Over time, cells, like a small house, accumulate "garbage"—damaged proteins, worn-out parts, or invading microbes. Autophagy acts like a cleaning service: it finds this waste, stores it in special "bags," processes it, and returns useful components to the body. This process maintains cellular health, protects against disease, and supplies the body with energy during exercise and fasting.
In the study, 10 healthy men (average age 23) were immersed in water at 14°C for an hour daily for a week. The researchers monitored blood proteins to assess the impact of cold on key cellular responses: autophagy, inflammation, and heat shock.
When cells are suddenly cooled, their protein structure is disrupted—they begin to fold incorrectly and clump together. In response, the body activates a protective mechanism. Specialized heat shock proteins (HSPs) help restore damaged proteins to their proper shape, prevent their accumulation, and direct irreversibly damaged molecules for disposal, including through autophagy.
Initially, the participants exhibited autophagy dysfunction, manifested by the accumulation of the p62 protein. This protein acts as a "marker"—it binds to damaged cellular components and prepares them for disposal through autophagy, and is then "disposed of" along with them. If p62 accumulates, the process is disrupted. Concurrently, levels of caspase-3, responsible for apoptosis (cell self-destruction), increased. These data demonstrate a key mechanism of the cellular response to stress: when autophagy (p62) is ineffective, the controlled cell death program (caspase-3) is activated.
By the fourth day of the experiment, p62 protein levels had decreased (though they remained above baseline), while caspase-3 levels remained high. Apparently, autophagy was unable to cope with the cold stress. However, by the seventh day, the situation had changed: autophagy-related activity began to prevail over cell death signals. The cells began to tolerate the cold better.
According to scientists, exposure to cold may help prevent disease and even slow aging at the cellular level. However, further research is needed.
