LITTLE ROCK — When ticking off the benefits of physical activity, few of us would include intracellular housecleaning. But a new study suggests that the ability of exercise to speed the removal of garbage from the body’s cells may be one of its most valuable, if least visible, effects.
For the new research, published by the journal Nature in January, scientists at the University of Texas Southwestern Medical Center in Dallas gathered two groups of mice.
One set was normal, with a finely tuned cellular scrubbing system. The other had been bred with blunted cleaning systems.
It has long been known that cells accumulate flotsam from the wear and tear of everyday living. Inside the cell, a kind of trash heap is formed of broken proteins, shreds of cellular membranes, invasive viruses or bacteria and worn out, broken-down cellular components.
Most of the time, cells sweep away this debris.
They even recycle it for fuel. Through the process autophagy, or “self-eating,” cells create specialized membranes that engulf junk in the cytoplasm and carry it to a region of the cell called the lysosome, where the waste is broken down and burned for energy.
Without this efficient system, cells could become choked and malfunction or die. In recent years, some scientists have begun to suspect that faulty autophagy mechanisms contribute to the development of a range of diseases, including diabetes, muscular dystrophy, Alzheimer’s disease and cancer. The slowing of autophagy in middle age is also believed to play a role in aging.
Most researchers think that the process evolved in response to the stress of starvation; cells would round up and consume superfluous bits of themselves to keep the important parts alive. In petri dishes, the rate of autophagy increases when cells are starved or otherwise placed under physiological stress.
Exercise, of course, is physiological stress. But until recently, few researchers had asked whether exercise might somehow affect the rate of autophagy and, if so, whether that mattered to the body as a whole.
“Autophagy affects metabolism and has wide-ranging health-related benefits in the body, and so does exercise,” said Dr. Beth Levine, a Howard Hughes Medical Institute investigator at UT Southwestern. “There seemed to be considerable overlap.” But it wasn’t clear how the two interacted, she added.
So she and her colleagues had lab mice run. The animals had been treated so that the membranes involved in autophagy would glow, revealing themselves. After just 30 minutes of running, the mice had significantly more membranes in cells throughout their bodies, the researchers found, indicating accelerated autophagy.
But that finding didn’t explain what the augmented cellular cleaning meant for the well-being of the mice. So the researchers developed a new strain of mice in which autophagy levels remained constant, even if the animals were starved or vigorously exercised.
Then the researchers had these mice run alongside a control group of normal mice. The autophagy-resistant mice quickly grew fatigued. Their muscles seemed incapable of drawing sugar from the blood as the normal mice did.
More striking, when Levine stuffed both groups of animals with high-fat kibble for several weeks until they developed a rodent version of diabetes, the normal mice subsequently reversed the condition by running, even as they continued on the fatty diet.
But after weeks of running, the autophagy-resistant mice remained diabetic. They also had higher levels of cholesterol than the other mice. Exercise had not made them healthier.
Levine and her colleagues concluded that an increase in autophagy, prompted by exercise, seems to be a crucial step in improving health.
The finding is “extremely exciting,” said Zhen Yan, of the Center for Skeletal Muscle Research at the University of Virginia, who is also studying autophagy and exercise. The study, he said, “improves our understanding of how exercise has salutary impacts on health.”
The implications of Levine’s results are broad. It’s possible, for instance, that people who don’t respond as robustly to aerobic exercise as their training partners may have sputtering or inadequate autophagy systems.
“It’s very difficult to study autophagy in humans,” Levine said. So it would be a leap to suggest that someday, autophagy-enhancing drugs or specialized exercises could help people fully benefit from exercise.
For Levine, the study underscores the importance of staying active. The control mice and the genetically modified group had “normal background levels of autophagy” during everyday circumstances, Levine noted. But this base-line level of cellular housecleaning wasn’t enough to protect them in the face of a poor diet.
“I never worked out consistently before,” Levine said. But now, having witnessed how exercise helped scour the cells of the running mice, she has bought a treadmill.
ActiveStyle, Pages 23 on 02/13/2012