An innovative model using human blood samples to study muscle protein growth may help advance scientists’ understanding of age-related muscle loss. The model is described in a study published in the American Journal of Physiology-Cell Physiology.
Age-related muscle loss, called sarcopenia, is a condition that can reduce quality of life and restrict independence as a person gets older. Lifestyle changes, such as decreased mobility, poor diet, hormonal fluctuation and increased inflammation in the body, may all play a role in the development of sarcopenia.
Studying the production and life cycle of muscle protein (muscle protein synthesis) in people can be expensive, difficult and sometimes invasive. However, finding new and easier methods for studying the causes of sarcopenia is critical to establish new treatments that could support muscle health and help improve healthspan—the length of time a person remains healthy in their life, a media release from the American Physiological Society explains.
Muscle Protein Synthesis and Signaling
Researchers from the University of Birmingham in the UK used myotubes—synthetic muscle—from mice to study muscle protein synthesis and signaling. They treated the cells with human blood donated by two groups of healthy male volunteers. One group was younger, with an average age of 26, and the other group was older, with an average age of 72. Some of the cells were also treated with the amino acid leucine to determine how cells responded to a growth-promoting stimulus.
The research team found the myotubes exposed to blood from older volunteers were smaller (indicating muscle loss), had impaired muscle protein synthesis and blunted signaling responses when compared to the cells treated with the younger volunteers’ blood, per the release.
“We have demonstrated here that there are many factors present in aged blood that impair pathways that regulate muscle cell size and may partly explain age-related muscle degeneration. Our next steps are to understand the factors in blood that may cause this response and to develop ways to reverse or prevent this.”
— Leigh Breen, PhD, corresponding author of the study
[Source(s): American Physiological Society, Newswise]