Research reveals the link between physical activity and healthy muscle cells
TORONTO, May 10, 2007 -- Regular exercise not only boosts energy but actually reduces cell death in muscles, York University researchers have proven.
Scientists have known for a century that cells require organelles known as mitochondria in order to produce energy. However, these mitochondria have also been shown to promote cell death – or apoptosis, in certain situations. But until now, no one has been able to show when or how that happens in muscle, according to David Hood, a professor in the School of Kinesiology and Health Science at York, and Canada Research Chair in Cell Physiology.
Hood and Peter Adhihetty, at the time a doctoral student in the Department of Biology, led an interdisciplinary team that recently published two studies, in the American Journal of Applied Physiology (see Study 1) and the American Journal of Physiology, Endocrinology and Metabolism (see Study 2).
The first study found that in rats there is a much greater incidence of cell death in muscle that is inactive, than in muscle that is regularly active. The second study, which mimicked chronic exercise training in rats, demonstrated that mitochondria from muscle that was repeatedly exercised released fewer of the proteins that break up DNA and cause cell death.
“The implications are that regular exercise will help prevent the decay of muscle cells and help maintain their structure and function,” said Hood, who is more interested in research that pertains to everyday people – or those with disease – than in research for athletes.
“Cells in muscles that are exercised regularly produce more mitochondria than cells in inactive muscles. So we’ve been telling people to exercise regularly because it will lead to greater endurance (less fatigue) and improve their daily lives, but until now, we haven’t been able to point to the way that exercise helps to preserve healthy muscle cells,” said Hood. “We’ve now traced this particular pathway to less cell death.”
The good news is that inactive people who have fewer mitochondria to prevent muscle cell death can change this by exercising, said Hood. That includes people with type 2 diabetes, a group that has recently been found to have fewer mitochondria than most of the population.
“You don’t have to be a high-performance athlete. I’m talking about regular physical activity,” says Hood. “For most people, having fewer mitochondria is completely reversible.”
Hood expects the findings will significantly improve understanding in the exercise physiology field of how boosting mitochondria can lead to better overall health. They may also benefit older people who are losing muscle mass, and astronauts, whose muscles atrophy in space, he said. Hood is also conducting research designed to benefit people with mitochondrial myopathies, or dysfunctional mitochondria.
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Media contact:
Janice Walls, Media Relations, York University, 416 736 2100 x22101 / wallsj@yorku.ca
