It is very common among the population, that arises the spontaneous and urgent need to “go on a diet” sporadically to achieve a desperate fat loss for an important event or for the summer, which are nothing more than a desperate and misguided attempt to achieve a timely aesthetic improvement. Not only will it be an attempt against health, but also the improvements in body composition will be a temporary mirage, since in these situations sometimes absurd and risky protocols are usually carried out that not only endanger your muscle mass, but also encourage the regain of body fat after the stipulated date.

Weight gain and loss is often observed in obesity and there is a regaining of lost weight after “dieting”. Recovery of lost weight is stipulated at a rate of over 30% of subjects in 1 year and 95% at 5 years, i.e., a total failure.

During weight gain, the increase in fat mass is high compared to changes in muscle mass, so during these weight fluctuations, we can assume that participants lose and regain fat, but at the same time experience a loss of muscle mass, leading to the onset of what we know as sarcopenic obesity which I will discuss later. This could be explained in part by the accumulation of lipids (lipotoxicity), which prevents the incorporation of amino acids and reduces protein synthesis in skeletal muscle.

In fact, the very loss of muscle mass of these “protocols” induces that subsequent fat regain, due to what we know as proteinostat. I explain:

When we lose body fat by being subjected to a caloric deficit, hormonal and metabolic alterations occur that make us increase our appetite. For a long time, this hunger-satiety mechanism has been said to be controlled by certain hormones emitted by adipose tissue, the best known being leptin, which is a hormone emitted mostly by adipose tissue and which exerts an appetite-suppressing effect. Logically, when fat is lost, together with a reduction in calories and carbohydrates, less leptin is emitted and the sensation of hunger is not emitted, so it increases (which is why many bodybuilders cannot stop eating after a competition). This widespread theory is known as the “leptinocentric” or “Adipostat” theory.

However, we know that muscle tissue has a lot to do with this, because as we see in the graph, in a study known as the Minnesota experiment, subjects were put in extreme caloric deficit. The people went down they lost fat (blue line) but also a lot of muscle mass (red line), and when they went back to eating normal calories, the hyperphagia (increased appetite) did not stop until they regained their previous fat levels but continued until they regained their muscle mass levels, but at the same time there was what is known as collateral fattening, since their fat levels (blue line) increased even more above their basal levels because they could not stop eating.

This tells us two things: first that the adipostat theory is not the only one that influences hunger-satiety control and that muscle tissue plays an important role in it and second that any weight loss strategy in which muscle mass is lost (especially by extreme restrictions or by not performing strength training) are doomed to failure and that a yo-yo effect occurs.

Okay, but let’s continue….

Once we have regained that lost adipose tissue (with some extra kilograms added) after that desperate attempt to improve the physique in a short time, surely, after a while, there is again a negative feeling of wanting to lose fat again, as there is usually a feeling of guilt for having regained those kilos of fat lost.

So we return to undergo periods of caloric restriction, which hopefully this time, is not for a one-time event and there is awareness of the process and the importance of putting yourself in the hands of a qualified professional. But even so, the rate of abandonment before a nutritional intervention is very high. This can be due to multiple reasons, involving both the person concerned, the professional, and the social, economic and work environment of the subject in question. Therefore, creating adherence is key in any fat loss intervention.

So what’s going on here? Let’s see…

Due to a lifestyle, a sedentary context and bad protocols and diets established for rapid fat loss, we now surely find ourselves with a double problem, not only does the subject in question have excess body fat, but also has low muscle quantity/quality, and may be what we call sarcopenic obesity or sarco-obesity.

Obesity creates a chronic low-level inflammatory environment that can influence muscle remodeling, leading to impaired myocyte formation and, in addition, deposition of fibrotic and adipose tissue, with a consequent reduction in muscle structural integrity and functional capacity.

In a recent study, Rossi et al 2019 show how subjects (60 men and 147 women with obesity) who experience a greater number of weight gain and weight loss cycles over their lifetime have lower muscle mass and strength

The risk of developing sarcopenia was almost six times higher in participants with large phases of fat gain and loss compared to subjects with fewer phases. In fact, participants who had more than five cycles of weight gain and loss during their lifetime showed a reduction in muscle mass that was approximately five times greater than those who did not have these cycles.

The data from this study highlight the negative consequences on both the quantity and quality of skeletal muscle caused by repetitive weight cycling in participants with obesity, and it is therefore not surprising that there is a higher prevalence of sarcopenia in people who have multiple attempts and failures to lose fat.

Thus, there is a real risk for those subjects with obesity who repeatedly undergo repeated fat loss cycles, leading to loss of muscle mass and strength. These changes in body composition predict functional decline, cardiovascular disease, disability and mortality in subjects with obesity.


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