The “love hormone” does more than trigger labor and cement emotional ties between people. Oxytocin also helps repair damaged muscles, at least in mice.
Oxytocin stimulates muscle stem cells to divide when muscle is damaged, researchers report June 10 in Nature Communications. Experiments with mice also showed that the hormone’s levels in the animals’ blood declines with age. Giving old mice shots of oxytocin restored their muscle-regeneration capabilities to match those of much younger rodents. But extra doses of the hormone did not boost muscle-building in young mice.
“This is not a performance-enhancing drug,” says study coauthor Irina Conboy, a stem cell scientist at the University of California, Berkeley.
The findings raise the possibility that oxytocin may stave off muscle atrophy in aging people.
“It is a possible new avenue for therapy,” says Kristian Gundersen, a physiologist at the University of Oslo, who was not involved in the new work. “But there is still a lot to do before we can recommend this as a drug.”
The work grew from studies in which scientists tethered the circulatory systems of young and old mice. Something in the blood of young mice rejuvenated their aging counterparts. Scientists recently described substances in the young mice’s blood that benefit old brains (SN: 5/31/14, p. 8), but old organs and muscle perked up, too. Conboy and her colleagues went looking for molecules that influence muscle repair.
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They knew that muscle stem cells contain oxytocin receptors, proteins on the cell’s surface that latch on to the hormone and then send a growth signal into the cell. The number of those receptors on stem cells declines with age, the researchers found, as do oxytocin levels in the blood. Young mice had three times as much oxytocin in their blood as old mice did.
That’s a one-two punch that researchers have rarely seen, says Nathan LeBrasseur, a physiologist at the Mayo Clinic in Rochester, Minn. Usually scientists think of aging processes at the cellular level as happening either in a cell or in molecules floating around outside the cell. “Here you see changes in both scenes,” he says. As a result, stem cells in older mice don’t get oxytocin’s message to repair damaged muscle.
When that happens in older people and animals, “Plan B kicks in,” Conboy says. Muscle stem cells stay dormant while other cells patch the injury with fat and fibrous, scarlike tissue, she says. The researchers reasoned that giving old mice oxytocin should wake up muscle stem cells and lead to better wound repair.
“That’s one of the first experiments we tried,” says coauthor Wendy Cousin, also a stem cell scientist at UC Berkeley. Sure enough, old mice that got injections of oxytocin repaired injured muscles as well as young mice did.
Mice engineered to lack oxytocin were less able to repair injured muscle compared with normal mice. That defect got worse with age. Mice lacking oxytocin also had less muscle mass than their normal counterparts. Normal mice, for instance, had a tibialis anterior leg muscle that weighed about 32 percent more than the ones from mice without oxytocin. These findings indicate that the hormone may also play a role in muscle atrophy or sarcopenia, the muscle loss that contributes to frailty in old age, the researchers conclude.
Gundersen and LeBrasseur both say the results strongly support the idea that oxytocin stimulates wound repair in muscles. But both scientists want more data before they would conclude that declining oxytocin levels cause sarcopenia.
Conboy and colleagues caution that people shouldn’t take oxytocin based on this mouse study. “There are people who will buy oxytocin hoping that they can remain forever young,” she says. But the team doesn’t yet know if oxytocin levels decline as people age, and if they do, what dose would be appropriate, when to give it, or what the long-term consequences of such supplementing might be. The hormone may be of most help to older people who are injured or need surgery, Conboy’s team speculates.