Muscle decline from inactivity can be countered by metformin, according to the RNF press service.
Skeletal muscles do more than help bodies move. They are central players in metabolism and energy balance. Muscles respond to how a person lives: regular training keeps them flexible, strength work increases size and power for lifting, and long stretches of rest lead to weakening and loss of mass. Bedridden patients and astronauts in weightless conditions feel this most acutely. Yet some animals pause movement for months during hibernation without severe muscle loss, which hints that a biological solution might be possible with the right approach.
A team led by Boris Shenkman at the Institute of Biomedical Problems of the Russian Academy of Sciences has explored a basic pathway to prevent muscle atrophy by addressing metabolic disturbances inside muscle cells. Atrophy arises when muscle protein creation and breakdown fall out of balance. During extended rest, cells burn far less fuel in the form of ATP, and the accumulation of AMP disrupts cellular function. This disruption is tied to a slowdown of AMP-activated protein kinase AMPK, a regulatory enzyme. When AMPK activity is low, muscles fail to sustain protein synthesis efficiently, accelerating atrophy. The researchers proposed activating AMPK with metformin, a drug already used to treat diabetes, to restore metabolic harmony in muscle tissue.
In their experiments, mice underwent a hind limb unloading protocol designed to simulate disuse. The animals were allowed to move freely in the cage and nourished normally, but their hind limbs were restrained, limiting load-bearing activity. The front claws remained active, creating a clear contrast between active and inactive muscles. The results showed a meaningful reduction in muscle loss when metformin was administered: a soleus muscle experienced about 21 percent mass loss with metformin versus 37 percent without it. Moreover, the treated mice retained greater muscle strength, with force production roughly one third higher than that seen in mice that endured disuse without the drug. These findings support the idea that metabolic modulation can blunt disuse atrophy by stabilizing the balance between protein synthesis and degradation in muscle tissue.
The authors envision potential benefits for people who face prolonged bed rest or limited mobility due to illness or disability. If these findings translate to humans, metformin could become part of a strategy to preserve muscle health during extended inactivity, reducing frailty and assisting recovery when activity resumes. More research will be needed to determine optimal dosing, timing, and safety in different populations, as well as to understand how this approach interacts with nutrition and exercise plans.
In related lines of inquiry, scientists continue to explore how metabolic regulators influence muscle aging and resilience. The pursuit of methods to maintain muscle mass under adverse conditions remains a priority for medicine and space biology alike, with the ultimate aim of keeping people strong and mobile no matter the circumstances.