Exercise would increase communication between skeletal muscles and adipose tissue, improving metabolic health and performance. This is suggested by recent research conducted in Brazil on mice and humans, which in the future could lead to new treatments for metabolic diseases associated with aging and obesity.
it would trigger the release of microRNA signaling molecules into the bloodstream, which in turn would free up more energy for muscle use.
Previous research had already established how aging and obesity impair the production of these signaling molecules, increasing the likelihood of metabolic diseases such as diabetes and dyslipidemia. Exercise, on the other hand, would help ward off these conditions by increasing the production of some microRNAs.
This new research appeared in the journal Proceedings of the National Academy of Sciences of the United States of America.
At the end of the observation period, the researchers found a significant increase in the production of a protein called DICER in the fat cells of the animals. This increase is related to the reduction in body weight and the amount of visceral fat in the abdomen.
DICER is an enzyme that allows fat cells to produce microRNA signaling molecules.
Later the scientists repeated the experiment with genetically modified mice, unable to produce any DICER in their fat cells, noting that they did not benefit as much from training as the others.
"At this stage the animals did not lose weight or visceral fat and their overall fitness did not improve," confirms Marcelo Mori.
This is because the fat cells in the genetically engineered mice failed to provide their muscles with the extra metabolic fuel they needed during strenuous exercise. "Without DICER - says Mori - fat cells actually consume more glucose during training, bringing less fuel to the muscles. This can lead to hypoglycemia or low blood sugar levels and in athletes it can limit performance."
In parallel, to confirm that fat and muscle were communicating via signaling molecules in the bloodstream, the researchers injected doses of blood from a mouse that had undergone the exercise program to one that hadn't.
This transfusion increased DICER production in the recipient's adipose tissue.
, whose average age was 63. However, there was considerable variation among individuals, which could help explain why some people benefit from exercise more than others., and think of converting this knowledge into a drug ».
The team has already taken a step in this direction by narrowing the scope to a particular microRNA molecule called miR-203-3p and finding that when muscles have exhausted all their glucose stores during prolonged exercise, it signals to the fatty tissue to make more fuel available. "This metabolic flexibility is essential for good health and performance enhancement," says Mori.
Positive effects of calorie restriction
Curiously, their previous research on mice found that calorie restriction would also increase the production of miR-203-3p.
Animal evidence and some human studies suggest that severely limiting calorie intake, such as through intermittent fasting, may help prevent conditions associated with aging, such as diabetes and heart disease.
In muscle cells, a molecular sensor called AMPK is activated when cells consume large amounts of ATP, which is the fuel that powers all cell activity.
Activation of AMPK is known to play a role in the metabolic benefits of both calorie restriction and aerobic exercise.
In their latest series of experiments, the researchers showed that aerobic exercise activates AMPK in the muscles and fat cells of mice. This in turn increases the production of DICER in the fat cells to release additional energy stores.
