Strength training reduces fat cells, leading to weight loss

The researchers wanted to understand what happens to adipose tissue at the very beginning of strength training, before weight loss begins to affect metabolism and mask the direct effects of physical activity. To do this, they worked with male mice: some of the animals received a regular diet, while others received a high‑fat diet to induce obesity. Then the obese mice were divided into two groups: one remained without physical activity, while the other performed strength exercises. At the same time, all the animals continued to receive high‑calorie food, so the experts could isolate the effect of the training.

The load itself looked like climbing a 70‑centimeter staircase with a weight attached to the tail. Each training session was conducted at 70 % of the animal’s maximum capacity: the mice performed 20 climbs with breaks of 60–90 seconds. A total of seven such sessions were held. According to the study’s lead researcher, Leandro Moura, this approach made it possible to simulate for the animals the same intense muscle contractions that occur in humans during strength training.

Particular attention was paid to mesenteric adipose tissue — the layer of fat around the intestines. In mice, it serves as an analogue of visceral fat in humans: the kind that accumulates deep in the abdominal cavity, near vital organs. It is this type of fat that is particularly dangerous, as in excess it releases inflammatory substances into the bloodstream and disrupts metabolism throughout the body.

Despite the fact that the overall weight of the exercising mice did not decrease, the volume of their mesenteric fat decreased, and the fat cells themselves (adipocytes) became significantly smaller. In obesity, adipocytes become greatly stretched, experience chronic stress, and begin to release pro‑inflammatory molecules. A reduction in cell size indicates that the tissue becomes metabolically healthier, even before any changes are visible on the scale.

To understand the mechanisms, scientists looked inside the cells. They monitored the activity of proteins that regulate lipolysis — the process of breaking down stored fat. The key players turned out to be PLIN1 (perilipin‑1), ABHD5, and ATGL. In simplified terms, the chain works as follows: under the influence of stress, PLIN1 changes and releases ABHD5, which then activates ATGL — an enzyme that initiates the first stage of fat breakdown. Furthermore, the activity of the Scd1 gene, which is responsible for the synthesis of new fat molecules, decreased; this means that the body becomes less inclined to store calories as fat.

In inactive, obese mice, this system functioned less effectively: the level of ABHD5 was reduced, and the fat breakdown mechanism was practically not activated. Strength training, by contrast, enhanced the interaction between ABHD5 and ATGL and activated other markers of lipolysis.

These data help dispel the common myth that strength training is only needed for muscle growth, and that only aerobic exercise helps burn fat. As the authors emphasize, both types of exercise engage overlapping and yet distinct molecular pathways, so combining them remains the best strategy for improving metabolic health and reducing weight.

It is important to remember that the study was conducted on animals: these results cannot be directly applied to humans. Only male mice were involved in the study; one type of fat deposit and a limited set of molecular signals were examined. In the future, scientists plan to track how these mechanisms develop during longer training sessions and against the backdrop of actual weight loss, as well as to study the effect of exercise on other fat deposits, including the fat around the heart.

The main practical conclusion for those who are just starting to exercise is that the absence of quick changes on the scale is not a reason to give up. Already in the first days of training, the body initiates important metabolic processes that improve health and lay the groundwork for future weight loss.