The new understanding "is a fundamental jump forward in the study of fatigue," said Dr. Luigi Ferrucci, one of the conference organizers, and brings with it some good news for the tired among us.
Scientists are now convinced that fatigue has a real, molecular basis, and that at least two major biological processes are involved: An excess of natural chemicals called pro-inflammatory cytokines, which the body pumps out in response to infection. And sluggish mitochondria, the tiny organelles inside cells that make energy.
Even if these two pathways work separately - and nobody knows yet if they do - the implications are profound. For one thing, unraveling these pathways could lead to new antifatigue drugs, said Ferrucci, who is also director of the Baltimore Longitudinal Study on Aging. That's part of the good news.
For another, because both cytokine and mitochondrial problems get worse with excessive rest and improve with moderate exercise, it means exercise is an obvious, and readily available, remedy. A large body of research has already shown that exercise dampens down the "bad" cytokines and boosts the number and efficiency of mitochondria.
This doesn't mean you should go run a marathon if you've got the flu. Quite the contrary. In the acute phase of any illness, your body needs all its available energy to heal. But it does mean that, as soon as possible, you should get out and walk, even if it's just around the block for starters.
The fatigue now under the microscope - "central" or brain, fatigue - is most recognizable as a "subjective perception, the feeling that you don't have the energy to engage in any physical or intellectual challenge," said Dr. Anthony Komaroff , a fatigue specialist and professor of medicine at Harvard Medical School.
Ferrucci puts it slightly differently: "Fatigue is a physiological signal that tells the brain that you cannot keep doing what you're doing." Nobody is sure where this signal comes from, he said, though it's probably from the muscles.
