Muscles are made to move. Stretching and contraction stimulate biochemical pathways within muscle that maintain tissue health. When movement slows—when a broken limb is immobilized in a cast, for example, or in old age—unstimulated muscle wastes away.
See “How Muscles Age, and How Exercise Can Slow It”
Now, researchers at Harvard University have built a mechanical implant that prompts muscle contraction and could help to slow this atrophy. Known as MAGENTA (mechanically active gel-elastomer-nitinol tissue adhesive), the experimental device prevents muscle wasting in animals, the team reports.
It’s an “exciting advance” for treating people for whom activity is not possible, such as intensive care patients, who can experience atrophy in as little as 24 hours, says Fabrisia Ambrosio, a stem cell biologist in physical medicine and rehabilitation at Harvard University who was not involved in the study.
The team also aims to scale up the device from a few millimeters to several centimeters to fit around human muscle.
MAGENTA’s core consists of a spring made of nitinol, a shape-memory alloy that shortens when heated to a specific temperature. The metal is encased in a rectangular box made of flexible plastic, which provides insulation and resistance that lengthens the spring. A biocompatible glue welds the device directly onto the muscle tissue.
The tool is designed to be surgically implanted and activated by an external battery, which intermittently discharges an electrical current to induce short cycles of contraction and relaxation. As the metal heats up, it shortens and causes the muscle to contract with it. When the electricity stops, the spring lengthens, relaxing the muscle fibers.
When the researchers tested the device in a mouse’s hind leg, they found that it exerted a similar force on the muscle to that achieved during exercise. Next, they implanted it into the hind legs of mice and immobilized the leg in a tiny cast for two weeks. While untreated mice and mice with an inactive version of the implant showed significant muscle atrophy, rodents treated with MAGENTA experienced little wasting despite being unable to move their leg. Analysis of the treated tissue revealed that the device activates the same biochemical pathways activated by movement, boosting the protein synthesis needed to maintain muscle.
In the absence of an external battery, the device can also be activated remotely by shining a laser through the skin. In mice, this approach was less effective than electrical activation, and it would likely be even less so in people, as we have a thicker dermis, says study coauthor Sungmin Nam, a bioengineer at Harvard’s Wyss Institute. But he hopes to improve this laser activation to avoid the need for wires and bulky equipment.
The team also aims to scale up the device from a few millimeters to several centimeters to fit around human muscle. But Jonathan Rossiter, a robotics engineer at the University of Bristol in the UK who was not involved in the work, notes that larger devices would generate more heat, which “must be managed to avoid damaging muscle tissues.”
MAGENTA is a creative way of putting already available materials together to solve an “important clinical problem,” says Harvard University bioengineer Subramanian Sundaram, who was not involved in the study. But the big drawback is that it requires surgery, which for some patients may be a deal breaker, he says.