Many of us may not realize that body fat can be metabolically healthy — or the reverse — no matter what someone’s weight or shape.
“Healthy fat is not about the amount of fat” someone carries, said Jeffrey Horowitz, a professor at the University of Michigan, who studies exercise and metabolism. It is about how well that fat functions, he said. “A person who has healthier fat is much better off than someone with the same body fat percentage whose fat is unhealthy.”
What principally differentiates healthy from al fat, Horowitz continued dysfunction, is the size of the fat cells. “The more small fat cells, the better,” he said.
And notably, you don’t have to lose weight or fat to make the body fat you already have metabolically healthier.
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Why fat cell size matters
Large fat cells, he said, are already filled with fat. They cannot store much more and tend to leak some of their overstuffed contents into the bloodstream as fatty acids. From there, the fatty acids slosh toward and lodge in other organs, such as the heart, muscles or liver. Fatty, well-marbled livers, muscles or hearts are undesirable (unless, perhaps, you raise steers).
Small fat cells, on the other hand, can expand, essentially slurping fat from your blood. You want fat to stay inside fat cells, Horowitz said.
Healthy fat cells also contain reams of active mitochondria, the power centers of any cell. Mitochondria convert oxygen and food into cellular energy. In general, the more mitochondria, the healthier and more resilient any cell will be, including fat cells.
Finally, healthy fat tissue teems with blood vessels, to ferry oxygen and nutrients to fat cells, along with battalions of other cells, most related to immunity, that helps fight inflammation. Without sufficient blood supply and immune protection, fat tissue often becomes inflamed and scarred and releases substances into the bloodstream that initiates similar, unhealthy inflammation in our bodies, even in people who are not overweight.
How exercise can remodel your fat cells
Until recently, though, scientists were not sure whether or how much of our fat could change. That is, they knew healthy fat tissue could deteriorate, filling with large, leaky cells, dysfunctional mitochondria and inflammation.
But whether this process could be reversed or slowed remained unclear. Some studies in recent years involving rodents were encouraging, suggesting physically active animals harbored metabolically healthier body fat compared with sedentary rodents, even if they were all overweight by rodent standards.
But we are not lab mice and many questions remained about the malleability of our body fat.
A study published in June brought glimmers of clarity, though. In the study, researchers at the University of Copenhagen in Denmark biopsied abdominal fat from young, sedentary men older sedentary men and physically active men, most of them longtime and frequent cyclists.
The fat cells from the older, sedentary men showed relatively poor mitochondrial health, with fewer mitochondrion than in the young men’s fat and less energy produced by each mitochondrion. But the physically active men’s fat cells held plenty of mitochondria, more even than in fat tissue from the young men, so that their fat cells, overall, were better supplied with energy. Their fat tissue also showed fewer signs of incipient inflammation than fat from the inactive men, whatever their ages.
“Exercise training meant more mitochondria and better functioning mitochondria” and, in essence, healthier fat, said Anders Gudiksen, a professor of cell biology at the University of Copenhagen, who led the study.
But for anyone who might not have had the foresight to be a lifelong cyclist, another new study offers hope that starting to exercise now, no matter how sedentary you may have been, could rapidly improve your fat’s fitness.
For the new study, published in the Journal of Physiology and overseen by Horowitz, researchers biopsied fat tissue from 36 sedentary men and women with obesity and then asked them to ride a stationary bike at a moderate pace for 45 minutes or more intensely for a 20 -minute interval workout four times a week for 12 weeks.
The volunteers’ diets were carefully monitored, so they would not lose weight. Otherwise, Horowitz said, changes in their fat tissue might have been due to weight loss, not exercise.
But without shedding pounds, the exercising volunteers still remade their fat. They wound up with substantially more small fat cells, as well as more capillaries to nourish those cells. Their fat tissue also held fewer biochemical markers of inflammation and less symptoms of scarring and hardening around the fat cells.
These effects were seen, whether the volunteers rode moderately or hard. “Intensity didn’t matter,” Horowitz said, only that they were active.
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In the short term, these alterations should make fat tissue more capable of slurping up and storing any excess calories someone takes in with large meals during the holidays, Horowitz said, a scenario that does not necessarily mean weight gain. This fat is usually stored temporarily, soon converted into energy for other tissues, like muscles. But in the meantime, he said, it is better to warehouse such fat in fat cells, not your liver or arteries.
The longer-term implications of exercise and fat revolve around inflammation, Horowitz said, and whether and how metabolically healthy fat contributes to a metabolically healthy body, even — and perhaps especially — if people have obesity.
We need more research to fully understand what constitutes healthy fat, he said, and the types and amounts of exercise that best generate or maintain it. But already it seems clear, he said, movement benefits fat, as well as the rest of your body, offering one more reason to ride, walk, jog, swim or, in whatever way you choose, be active today.
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