overview: Studies have revealed that exercise is associated with muscle nuclear remodeling, which may contribute to the protective effects of exercise on muscle function throughout life.
sauce: King’s College London
Studies have shown that exercise is associated with changes in the nuclei of muscle fibers, which may contribute to the protective effects of exercise on muscle function throughout life.
The authors of this paper isolated single muscle fibers from young and elderly exercise-trained individuals from the School of Cardiovascular and Metabolic Medicine and Sciences and the Center for Human and Applied Physiological Sciences.
In particular, they used the organization of young marathon runners and older master cyclists. The latter he has the ability to cycle 100 km in less than 6.5 hours (average age he is 76).
Surprisingly, they discovered that muscle nuclei, commonly referred to as the “control centers” of muscle fibers, are more spherical, less deformable, and contain more of a protein called lamin A than in untrained individuals. Parallel studies in mice confirmed changes in lamin A, indicating that muscle nuclei become stiffer as a result of exercise.
write in Journal of PhysiologyThey concluded that exercise is associated with the remodeling of preserved muscle nuclei in older adults, which may contribute to the protective effects of exercise on muscle function throughout life.
Age-related declines in skeletal muscle function, such as strength and endurance, can lead to decreased quality of life. It is understood that exercise can mitigate the loss of muscle function, but the precise mechanisms that control this process are not fully understood.
Thus, characterizing exercise-associated intracellular changes may advance our understanding of how exercise can extend geriatric function.
Apart from housing the cell’s genome, the nucleus can sense and respond to physical forces. This changes the shape of the nucleus and activates cell communication pathways.
Defects in proteins that control nuclear mechanisms, such as Lamin A, are a hallmark of several diseases such as heart disease, muscular dystrophies and premature aging disorders.
Under these conditions, the nucleus is susceptible to deformation and deformation, resulting in abnormal cellular communication. However, it was previously unknown whether these specific traits are affected by aging or exercise.
The researchers speculated that the nuclei of muscle cells, called myonuclei, show abnormalities similar to laminitis in older people.
Dr. Matthew Stroud, Principal Investigator at Stroud Lab, said: Here, using both humans and mice, we have shown that changes in muscle nucleus shape and structure are strongly associated with exercise. “
As the gatekeeper of the genome, the nucleus governs cell fate and function, and the nuclear changes we observed may facilitate muscle adaptation to exercise. This can reduce age-related muscle dysfunction. “
Human lifespans have increased significantly over the past half century, and this trend is projected to continue. One concern, however, is that healthy life expectancy (the portion of a person’s life who is generally healthy) has not been extended commensurately in old age.
Instead, it resulted in longer morbidity and reduced independence and quality of life. The authors hope that elucidating the beneficial effects of exercise will guide therapeutics to improve healthy life expectancy in the growing aging population.
About this exercise, aging and muscle function research news
author: press office
sauce: King’s College London
contact: Press Office – King’s College London
image: image is public domain
See also
Original research: open access.
“Exercise-related myonuclear changes are independent of human age.” Matthew Stroud et al. Journal of Physiology
overview
Exercise-related myonuclear changes are independent of human age
The age-related decline in skeletal muscle structure and function can be mitigated by regular exercise. However, the exact mechanisms governing this are not fully understood. The nucleus plays an active role in transducing force into biochemical signals (mechanotransduction) using nuclear lamina proteins.
Lamin A regulates nuclear shape, nuclear dynamics, 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 exercise adaptation remains obscure.
Here, we have isolated single muscle fibers and performed detailed morphological and functional analyzes of muscle nuclei from exercise-trained young and aged individuals.
Strikingly, the muscle nuclei of trained individuals were more spherical, less deformable and contained thicker nuclear lamina than untrained individuals. Complementing this, exercise 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 throughout life.
