Despite the results, this isn't a transfusion you would want.
In a lab at Stanford University, researcher Thomas Rando and his colleagues connected the circulation systems of old mice with those of young ones. For more than five weeks, the animals shared a blood supply through a physical link.
Macabre, maybe, but the outcome will probably excite anyone over 40 with a gym membership. Simply by having their muscles bathed in young blood, the old mice regained youthful muscle regeneration.
The results -- reported this year in the journal Nature -- have confirmed a theory with profound implications for regenerative medicine. At least some old stem cells, it seems, act young in the presence of young blood.
While it is no small feat, finding what blood factors are responsible could do more than boost muscle mass in the elderly, providing new treatments for everything from heart disease to Alzheimer's. "We think it's going to be a fairly general phenomenon," said Dr. Rando, an associate professor of neurology and neurological sciences at Stanford's school of medicine.
Even if the findings lead to only muscle saving, the results could be profound. (As for enhancing bodybuilding, Dr. Rando said nothing to date suggests that this would work. Nor is he certain that the findings could lead to enhanced muscle healing in the young.)
From the age of 20 to 80, people lose 20 to 30 per cent of their skeletal muscle mass. The impact is more than cosmetic. Less muscle mass means a lower metabolism, increasing the risk of obesity and related ailments. Weaker muscles also increase the risk of falls and related injuries.
Part of the problem lies with muscle stem cells called satellite cells. Waiting in reserve in muscle fibres, these cells are responsible for the growth, healing and regeneration of skeletal muscle.
When we're young, the cells are quick to do their job. However, like all stem cells, their capabilities decline with age, along with the regenerative capacity of muscle.
"As you get older, your stem cells get less active," said Michael Rudnicki, director of the Molecular Medicine Program at the Ottawa Health Research Institute.
The problem isn't that the number of satellite cells declines with age. "We know that the cells are present in old and young mice in equal numbers," Dr. Rudnicki said. Rather, in muscle -- as well as such tissues as blood, liver and brain -- the cells become less responsive with age.
If responsiveness could be restored, it might bypass the need for other forms of treatment such as the transplant of stem cells from external sources.
In previous work, Dr. Rando and colleagues demonstrated that stem-cell responsiveness could be restored in muscle through an artificial signal.
They found that age-related declines in muscle regeneration result from the failed activation of a cellular trigger called Notch. The trigger is normally pulled by another molecule called Delta. With age, less Delta is produced during muscle injury.
In their earlier work, Dr. Rando and colleagues used a Delta mimic to restore Notch activation and, in turn, the youthful action of aged satellite cells, showing that the cells themselves aren't the problem. "It was a demonstration that you can bypass the aging process," he said.
Muscle regeneration has also been restored through transplantation. Aged mouse muscle is rejuvenated when grafted into young mice. Conversely, young mouse muscle is inhibited when grafted into old mice.
This showed that something is missing in older animals, Dr. Rando says. What it didn't show definitively, however, is whether factors in blood are responsible or whether muscle-building cells from young mice simply repair transplanted old muscle.
The new study by Dr. Rando and his colleagues settles the matter, as the mice in their study were exposed only to blood factors. Furthermore, the young mice were altered with a green fluorescent protein, ensuring that any muscle-rebuilding cells from them would be easily located in the muscle of older mice.
When the researchers injured limb muscles in old mice that shared blood with young, the damage was repaired at about the same speed as with their young counterparts. When they looked to see whether young muscle-building cells were responsible, they found this wasn't the case, as less than 0.1 per cent of regenerated muscle structures in the old mice glowed green. "Unequivocally, the enhanced regeneration was from the old muscles," Dr. Rando says.
Similar findings were made with liver cells from old mice. As with muscle, liver tissue regenerates less actively in older animals, so finding youthful healing here supports a more general phenomenon.
The next step, Dr. Rando says, is to determine why young blood has such an impact. There could be inhibitory factors in old blood, regenerative factors in young blood, or both.
Screening, separating out and testing every component of blood would be a daunting task, Dr. Rando says, so his team plans to gamble and target likely candidates. "We're taking our best guess."
There's no telling how long it might take to track down the active factors, or to turn these findings into treatments. But at this point, one thing seems clear: The fountain of youth flows through the veins of the young.
Simon Smith is a Toronto-based freelance writer.