summary: The study revealed that exercise is associated with remodeling of the myofascial core 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 nucleus of muscle fibers and may contribute to the protective effects of exercise on muscle function across the lifespan.
The paper’s authors, from the College of Medicine and Cardiovascular and Metabolic Sciences and the Center for Human Physiological and Applied Sciences, isolated single muscle fibers from exercise-trained young and elderly individuals.
In particular, they used tissues from young marathon runners and older cyclists – with the latter able to cycle 100km in less than 6.5 hours (with an average age of 76).
Remarkably, they found that the myocytes — commonly referred to as the ‘control center’ of muscle fibers — were more spherical, less deformed, and contained more of a protein called lamin A than the untrained individuals. Parallel studies in rats confirmed changes in lamin A, and showed that muscle cores were stiffer as a result of exercise.
write in Journal of Physiologyconcluded that exercise is associated with myofascial remodeling, which is maintained in the elderly, 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 decreased quality of life. While it is known that exercise can mitigate the decline in muscle function, the exact mechanisms that control this process are not fully understood.
Characterizing exercise-related cellular changes may improve our understanding of how exercise extends functions in aging.
Apart from 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 nucleolar mechanisms, such as lamin A, are hallmarks of some diseases including heart disease, muscular dystrophy and disorders of premature aging.
In these conditions, the nuclei are distorted and more ductile, with anomalous cellular communication. However, whether these specific characteristics are affected by aging and exercise was not previously known.
The researchers speculated that the nuclei in the muscle cells, called myocytes, would show abnormalities similar to laminopathy in aging individuals.
Dr Matthew Stroud, Principal Investigator in Stroud’s lab, said: “While we know that exercise can counteract 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 the shape and structure of the nucleus in Muscles are closely related to exercise.”
As guardians of the genome, eukaryotes control cell fate and function, and the nuclear modifications we observed may enhance muscle adaptation to exercise. This may help alleviate muscle weakness with 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 associated with an equivalent extension of the healthy period – the part of a person’s life when they are generally healthy – into old age.
Instead, the duration of the disease is prolonged, and independence and quality of life diminished. The authors hope that revealing the beneficial effects of exercise may guide treatments to improve the health of our ever-growing population.
About that exercise, aging, and muscle function research news
Original search: open access.
“Exercise-related myoclonic alterations are age-independent in humansBy Matthew Stroud et al. Journal of Physiology
Exercise-related myoclonic alterations are age-independent in humans
Age-related decline in the structure and function of skeletal muscles can be mitigated by regular exercise. However, the exact mechanisms governing 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 regulates nuclear shape, nuclear mechanics, and ultimately gene expression. Defective lamin A expression causes muscle diseases and syndromes of premature aging, but the roles of nuclear structure and function in physiological aging and in athletic adaptations remain enigmatic.
Here, we isolated single muscle fibers and performed detailed morphological and functional analyzes on myofibrils from exercise-trained young and elderly individuals.
Remarkably, myogenic cores from trained individuals were more spherical, less deformed, and contained a thicker nuclear lamina than untrained individuals. Complementary to this, exercise led to increased levels of lamin A and increased stiffness of myofibrils in rats.
We conclude that exercise is associated with remodeling of the myofascial cores, regardless of age, which may contribute to the protective effects of exercise on muscle function across the lifespan.