Scientists recently found a molecule that can maintain, and even augment, the muscle mass and bone density of space-faring mice.
That might sound irrelevant (why would mice need to maintain muscle mass in space?), but this could actually help astronauts with a common problem with space travel. Astronauts in space must exercise regularly and intensely to avoid muscle atrophy; due to the microgravity, astronauts have little regular physical exertion and quickly lose muscle mass otherwise. Studies have shown that space journeys as brief as 5 to 11 days lead to a 20% loss of muscle mass for astronauts. The calf muscles, quadriceps, and back and neck muscles (which can be collectively termed antigravity muscles) require minimal contraction for astronauts to move around in space, allowing the muscles to weaken rapidly.
Muscle atrophy isn’t only a problem for astronauts, though. Others to benefit from this research could include “people who are bedridden or in a wheelchair, as well as people with cancer, chronic obstructive pulmonary disease or other causes of muscle wasting.”
The main focus of this study was the gene myostatin, common to various species, including mice, cattle, and humans. Myostatin plays a role in both the number of muscle fibers in the developing animal and the level of fiber growth in the adult stage, negatively regulating muscle growth in species from dogs to humans. Several studies have shown that myostatin inhibition can help with disorders that cause wasting of the muscles by increasing muscle mass. Some evidence even suggests that myostatin inhibition might increase muscle strength as well. This study, however, targeted a different cause of muscle atrophy.
Study author Se-Jin Lee eliminated the myostatin gene from mice, allowing them to achieve double the muscle mass of regular mice. In December 2019, the mice were launched on a SpaceX craft from Florida’s Kennedy Space Center for a 33 day space journey. In contrast to the normal mice, that lost muscle mass, the myostatin-inhibited mice maintained their augmented muscle mass.
Of course, eliminating the gene from human astronauts is not a feasible approach. To better model a treatment that could be applied to humans, Lee’s team came up with a solution to inhibit myostatin’s expression. Myostatin prohibits growth by attaching to a specific receptor on muscle cells. To prevent this binding, the researchers came up with a molecule that was a “decoy” receptor to be injected into the mice’s bloodstreams, capturing myostatin proteins and activin A proteins, which prevent both muscle and bone growth. The unique chemical structure and folding of the receptor allows it to bind to these two proteins for this effect, and as we learned in class, the shape is very important to the functionality. The mice in the International Space Station injected with this molecule experienced bone and muscle growth while still in space. The treatment also recovered bone and muscle mass for untreated mice landing from space.
Treatments inspired by this research could hopefully be used to help astronauts maintain bone density and muscle mass in space. Though myostatin inhibition alone has not proven effective in humans, such a treatment that inhibits other proteins, like activin A, as well may be plausible.