Muscle is often seen as a visible marker of fitness and strength, but it is also one of the most important organs for longevity. It helps your body with blood sugar control1, circulation, and bone health2, and that's not even mentioning all of the lifting, carrying, and mobility that strong muscles enable.
Yet muscle loss is one of the most common, and most accepted, realities of getting older. Muscle mass can decline about 8% per decade after you turn 30 if you don't actively work to support it, but most people consider it inevitable with aging and move on.
But a growing body of research suggests the story of muscle loss is more nuanced than most people realize. It's not that you are just losing muscle, but the muscles are actually losing the ability to repair themselves. The internal signal telling your muscles to start repairing gets chemically "rusted" over time.
Luckily, researchers at Kyushu University have identified a compound that might be able to protect and enhance that signal.
Why your muscles need a repair signal
Muscle is remarkably good at healing itself, but only when it's systems are working properly. At the center of that repair system is a protein called hepatocyte growth factor, or HGF, which acts as a kind of wake-up call for your muscle's built-in repair crew.
In healthy muscle, HGF sits in the supportive tissue surrounding muscle fibers. When muscle is injured or put under physical stress, HGF gets released and travels to specialized stem cells embedded in the muscle tissue. Once it docks with those stem cells, it activates them, prompting them to multiply, mature, and get to work repairing damaged fibers.
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The rusted key problem
According to the study, the issue with aging muscle isn't that HGF disappears. Instead, HGF undergoes a chemical change, a process called nitration, that alters the part of the protein responsible for docking with muscle stem cells.
Picture HGF as a key that fits a specific lock perfectly. Nitration causes corrosion to build up on the teeth of that key. The key is still there, but it no longer fits.
The same goes for HGF—it still exists in the muscle, but it can't properly fit into the stem cell and activate the repair signal. When this process stalls, the fibers in your muscles begin to weaken, scar tissue and fat accumulates, and the fast-twitch fibers that power quick, forceful movements slow down.
Enter LASSS
The Kyushu University research team wanted find a compound that could either prevent this chemical damage, or at least compensate for it. They focused on two sulfur-based molecules known for their antioxidant properties: glutathione trisulfide (GSSSG) and lipoic acid trisulfide (LASSS). Both belong to a class of compounds called trisulfides, which have attracted recent interest for their unusual chemistry and potential therapeutic applications.
In early experiments, both compounds reduced the chemical damage to HGF. Restoring the protein's ability to bind to muscle stem cells proved more difficult, until the researchers adjusted the ratio of HGF to trisulfide in their experiments.
At a higher concentration, something unexpected happened with LASSS.
Rather than simply protecting HGF from damage, LASSS appeared to enhance it. When combined with a larger amount of LASSS, HGF's ability to bind to muscle stem cells increased more than two-fold compared with untreated HGF, and became more resistant to the chemical damage that normally impairs it. GSSSG showed no such effect.
The researchers believe LASSS may interact directly with HGF and induce a subtle structural change, effectively creating a more powerful and resilient form of the protein. The the team described it as a "Super HGF," because it wasn't just a partial restoration of function. It was a full-on upgrade.
From the lab to living tissue
To see whether the effect held up outside of a controlled lab setting, the team tested LASSS in a mouse model of muscle atrophy. Mice pretreated with LASSS showed significantly less chemical damage to HGF compared with untreated animals. GSSSG, again, showed no protective effect.
Studies like this are often first conducted in mice because they share over 95% of their genes with humans and are much easier to manipulate and observe. Further studies need to be conducted in aging animals and eventually humans to confirm if LASSS is safe and effective over time, but the mouse model provides encouraging evidence that LASSS's effects aren't limited to test tubes.
What this means for muscle health and aging
Muscle loss with age affects a significant portion of older adults and is closely linked to reduced independence, increased fall risk, and lower quality of life. Most current approaches focus on resistance training and protein intake, which are undoubtedly important, but research like this points to a molecular layer of the problem that these lifestyle interventions alone may not fully address.
If LASSS or similar compounds can be developed into safe, effective therapies, they could offer a new tool for preserving muscle repair capacity during aging, prolonged bed rest, or other conditions that accelerate muscle decline. The researchers also note that HGF's role in muscle repair is likely conserved across species, meaning the findings could eventually benefit companion animals like cats and dogs as well.
The takeaway
This research is brand new, and while this compound won't be available at your pharmacy any time soon, the mechanism it highlights is important for understanding age-related muscle loss.
The assumptions has been that muscles wear out over time, but it may actually be a matter of a repair signal being chemically blocked so it can no longer do its job. The discovery that a compound can not only protect that signal but amplify it opens a whole new world of ways to preserve muscle strength and function later in life.
For now, the most evidence-backed strategies for maintaining muscle as you age remain consistent: prioritize resistance training, eat enough protein, and stay active. If you want to dig even deeper, check out our guide on the best nutrients to help fight muscle loss as you age.
