In humans, the process of autophagy occurs during aging, at least in part, when the body breaks down the myosin fibers in our muscles and joints. The breakdown of myosin fibres can occur due to stress, such as injury and surgery, and due to increased metabolic activity.
In most cases, the human body doesn’t perform autophagy fully; some of the myosin fibres in muscle remain undigested for years, causing the muscles to atrophy. However, the body can also take advantage of the breakdown process to produce new myosin fibres. The muscle fibers become extremely fragile as a result. When the body cannot absorb the nutrients it needs, these nutrients are then absorbed by the skin. This is why we get dry skin after we exercise.
Another benefit of autophagy in muscle cells is that the breakdown of myosin fibres creates high concentrations of amino acids that can be used by the body. These amino acids may act as nutrients to repair damaged tissue or to boost the immune system. Autophagy in muscle cells may also allow the production of fatty acids, which in turn can help the body burn fat.
In order for autophagy to take place properly in the body, a specific organelle must be activated. This activates a process in the cells called “peristaltic motility,” in which the movement of molecules through the cell membranes is facilitated by a chemical reaction between amino acids. One particular type of enzyme, referred to as AMP is responsible for this process. AMP can only be activated by the enzyme glycogenolysis.
Glycogen is a special sugar found in the muscle and liver cells of the body. When glycogen levels in these cells drop, they can no longer function properly; they can no longer carry out peristaltic motility and therefore can no longer stimulate the movement of molecules within the cell. A number of proteins, including a series of enzymes known as glycogen synthetases, convert glycogen to glucose and then use the glucose as energy to provide the movement of molecules in the cell membranes.
When autophagy in muscle cells stops, glycogen synthetases turn to a protein called glycogen degradation protein. This is a protein that will not break down as it was designed to do and is used instead as a source of energy to enable the breakdown of myosin fibres in the muscle cells.
Many glycogen synthetases have been isolated and identified so far, including one called “Gly482”. This enzyme can degrade glycogen and provide the body with energy and other nutrients, thereby allowing the muscle cells to perform autophagosome (protein-making) activity. Gly482 has been shown to play an important role in the process of autophagy in muscle tissues.
Gly482 is not the only enzyme that is needed in order for glycogen to be broken down. Another type of enzyme, called the glycogen phosphatidyl-transferase, is also required. The enzyme glycogen phosphatidyl-transferase (GPT) is known to contribute to the process by which glucose and other nutrients are transferred into the cell. However, GPT cannot be activated without the presence of glycogen enzymes.
Some studies suggest that GPT and the glycogen phosphatidyl-transferase can be activated by the liver, pancreas, or stomach. While some of these studies were conducted on mice, some studies have been conducted on human volunteers. Studies in humans have shown that in cases where GPT has been injected intravenously, some benefits have been noted. However, these studies have not been conclusive.
The process of autophagy is important in the growth of muscle tissue. It is possible that there are more than one autophagy protein-producing organelles in the muscle tissue of the body.
