MELBOURNE, Nov. 5 (Xinhua) -- Lacking a common protein may affect how muscles respond to testosterone, potentially affecting athletic performance and age-related muscle loss, according to a new study led by an Australian research institute.
The research has uncovered a surprising link between ACTN3, the gene for speed, and the body's response to testosterone, the hormone that helps maintain muscle mass, according to a statement released Wednesday by Australia's Murdoch Children's Research Institute (MCRI).
The α-actinin-3 protein is found in muscles important for explosive activities. About one in five people lack this protein due to a variation in the ACTN3 gene, said the study published in Science Advances.
The research showed this genetic variation reduced levels of the androgen receptor in muscle tissue in both men and women, impacting how muscles grow or shrink in response to testosterone, said MCRI Senior Research Officer Jane Seto.
"This gene has long been associated with elite sprinting ability, but we're now seeing it plays a much broader role in muscle biology. It's not just about speed but about how your muscles respond to testosterone," Seto said.
The study, using both mouse models and human samples, found that missing the α‑actinin‑3 protein worsened muscle loss in male mice when testosterone was blocked, and blunted muscle growth in female mice treated with supplementary testosterone during puberty.
Researchers identified seven key genes that appear to drive this effect, as they are sensitive to testosterone and depend on the α-actinin-3 protein for proper expression. These genes influence important cell processes such as breaking down amino acids, cleaning out damaged cells and regenerating newer, healthier ones and producing energy in mitochondria, the study said.
Seto said the findings could explain why some people lose muscle more rapidly with age or illness, or respond to testosterone-based therapies differently, and suggest this protein as a potential target for treatments preserving muscle mass. ■
