This study from the University of São Paulo (USP) will certainly contribute to the development of alternatives to treat muscle weakness and atrophy. The Brazilian researchers, in partnership with American and Norwegian colleagues, show here, in Scientific Reports, that the absence of muscle stimulus results in an accumulation of toxic proteins in the cells which leads to muscle weakness or loss. of muscle mass. It is typically this type of muscle dysfunction that affects the elderly or people with sciatic nerve damage, bedridden patients or even workers who spend long hours sitting, specify the authors.
This buildup of toxic proteins is found to be linked to impaired autophagy, the cellular process responsible for identifying and eliminating damaged proteins and toxins. The study deciphers this process on a group of rats subjected to an exercise program preceding an injury and shows that physical exercise can keep the autophagic system working, optimizing its activity if necessary, as in the case of a dysfunction. muscle related to an injury or a temporary lack of exercise.
Without autophagy, a molecular cascade leads to cell death: Here, the demonstration is performed in rats undergoing sciatic nerve ligation surgery, to create an effect equivalent to that of sciatic nerve compression in humans. The pain prevents the human or animal subject from using the affected leg and the muscles involved weaken and atrophy. During the 4 weeks preceding the surgery, the rats had been divided into 2 groups, one sedentary and the other trained to run at 60% of maximal aerobic capacity for 1 hour a day, 5 days a week. The experiment shows that the muscular dysfunction induced by the lesion of the sciatic nerve turns out to be less aggressive in the “aerobic” group than in the sedentary group. The researchers observe that the physical training increases autophagic flow and thus reduces dysfunctional protein levels in the muscles. At the same time, exercise improves the contractility of muscle tissue.
Thus, daily exercise sensitizes the autophagic system , facilitates the elimination of proteins and organelles that are not or no longer functional in the muscles. Elimination of these dysfunctional components is essential, because when built up, they become toxic and contribute to the breakdown and death of muscle cells.
Muscles work like a refrigerator , which needs electricity to operate. If this signal ceases because you remove the plug from the refrigerator or block the neurons that innervate the muscles, the foods, such as the proteins in the muscles, will start to “spoil”. Initially, an early warning mechanism present in the cells activates the autophagic system, which identifies, isolates and eliminates faulty material but if the mechanism ceases to function properly, the cells also malfunction. The proteins that then form toxic aggregates begin to damage and cause cell death.
Exercise is a transient stress that leaves a memory in the body, here via the autophagic system. When the body is subjected to other stresses, it is then better prepared to react and combat the effects.
The idea, at the end of this work, would be to be able to identify a molecule that selectively keeps the autophagic system on alert, similar to what happens during physical exercise, and to develop a drug to treat muscle dysfunction. . In particular, in bedridden or immobilized patients, or suffering from degenerative muscular diseases.
