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How exercise can moderate the age-related decline in skeletal muscle structure and function

How exercise can moderate the age-related decline in skeletal muscle structure and function

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Summary: The study revealed that exercise is associated with myonuclear remodeling and may contribute to the protective effects of exercise on muscle function across the lifespan.

source: King’s College London

Research has found that exercise is associated with changes in the core of muscle fibers and may contribute to the protective effects of exercise on muscle function throughout life.

The paper’s authors, from the School of Cardiovascular and Metabolic Medicine and Sciences and the Center for Human and Applied Physiological Sciences, isolated single muscle fibers from young and older trained individuals.

In particular, they used tissue from young marathoners and elderly master cyclists – the latter capable of cycling 100km in under 6.5 hours (with an average age of 76).

Surprisingly, they found that the myonuclei – commonly referred to as the “control center” of muscle fibers – were more spherical, less deformable and contained more of a protein called lamin A than untrained individuals. Parallel studies in mice confirmed the changes in lamin A and showed that myonuclei were stiffer as a result of exercise.

Writing in Journal of Physiologythey concluded that exercise is associated with myonuclear remodeling that persists in older adults and may contribute to the protective effects of exercise on muscle function across the lifespan.

Age-related decline in skeletal muscle function, such as muscle strength and endurance, can lead to reduced quality of life. Although it is appreciated that exercise can mitigate the decline in muscle function, the exact mechanisms that control this process are not fully understood.

Therefore, characterizing the subcellular changes associated with exercise may improve our understanding of how exercise may enhance functionality in old age.

In addition to containing the cell’s genome, the nucleus is capable of sensing and responding to physical forces that can change the shape of the nucleus and activate cellular communication pathways.

Defects in proteins that control nuclear mechanics, such as lamin A, are hallmarks of some diseases, including heart disease, muscular dystrophy, and premature aging disorders.

Under these conditions, nuclei are deformed and more deformable, with aberrant cell communication. However, whether these specific properties are affected by aging and exercise was until now unknown.

The researchers speculated that nuclei in muscle cells, called myonuclei, would show similar abnormalities to laminopathies in aging individuals.

Dr Matthew Stroud, Principal Investigator of the Straud Lab, said: ‘Although we know that exercise is able to reverse various harmful aspects of the aging process, our molecular understanding of this is incomplete. Here, we used both humans and mice to show that changes in muscle core shape and structure are strongly associated with exercise.

Age-related decline in skeletal muscle function, such as muscle strength and endurance, can lead to reduced quality of life. Image is in the public domain

As guardians of the genome, nuclei govern cell fate and function, and the nuclear changes we observed may promote muscle adaptation to exercise. This may help mitigate muscle dysfunction with age.”

Human life expectancy has increased significantly over the past half century and this trend is expected to continue. One concern, however, is that this has not been accompanied by an equivalent increase in health expectancy – the portion of a person’s life when they are generally in good health – in old age.

Instead, morbidity is increased and independence and quality of life are reduced. The authors hope that unraveling the beneficial effects of exercise can guide treatments to improve the health status of our ever-growing aging population.

About this exercise, aging and muscle function research news

Author: Press office
source: King’s College London
Contact: Press Office – King’s College London
Image: Image is in the public domain

See also

How exercise can moderate the age-related decline in skeletal muscle structure and function

Original research: Free access.
Exercise-related myonuclear changes are independent of age in humans” by Matthew Stroud et al. Journal of Physiology


Summary

Exercise-related myonuclear changes are independent of age in humans

Age-related decline in skeletal muscle structure and function can be mitigated by regular exercise. However, the exact mechanisms that govern this are not fully understood. The nucleus plays an active role in converting forces into biochemical signals (mechanotransduction), with nuclear lamina protein

Lamin A regulating nuclear shape, nuclear mechanics, and ultimately gene expression. Defective Lamin A expression causes muscle pathologies and premature aging syndromes, but the roles of nuclear structure and function in physiological aging and in adaptations to exercise remain unclear.

Here, we isolated single muscle fibers and performed detailed morphological and functional analyzes of myonuclei from young and older exercise-trained individuals.

Strikingly, myonuclei from trained individuals were more spherical, less deformable, and contained a thicker nuclear lamina than untrained individuals. In addition, exercise resulted in increased levels of Lamin A and increased myonuclear stiffness in mice.

We conclude that exercise is associated with age-independent myonuclear remodeling, which may contribute to the conservative effects of exercise on muscle function across the lifespan.


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