Summary: Study finds exercise is associated with myonuclear remodeling and may contribute to lifelong protective effects of exercise on muscle function.
Source: King’s College London
Research has shown 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 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 exercise-trained individuals.
In particular, they used fabrics from young marathon runners and elderly master cyclists – the latter able to cycle 100 km in less than 6.5 hours (with an average age of 76).
Surprisingly, they found that myonuclei – commonly referred to as muscle fiber “control centres” – were more spherical, less deformable and contained 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 following exercise.
Write in the Journal of Physiologythey concluded that exercise is associated with myonuclear remodeling, which is preserved in the elderly, 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 reduced quality of life. While it is recognized that exercise can attenuate muscle function decline, the precise mechanisms that control this process are not fully understood.
Characterizing exercise-associated subcellular changes may therefore improve our understanding of how exercise can extend functionality in old age.
In addition to housing the cell’s genome, the nucleus is able to sense and respond to physical forces, which can alter the shape of the nucleus and activate cellular communication pathways.
Defects in proteins that control nuclear mechanics, such as lamin A, are hallmarks of certain diseases, including heart disease, muscular dystrophy and premature aging disorders.
Under these conditions, the nuclei are misshapen and more deformable, with aberrant cell communication. However, it was not known whether these particular properties were affected by aging and exercise.
The researchers hypothesized that muscle cell nuclei, called myonuclei, would show abnormalities similar to laminopathies in aging people.
Stroud Lab Principal Investigator Dr. Matthew Stroud said: “While we know that exercise is able to overcome various detrimental 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 govern cell fate and function, and the nuclear alterations we observed may promote muscle adaptation to exercise. This may help alleviate muscle dysfunction as you age.
Human lifespan has increased dramatically 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 extension of lifespan – the part of a person’s life during which they are generally healthy – in old age.
Instead, morbidity was prolonged and independence and quality of life decreased. The authors hope that unraveling the beneficial effects of exercise can guide treatments to improve the health of our ever-expanding aging population.
About This Exercise, Aging, and Muscle Function Research
Author: Press office
Source: King’s College London
Contact: Press Office – King’s College London
Picture: Image is in public domain
See also
Original research: Free access.
“Exercise-Associated Myonuclear Alterations Are Independent of Age in Humans” by Matthew Stroud et al. Journal of Physiology
Summary
Exercise-associated myonuclear alterations are independent of age in humans
Age-related decline in skeletal muscle structure and function can be alleviated by regular exercise. However, the precise mechanisms that govern this are not fully understood. The nucleus plays an active role in translating forces into biochemical signals (mechanotransduction), with the nuclear lamina protein
Lamin A regulating nuclear shape, nuclear mechanics and ultimately gene expression. Defective expression of lamin A causes muscle pathologies and premature aging syndromes, but the roles of nuclear structure and function in physiological aging and in exercise adaptations remain unclear.
Here, we isolated single muscle fibers and performed detailed morphological and functional analyzes on myonuclei from young and older exercise-trained individuals.
Strikingly, the myonuclei of trained individuals were more spherical, less deformable, and contained a thicker nuclear lamina than untrained individuals. Complementing this, exercise resulted in increased lamin A levels and increased myonuclear stiffness in mice.
We conclude that exercise is associated with myonuclear remodeling, independent of age, which may contribute to the conservative effects of exercise on muscle function across the lifespan.