Why is physical exercise so beneficial to our health? A new study reveals part of the answer, as a fat molecule — which improves cardiometabolic health — is found to be released during exercise.

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When we’re cold, we burn fat, and a new study helps to explain why and how.

Physical activity and our heart and metabolic health are known to be intimately linked.

Even the slightest increase in physical activity levels lowers cardiometabolic risk, studies have shown, while less physical activity raises the risk of cardiovascular disease and diabetes.

But why is exercise so good for our body, and how does it help us to manage fat levels and keep a healthy weight?

Researchers at the Joslin Diabetes Center — affiliated with Harvard Medical School in Boston, MA — in collaboration with scientists at the Ohio State University in Columbus set out to investigate.

The researchers found that even a short, moderate bout of exercise boosts the levels of a key lipid that is released by brown fat, or the “good” type.

Brown fat is considered to be “good” because, unlike white fat — which has been tied to conditions such as heart disease and diabetes — it burns calories; the main purpose of brown fat is to convert the food we eat into energy.

The new findings — which are now published in the journal Cell Metabolism — “highlight another mechanism for the beneficial effects of exercise,” explains study co-author Laurie Goodyear, a senior investigator at the Joslin Diabetes Center.

The lipid in question is called 12,13-dihydroxy-9Z-octadecenoic acid (or 12,13-diHOME), and one of the interesting things about it is that our body also releases it when we’re cold.

Previous research has shown that exposure to cold makes the lipid 12,13-diHOME stimulate brown fat activity, and that people with a higher level of 12,13-diHOME have better insulin sensitivity and a lower body mass index (BMI).

What the new study found, for the first time, is that exercise also boosts 12,13-diHOME levels. Using lipidomics analysis, the researchers saw that a single “bout of moderate-intensity exercise causes a pronounced increase in the circulating lipid [12,13-diHOME] in male, female, young, old, sedentary, and active human subjects.”

An additional examination of mice revealed that in rodents, too, both a short bout of exercise and long-term physical training boosted levels of the lipid. Finally, removing the rodents’ brown fat canceled this effect, confirming the fact that the lipid is produced by this type of fat.

As Goodyear explains, “Our data provide some of the first evidence that exercise can alter the endocrine function of brown fat by increasing 12,13-diHOME.”

Treating mice with 12,13-diHOME “increased skeletal muscle fatty acid uptake and oxidation, but not glucose uptake,” write the researchers.

This suggests that, while white fat breaks down the stored adipose tissue into fatty acids that then circulate in our blood, brown fat produces 12,13-diHOME, which encourages the muscles to absorb these fatty acids during exercise.

“I think it is surprising that one type of fat provides the fuel and the other signals the muscle to use the fuel,” says Goodyear.

The researchers say that they found the results surprising, especially in light of previous studies, which so far have suggested that exercise lowers the activity of brown fat in the human body.

“Most data,” says study co-author Kristin Stanford, who is a researcher at the Ohio State University’s Wexner Medical Center, “have suggested that cold and exercise have opposite effects on [brown fat].

“[S]o,” she adds, “to see that 12,13-diHOME was released from [brown fat] after both exercise and cold exposure was unexpected.”

“We still have more to learn about how [brown fat] is activated by cold and exercise and how these two stimuli could work in parallel,” concludes Stanford.