile function (force, power, shortening velocity, Ca2+ sensitivity, and rates of force development [RFD]) of the MHC I fibres appear well-preserved with ageing. In contrast, several studies observe profound age-related decrements in function – namely force and power – of the MHC II fibres. The decrements in MHC II fibre function are primarily attributable to fibre atrophy, rather than age-related alterations in the intrinsic contractile mechanics, per se. Since MHC II fibres can generate greater force and power than MHC I fibres, these findings implicate fast fibre atrophy as an important therapeutic target for attenuating age-related decrements in whole-muscle strength and power.