Exercise and cellular renewal PDF Print E-mail
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Written by Karel Nunnink   



Study Provides First Evidence that Exercise Stimulates Cell Renewal Mechanism


We all know that exercise lowers the risk of just about any bodily malady you can name, including aging. But did you know that it consumes the debris in cells all over the body? I didn’t either until I read about it in The New York Times, Science Daily, and the HHMI News. The Howard Hughes Medical Institute (HHMI) at the University of Texas Southwest Medical Center in Dallas is where much of the research on this cleansing mechanism—the technical name is autophagy—is being conducted. (The new studies were reported January, 2012, in the journal Nature.)


Autophagy means “self-eating.” Autophagy is the process by which cells collect, breakdown, and digest damaged or unneeded parts. It doesn’t sound very pleasant, but it’s the body’s resourceful way of turning the waste products of cellular function into raw material for new structures or energy. Scientists believe this means of recycling evolved in response to starvation or stress; cells would gather and consume damaged or worn out fragments to keep the rest of the cell alive and healthy. In Petri dishes, the rate of autophagy increases when cells are starved or otherwise put under physiological stress. Exercise is a physiological stress. This led researchers to believe that autophagy may explain how exercise fends off metabolic disorders like diabetes and protects against other diseases.


“Autophagy is…known to have several health benefits and those benefits correspond closely to the effects of exercise,” said Dr. Beth Levine, professor of internal medicine and microbiology and director of the Center for Autophagy Research at UT Southwestern. “We hypothesized that some of the health benefits of exercise might be explained through autophagy.” Levine is the senior researcher in the new studies and responsible for many of the fundamental discoveries in this area.


The new research progressed in a logical, two-step progression.  The first step isolated the effect of exercise on autophagy; and the second step looked at the effect of autophagy.


Exercise Sparks Autophagy


As part of the autophagy process a double membrane forms around the unwanted cell fragments as a prelude to breakdown and recycling. The membranes are a marker of autophagy. To test the idea that exercise triggers autophagy, Levine and her colleagues used mice that had been medically treated so that the membranes encasing the debris inside their cells would give off a green glow, signaling that autophagy was taking place. They then placed the mice on treadmills; after 30 minutes of running, the mice had more glowing membranes in cells throughout their bodies. This told the researchers that exercise was sparking autophagy.


“That was a brand new finding,” Dr. Levine said. They established--for the first time--that exercise stimulates autophagy.


Next, Levine and her colleagues tested the purpose served by autophagy. What does it do? This phase was extended as the effects of autophagy unfolded.


Endurance Improved, Diabetes Gone


The team engineered mice that showed autophagy under normal circumstances, but lacked the ability to ramp up the debris-eating process when stressed. This set the stage for testing the role of autophagy. They then subjected the mutant mice to several phases of testing.


When the researchers placed the mutant mice on treadmills, they found that they couldn’t run as long as normal mice. A closer look showed that the mice weren’t metabolizing sugar normally; they weren’t burning sugar to fuel their running. As a result, blood sugar levels soared and endurance tanked


Autophagy aids endurance—it allows normal mice to run longer—but that’s not all it does.


This suggested to the Levine team that the autophagy-challenged mice might also be unable to derive the long-term benefits of exercise. To test this proposition, they fed both mutant and normal mice a high-fat diet for four weeks. Both mice groups remained sedentary. Not surprisingly, the mice gained weight and developed signs of type 2 diabetes.


They then put the mice (both groups) on a stringent exercise program for eight weeks while continuing to feed them a high-fat diet. The normal mice responded, losing weight and pulling back from diabetes. The mutant mice that exercised on the treadmill also lost weight, but did not get the metabolic benefits; their blood sugar remained high. To get the benefits of exercise, “autophagy really was necessary,” Levine said.


Significantly, the Levine team had earlier reported that exercise sparked an increase in autophagy in cells in the liver and pancreas, organs involved in the metabolism of glucose (sugar). This, of course, added another link between exercise, autophagy, and blood sugar regulation.


“Our finding that exercise fails to improve glucose metabolism in autophagy-deficient mice strongly suggests that autophagy is an important mechanism by which exercise protects against diabetes,” said Dr. Levine. “It also raises the possibility that activation of autophagy may contribute to other health benefits of exercise, including protection against cancer, neurodegenerative diseases and aging.”

live long and strong.

Information from Ripped, Clarence Bass.


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