Brown Adipose Tissue

When the skin senses cold, cold receptors transmit signals to the hypothalamic thermoregulatory center and simultaneously activate brown fat through a direct pathway.

Using infrared thermal imaging, Søberg observed that after 4 minutes of immersion in 4°C cold water, the temperature of brown fat in the supraclavicular region rose markedly.

Brown adipocytes are rich in mitochondria and use uncoupling protein 1 (UCP1) to short-circuit the proton gradient, causing energy to be released as heat without generating ATP; this process is called non-shivering thermogenesis.

Human brown fat is mainly distributed in the neck and supraclavicular regions, is regulated by sympathetic nerves and cold stimulation, and its activity can be assessed in vivo by techniques such as PET-CT and infrared thermal imaging.

Shivering further activates brown fat through signals such as succinate, helping the body rewarm.

Søberg proposes the "end with cold" principle: ending with cold exposure, the body continues to generate heat on its own for hours afterward, brown fat and muscle cells remain active, and mitochondrial number and efficiency increase accordingly.

A 2017 study by Hansen et al. found that after subjects slept in a 19°C room for one month, both brown fat activity and insulin sensitivity increased; after returning to 24°C for one month the indicators fell back; after raising the temperature to 27°C, brown fat activation and insulin sensitivity declined further.

Even exposure of only areas such as the face to cooler air is enough to produce systemic metabolic effects.

There is currently insufficient evidence to quantify the specific magnitude of brown fat activation by different cold exposure protocols, and the optimal combination of water temperature, duration and frequency still awaits answers from more controlled studies.