Recent research has found that being physically active alters fat at a molecular level in ways that improve the fat’s health.
The findings have broad implications for the state of our metabolisms, muscles and even how well our bodies deal with the approaching holiday season of cheery gluttony, reports The Washington Post.
Many people may not realise that body fat can be metabolically healthy – or the reverse –no matter your weight or shape.
“Healthy fat is not about the amount you carry,” said Professor Jeffrey Horowitz from the University of Michigan, who studies exercise and metabolism. It is about how well that fat functions, he said. “Someone with healthier fat is much better off than someone with the same body fat percentage whose fat is unhealthy.”
What principally differentiates healthy from dysfunctional fat 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.
Hibernating fat bears are complex. They may hold lessons for human health.
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, like the heart, muscles or liver. Fatty, well-marbled livers, muscles or hearts are undesirable.
Small fat cells, alternatively, 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 centres of any cell. Mitochondria convert oxygen and food into cellular energy. Generally, 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 help fight inflammation. Without sufficient blood supply and immune protection, fat tissue often becomes inflamed and scarred and releases substances into the bloodstream that initiate similar, unhealthy inflammation elsewhere 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 our fat could change. 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 harboured 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 early this year (see link below) brought glimmers of clarity, though, when researchers at the University of Copenhagen, Denmark, biopsied abdominal fat from young, sedentary men, older sedentary men and physically active older men, most of them longtime and frequent cyclists.
The fat cells from the older, sedentary men showed relatively poor mitochondrial health, with fewer mitochondria 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 more recent study offers hope that starting to exercise now, no matter how sedentary you may have been, could rapidly improve your fat’s fitness.
For this latest 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 kilos, the exercising volunteers still remade their fat. They ended 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.
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, 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.
Study details
Exercise training remodels subcutaneous adipose tissue in adults with obesity even without weight loss
Cheehoon Ahn, Benjamin Ryan, Michael Schleh, Pallavi Varshney, Alison Ludzki, Jenna Gillen, Douglas Van Pelt, Lisa Pitchford, Suzette Howton, Thomas Rode, Scott Hummel, Charles Burant, Jonathan Little, Jeffrey Horowitz.
Published in The Journal of Physiology on 6 March 2022
Abstract
Excessive adipose tissue mass underlies much of the metabolic health complications in obesity. Although exercise training is known to improve metabolic health in individuals with obesity, the effects of exercise training without weight loss on adipose tissue structure and metabolic function remain unclear. Thirty-six adults with obesity (body mass index = 33 ± 3 kg · m–2) were assigned to 12 weeks (4 days week–1) of either moderate-intensity continuous training (MICT; 70% maximal heart rate, 45 min; n = 17) or high-intensity interval training (HIIT; 90% maximal heart rate, 10 × 1 min; n = 19), maintaining their body weight throughout. Abdominal subcutaneous adipose tissue (aSAT) biopsy samples were collected once before and twice after training (1 day after last exercise and again 4 days later). Exercise training modified aSAT morphology (i.e. reduced fat cell size, increased collagen type 5a3, both P ≤ 0.05, increased capillary density, P = 0.05) and altered protein abundance of factors that regulate aSAT remodelling (i.e. reduced matrix metallopeptidase 9; P = 0.02; increased angiopoietin-2; P < 0.01). Exercise training also increased protein abundance of factors that regulate lipid metabolism (e.g. hormone sensitive lipase and fatty acid translocase; P ≤ 0.03) and key proteins involved in the mitogen-activated protein kinase pathway when measured the day after the last exercise session. However, most of these exercise-mediated changes were no longer significant 4 days after exercise. Importantly, MICT and HIIT induced remarkably similar adaptations in aSAT. Collectively, even in the absence of weight loss, 12 weeks of exercise training induced changes in aSAT structure, as well as factors that regulate metabolism and the inflammatory signal pathway in adults with obesity.
Key points
• Exercise training is well-known to improve metabolic health in obesity, although how exercise modifies the structure and metabolic function of adipose tissue, in the absence of weight loss, remains unclear.
• We report that both 12 weeks of moderate-intensity continuous training (MICT) and 12 weeks of high-intensity interval training (HIIT) induced modifications in adipose tissue structure and factors that regulate adipose tissue remodelling, metabolism and the inflammatory signal pathway in adults with obesity, even without weight loss (with no meaningful differences between MICT and HIIT).
• The modest modifications in adipose tissue structure in response to 12 weeks of MICT or HIIT did not lead to changes in the rate of fatty acid release from adipose tissue.
• These results expand our understanding about the effects of two commonly used exercise training prescriptions (MICT and HIIT) on adipose tissue remodelling that may lead to advanced strategies for improving metabolic health outcomes in adults with obesity.
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The Washington Post article – Have you exercised your body fat lately? (Open access)
See more from MedicalBrief archives:
Link with fat on the hips and stroke and heart attack risk
Interval training rapidly improves diabetics’ glucose metabolism
High-Intensity Interval Training (HIIT) burns more fat – Australia study
Walking faster more beneficial than walking further – Australian cohort study