|McMaster University in Ontario recently released the findings of two interesting studies about exercise. McMaster researchers examined how exercise boosts health by triggering stem cells to become bone; and discovered that a missing muscle gene impairs the ability of mice to exercise.
In the stem cell project, researchers found that exercise triggers influential stem cells to become bone instead of fat, improving overall health by boosting the body’s capacity to make blood.
The body’s mesenchymal stem cells are most likely to become fat or bone, depending on which path they follow. Using treadmill-conditioned mice, a team led by Gianni Parise found that aerobic exercise triggers those cells to more often become bone. The exercising mice ran under an hour, three times a week, enough time to significantly impact their blood production. In sedentary mice, stem cells were more likely to become fat, impairing blood production in the marrow cavities of bones.
“A modest exercise program significantly increased blood cells in the marrow and in circulation,” says Parise. “What we’re suggesting is that exercise is a potent stimulus — enough of a stimulus to actually trigger a switch in these mesenchymal stem cells.”
The findings add to the growing list of established benefits of exercise, Parise says, and suggest that novel non-medicinal treatments for blood-related disorders may be in the future. “Some of the impact of exercise is comparable to what we see with pharmaceutical intervention,” he says.
In the other study, researchers made the unexpected finding that a lack of desire to exercise may be due to missing genes-not laziness. The researchers were working with healthy, specially-bred mice, and they removed in some of the mice two genes in muscle that are essential for exercise. The genes control the protein AMP-activated protein kinase (AMPK), an enzyme that is switched on when you exercise.
“While the normal mice could run for miles, those without the genes in their muscle could only run a short distance,” said Gregory Steinberg, associate professor of medicine. “It was remarkable. The mice looked identical, but within seconds we knew which ones had the genes and which ones didn’t.”
The researchers found the mice without the muscle AMPK genes had lower levels of mitochondria and an impaired ability for their muscles to take up glucose while they exercise.
“When you exercise you get more mitochondria growing in your muscle. If you don’t exercise, the number of mitochondria goes down. By removing these genes we identified the key regulator of the mitochondria is the enzyme AMPK,” said Steinberg. He said the findings are important for individuals who find it difficult to exercise, such as the obese, asthmatics and people in wheelchairs. Their inability to exercise may lead to other complications such as diabetes and heart disease.
Steinberg warns couch potatoes, “As we remove activity from our lives due to emerging technology, the population’s base level of fitness is going down, reducing the mitochondria in people’s muscles. This makes it so much harder to start exercising.”