New Signaling Pathway Between Muscles and the Brain Influences Reproductive Hormones

According to research, a newly discovered communication pathway between the body’s muscles and the pituitary gland may play an unexpected role in female fertility. Scientists at McGill University found that a protein produced in the muscles regulates the release of a hormone produced in the pea-sized gland at the base of the brain. The findings, published in Science, could lead to new treatment options for infertility, according to the researchers. “Until now, it was not known that these two organs communicate with each other or how they do so,” said lead author Daniel Bernard, a professor at McGill University’s Department of Pharmacology and Therapeutics. “This discovery opens a new chapter in our understanding of the body and its complex connections.”

How Muscle Building Could Backfire

The pituitary hormone studied, known as follicle-stimulating hormone (FSH), promotes the maturation of egg cells in the ovaries. A deficiency can lead to infertility. Myostatin is a protein produced naturally by the body that plays a central role in controlling muscle growth and development. It belongs to the family of so-called TGF-β signaling proteins (Transforming Growth Factor Beta), which regulate numerous processes in the body—from cell growth and differentiation to tissue repair. Myostatin acts as the body’s natural brake on muscle growth. It thus ensures that muscles do not grow uncontrollably. The experiments on mice yielded particularly insightful results. When myostatin levels were artificially lowered—which leads to increased muscle growth—there was a simultaneous delay in puberty as well as impaired fertility. This observation suggests that a certain balance is necessary: too little myostatin may promote muscle growth, but at the same time it can throw the hormonal system out of sync. Conversely, restoring normal myostatin levels led to an increase in FSH levels, which is considered evidence that this signaling pathway is indeed functionally relevant. Whether this can also fully normalize fertility, however, remains the subject of further investigation.

Drugs designed to block myostatin to build muscle are being developed to treat conditions such as muscular dystrophy. Pharmaceutical companies are also testing whether blocking myostatin can help preserve muscle mass in people taking GLP-1 receptor drugs for weight loss, such as Ozempic, which can lead to both fat and muscle loss. However, this study raises concerns about the potential health risks of myostatin blockade.

Results May be Applicable to Humans in the Future

“We found that experimental drugs for treating muscle-wasting diseases lowered FSH levels in female mice. While these drugs may effectively promote muscle growth, there is a risk of disrupting reproductive hormones and fertility,” said first author Luisina Ongaro, a research associate in Daniel Bernard’s lab. The breakthrough also opens up the possibility of investigating whether natural fluctuations in myostatin levels could explain the timing of puberty, missed periods in female athletes, and infertility with no apparent cause.

In the future, the researchers plan to test whether their findings in mice can also be applied to humans—a prospect they describe as promising. Overall, this research demonstrates how closely interconnected various systems in the body are. Muscles, which were long viewed primarily as mechanical structures, are increasingly proving to be active players in the hormonal network. If this newly discovered communication pathway is confirmed in humans, it could not only explain certain risks but also enable new therapeutic approaches—such as targeted treatments for fertility disorders that have not yet been sufficiently understood.