Myonuclear Loss, Rather Than Senescent Myonuclei, Associates With Fiber Type-Specific Atrophy In Aging Human Skeletal Muscle
As we age, many of us notice a decline in muscle strength and size, particularly in the muscles responsible for powerful, quick movements. This phenomenon, known as age-related muscle wasting or sarcopenia, has long been a subject of scientific investigation. A recent study sheds new light on the underlying mechanisms behind this decline, focusing on the tiny control centers within our muscle cells: the nuclei.
Muscle cells are unique because they contain multiple nuclei, called myonuclei, which are essential for maintaining the cell’s size and function. It was previously thought that an accumulation of ‘senescent’ myonuclei—nuclei that have stopped dividing and may contribute to cellular aging—could be a key factor in muscle wasting. However, this research suggests a different primary culprit.
The study compared muscle biopsies from younger and older adults, specifically looking at two main types of muscle fibers: Type I (slow-twitch, endurance-focused) and Type II (fast-twitch, power-focused). They observed a significant reduction in the size of fast-twitch (Type II) muscle fibers in older individuals, which aligns with common observations of age-related strength loss. Interestingly, the size of slow-twitch (Type I) fibers remained largely unchanged with age.
Crucially, the researchers found no difference in the number of senescent myonuclei between young and old adults, and these senescent nuclei were not linked to muscle fiber size. Instead, the study revealed a notable decrease in the total number of myonuclei within the fast-twitch muscle fibers of older adults. This loss of myonuclei was strongly associated with the shrinking of these muscle fibers.
These findings suggest that the age-related decline in fast-twitch muscle size is not primarily due to an increase in dysfunctional, senescent nuclei, but rather a reduction in the overall number of myonuclei available to support and maintain these larger, more powerful muscle fibers. This understanding could pave the way for new strategies to combat age-related muscle loss, focusing on preserving or increasing myonuclear content in fast-twitch muscle fibers.
Source: link to paper