When Exercise Can Kill Hunger

The idea of ​​running (jogging) makes intuitive and evolutionary sense, says pathology professor JZ Long. “If you’re running from a rhinoceros or some other threat, the autonomic nervous system tells the brain to turn off digestion and any other non-essential processes.”

In a new study published June 15 in the journal Nature, an international team of scientists say they have found a molecule produced by the body after exercise that can partially satisfy hunger.

The component, found in the blood of mice, humans and racehorses, appeared in much greater amounts after strenuous exercise than after light exercise, which allowed scientists to draw interesting conclusions.

Research has shown that people who start exercising without controlling their calorie intake usually don’t lose much weight over time and may even gain it. Many factors play a role in this effect, including current fitness, body weight, diet, and even time of day.

Appetite also matters. If you feel hungry after a workout, you can easily consume more calories than you burn. But what makes us feel hungry after a workout remained a mystery.

For decades, scientists have known that various substances, such as the hormones leptin and ghrelin, are transferred to the brain and make us more or less hungry. Research shows that exercise changes blood levels, but so does diet and sleep habits. Scientists from Stanford University School of Medicine, Baylor School of Medicine, University of Copenhagen and other institutions used newly developed methods to look for molecules that appear in large amounts in the blood after exercise. They started with mice, having them run on tiny treadmills at increasing speeds until they got tired. Blood samples were taken before and after the “training”. The scientists compared the levels of thousands of molecules in the blood of rodents.

One of the molecules stood out for its indicator. The scientists found that it was a mixture of lactic acid and the amino acid phenylalanine, which seemed to be produced extensively in response to the high levels of lactic acid released during exercise, and named it lac-phe.

The researchers hypothesized that lac-phe may be related to post-exercise energy balance, as cells in the blood and elsewhere that produce it are associated with energy intake and body weight. Perhaps, they thought, it affects the appetite. To find out, they gave the drug lac-phe obese mice that usually eat with pleasure. Food consumption has been reduced by more than 30%. Apparently, they were less hungry with the additional presence of lac-phe in the blood.

The researchers then returned to the exercises. They bred mice that produced little or no lac-phe and made them run on treadmills five times a week for several weeks. After each run, the animals were allowed to eat as many fatty morsels as they wanted. Regular running helps mice avoid weight gain even on a high-calorie diet. But animals that couldn’t produce much lac-phe got fatter as they ate more pellets and gained about 25% more weight. lac-phe seems to have been the key to how vigorous exercise helped the mice avoid weight gain. Without it, the same exercises led to overeating.

The researchers also tested for lac-phe in other test subjects. First, they found the molecule in the blood of racehorses, and then asked eight healthy young men to work out three times: once by cycling at a leisurely pace for 90 minutes, another by lifting weights, and a third by various 30-second sprints on a stationary bike.

Blood lac-phe levels peaked after all types of exercise, but were highest after running, followed by weight training. Prolonged light exercise gave the least result. In other words, the more intense the exercise, the more lac-phe and, at least in mice, the more their appetite decreased.

“The results are exciting and give new meaning to the theory of exercise benefits and body weight regulation,” said Richard Palmiter, a professor of biochemistry at the University of Washington in Seattle and an expert in behavioral neuroscience.

“Assuming this process works the same way in humans as it does in mice, the discovery of lac-phe is very useful,” says Jonathan Z. Long, professor of pathology at Stanford University School of Medicine and lead author of the new study.

However, his research doesn’t say how lac-phe interacts with brain cells to affect appetite, or how intense exercise must be to increase lac-phe production, or how long the effect of the molecule lasts. In addition, the people involved were healthy young males, so there is still a lot to be learned before firm conclusions can be drawn.

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