Overview: Study reveals exercise is associated with myonuclear remodeling and may contribute to exercise’s protective effects on muscle function throughout life.
Source: King’s College London
Research has shown that exercise is associated with core changes in muscle fibers and may contribute to the protective effects of exercise on muscle function throughout life.
The authors of the paper, from the School of Cardiovascular and Metabolic Medicine & Sciences and the Center for Human & Applied Physiological Sciences, isolated single muscle fibers from young and older trained individuals.
In particular, they used tissue from young marathon runners and older master cyclists, the latter being able to cycle 100 km in less than 6.5 hours (with an average age of 76).
Strikingly, they found that myonuclei—commonly referred to as the “control center” of muscle fibers—are more bulbous, less malleable, and contain more of a protein called lamin A than untrained individuals. Parallel studies in mice confirmed changes in lamin A and showed that myonuclei were stiffer as a result of exercise.
Write in the Journal of Physiologythey concluded that exercise is associated with myonuclear remodeling, which is preserved in older people, and may contribute to the protective effects of exercise on muscle function throughout life.
Age-related decline in skeletal muscle function, such as muscle strength and endurance, can lead to a reduced quality of life. While it is clear that exercise can reduce the decline in muscle function, the precise mechanisms controlling this process are not fully understood.
Characterizing the subcellular changes associated with exercise may therefore improve our understanding of how exercise can increase functionality in old age.
Aside from housing the genome of the cell, the nucleus is capable of sensing and responding to physical forces, which can change the shape of the nucleus and activate cell communication pathways.
Defects in proteins that control the mechanics of nuclei, such as lamin A, are hallmarks of some diseases, including heart disease, muscular dystrophy and premature aging disorders.
Under these conditions, nuclei are misshapen and more deformable, with aberrant cell communication. However, whether these specific traits are affected by aging and exercise was previously unknown.
The researchers speculated that nuclei in muscle cells called myonuclei would show similar abnormalities to laminopathies in aging individuals.
Dr. Matthew Stroud, lead researcher at the Stroud Lab, said: “While we know that exercise can overcome several adverse aspects of the aging process, our molecular understanding of this is incomplete. Here we used both humans and mice to show that changes in core shape and structure in muscles are strongly associated with exercise.”
As gatekeepers of the genome, nuclei determine cell fate and function, and the nuclear changes we observed may promote muscle adaptation to exercise. This may help reduce muscle dysfunction with age.”
Human lifespan has increased significantly over the past half century and this trend is expected to continue. A concern, however, is that this has not been accompanied by an equivalent extension of the health span – the part of a person’s life in which they are generally in good health – in old age.
Instead, morbidity has increased and independence and quality of life have decreased. The authors hope that unraveling the beneficial effects of exercise can guide treatments to improve the health of our increasingly aging population.
About this news about exercise, aging and muscle function research
Writer: Press Office
Source: King’s College London
Contact: Press Service – King’s College London
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Original research: Open access.
“Myonuclear changes associated with exercise are independent of age in humans” by Matthew Stroud et al. Journal of Physiology
Myonuclear changes associated with exercise are independent of age in humans
Age-related decline in skeletal muscle structure and function can be mitigated by regular exercise. However, the precise mechanisms governing this are not fully understood. The nucleus plays an active role in translating forces into biochemical signals (mechanotransduction), with nuclear lamina protein
Lamin A regulatory nuclear form, nuclear mechanics and ultimately gene expression. Defective Lamin A expression causes muscle pathologies and premature aging syndromes, but the role of nuclear structure and function in physiological aging and in exercise adaptation remains unclear.
Here we isolated single muscle fibers and performed detailed morphological and functional analyzes on myonuclei from young and older trained individuals.
Strikingly, myonuclei from trained individuals were more spherical, less deformable, and contained a thicker nuclear lamina than untrained individuals. In addition to this, exercise resulted in increased levels of Lamin A and increased myonuclear stiffness in mice.
We conclude that exercise is associated with myonuclear remodeling independent of age, which may contribute to the preservative effects of exercise on muscle function throughout life.