Washington: Exercise may make body cells healthier and lead to a longer life, a study suggests. The study in mice shows that just one bout of moderate- to-intense exercise acts as a “stress test” on mitochondria in muscles.
Researchers discovered that this “stress test” induced by aerobic exercise triggers a process called mitophagy, where the muscle disposes of the damaged or dysfunctional mitochondria, making the muscle healthier. Mitochondria – the cellular power plant – creates the fuel so the body can function properly.
Yan compared exercise-induced mitophagy to a state vehicle inspection that removes damaged cars from the streets. “Aerobic exercise removes damaged mitochondria in skeletal muscle,” said Zhen Yan of the University of Virginia School of Medicine in the US. “If you do it repeatedly, you keep removing the damaged ones. You have a better muscle with better mitochondrial quality,” said Yan.
Yan and colleagues assessed the skeletal muscle of a mouse model where they had added a mitochondrial reporter gene called “pMitoTimer.” The mitochondria fluoresce green when they are healthy and turn red when damaged and broken down by the cell’s waste-disposal system, the lysosomes. The mice ran on a small treadmill for 90 minutes and researchers observed mitochondrial stress (signs of “state inspection”) and some mitophagy (towing of the clunkers) at six hours after exercise.
Yan explained that exercise in these mice also stimulated a kinase called AMPK, which in turn switched on another kinase, Ulk1. These chemical reactions appear to be important in control of the removal of dysfunctional mitochondria.
“When it is turned on, Ulk1 activates other components in the cell to execute the removal of dysfunctional mitochondria,” Yan said. Yan’s lab also deleted the Ulk1 gene in mouse skeletal muscle and found that, without the gene, the removal of damaged or dysfunctional mitochondria is dramatically inhibited, suggesting a new role for the Ulk1 gene in exercise and mitophagy.