Working out could help us fight off colds and other infections, according to a timely new study. The study, which found that regular exercise strengthens the body’s immune system in part by repeatedly stressing it, was conducted in animals. But the results most likely apply to people, the researchers say, and could offer further incentive for us to remain physically active this winter.
In broad terms, our immune system reacts to invading microbes through a variety of cells. Some of these cells don’t directly combat the infection, but instead promote the development of inflammation. When we think of inflammation, we usually think of fever, swelling and redness. But inflammation can also be a good thing, helping the body to heal itself as it fights invading microbes.
The problem is that inflammation can easily get out of hand. If the inflammatory response to an infection or injury is too robust or indiscriminate, the inflammation can ultimately cause more tissue damage and lingering health problems than it prevents.
Scientists have long tried to determine why inflammation sometimes grows rampant in the body. One thing they’ve noticed is that fat cells are particularly adept at producing substances that promote inflammation, in part as a response to messages from the immune system.
But fat cells also often produce inflammatory substances in greater amounts than needed to fight germs, in some cases even when there is no actual infection. As a result, past studies have found, obesity in animals and people can lead to elevated levels of inflammation throughout the body and, interestingly, a weaker overall immune response to an infection or illness.
Because of these links between fat cells and the immune response, scientists at Chosun University in Gwangju, South Korea, and other institutions recently began to consider whether exercise might affect the body’s response to germs. Among the many effects of physical activity, exercise generally reduces the amount of fat in the body and also alters levels of inflammation.
So for the new study, which was published last month in Scientific Reports, they gathered 28 average-weight male laboratory mice and tested their blood and fat cells for markers of inflammation and other immune cells. They then had half of the mice begin a swimming regimen, during which the animals paddled around a warmish pool for 10 minutes, five days a week, for three weeks.
Mice aren’t natural or eager swimmers and tend to thrash in the water, so the exercise was moderately strenuous for them, the equivalent of what 30 minutes or so of jogging might be for us.
The other mice remained sedentary.
Throughout the three weeks, the scientists monitored all of the animals’ levels of inflammation and what was happening, if anything, to their fat cells.
As expected, the swimmers showed increases in markers of inflammation, especially in their muscles, as their bodies worked to heal the slight tissue damage that occurs during regular exercise. Over all, they displayed higher levels of inflammation than the unexercised animals. Meanwhile, their fat cells were shrinking in size and number.
After three weeks, to test the animals’ immune response, half of the swimmers and half of the inactive mice were inoculated with Staphylococcus germs. In both mice and people, these germs cause skin infections and serious lung problems that resemble pneumonia.
Both the mice that had exercised and those that had remained sedentary began to grow ill from the Staph infections. But the differences in the animals’ immune responses proved to be considerable, the scientists found.
Inflammation rapidly blossomed in the sedentary, infected animals, as their immune systems pumped out high numbers of cells that promote inflammation. Many of these cells migrated to the animals’ lungs, suggesting that excessive inflammation was taking hold there.
Meanwhile, the infected swimmers had much lower levels of these pro-inflammatory cells, lower even than in the uninfected swimmers. The numbers of these cells in their lungs were particularly low. At the same time, the sickening swimmers were producing far more of a potent type of antimicrobial immune cell that, like internal Purell, directly kills germs, especially in their lungs.
Over all, the infected swimmers did not become as sick as the infected sedentary mice. They also experienced much less lung damage.
Precisely how swimming had changed these animals’ immune systems remains somewhat unclear. But, said Yoonkyung Park, a professor of biomedical science at Chosun University who oversaw the new study, the exercise seemed to have had two signal effects.
Most obviously, it reduced fatness, which, in turn, lessened the often-excessive levels of pro-inflammatory substances produced by fat cells.
At the same time, however, the workouts caused small amounts of continuous tissue damage and inflammation. This process, the researchers said, seems to have familiarized the animals’ bodies with trauma and how best to initiate healing.
The swimmers, in effect, appeared to have developed a more refined and effective immune response. Their immune systems appear to have learned to produce a beneficial amount of inflammation, but not too much. So when germs invaded, the system could rely less on indiscriminate, blunt-force inflammation and instead turn to targeted, antimicrobial killers.
Of course, as we all know, rodents are not people.
But Dr. Park believes that the effects are likely to be similar in people. “We strongly believe that long-term, regular exercise can considerably improve the immune defense mechanism,” he said, including, thankfully, “against viral infections such as colds and the flu.”