What Cold Showers and Exercise Have in Common Getting Stronger

Can cold showers, winter plunges, and brisk walks in the chilly outdoors provide some of the same benefits as intense exercise—including weight loss and increased energy levels? Such a link has been suspected, because cold exposure is known to convert metabolically docile white adipose tissue (WAT) into metabolically active brown adipose tissue (BAT). This “brown fat” helps you stay warmer and burn more energy

But now there is some evidence that cold exposure doesn’t merely help you turn up your inner furnace, and burn off a little fat in the short term. It may actually lower your body’s weight set point by activating a hormone that is also released during intense exercise.

That hormone is irisin (pronounced “EYE-rissin”), a cytokine produced in skeletal muscle. From the initial evidence, irisin and its partner hormone FGF21 may provide lasting benefits by boosting your metabolism and inducing you to shed excess pounds

Brown fat. BAT, or brown fat, is a very different kind of fat than WAT, or white fat. The mitochondria in BAT cells can quickly turn calories into heat. They do that by using the protein thermogenin (also called uncoupling protein 1 or UCP1) to bypass the normal efficient conversion of glucose or fatty acids into ATP, our energy storage medium, via oxidative phosphorylation. Instead, thermogenin “wastefully” oxidizes fatty acids to generate more heat, with minimal conversion to ATP

BAT is activated after cold exposure, and is beneficial for weight management because it can increase resting metabolic rate by up to 20%. As if that weren’t praise enough, brown fat it has been reported to have several additional health benefits, including reduced triglyceride levels, reduced incidence of fatty liver, and increased bone mineral density.

Discovered only in 2012, irisin is a special type of hormone known as a cytokine, and because it is produced by muscle it is classified as a myokine

Gretchen Reynolds, in a recent New York Times article, “Shivering as a form of exercise“, highlighted a just-published study in Cell Metabolism by Paul Lee and coworkers at NIH, demonstrating that vigorous exercise and exposure to the cold each activate production of a singular hormone — irisin — by a common mechanism

The researchers concluded that muscle contraction is the common mechanism causing release of irisin in exercise and shivering. They hypothesize that shivering — the rapid contraction of muscle — evolved as an early means of generating warmth, so that irisin secretion is as an inherent product of muscle contraction, whether from cold exposure or from exercise

Through irisin, shivering induces a basic type of cold-induced thermogenesis, called shivering thermogenesis or ST. The researchers found that ST is necessary to make muscles secrete irisin, causing the formation of brown fat. However, as brown fat accumulates, a second type of cold-induced thermogenesis kicks in, called non-shivering thermogenesis or NST. And non-shivering thermogenesis activates another hormone called fibroblast growth factor 21 or FGF21

So basically, this is the way you adapt to the cold: at first you need to get cold enough to shiver so that your muscles produce irisin, which increases brown fat. And as brown fat accumulates, you no longer need to shiver as much because mere cold exposure produces FGF21, which reinforces brown fat accumulation. The good news is that once you are adapted, you no longer have to shiver to get the benefits of cold exposure, because FGF21 acts to sustain brown fat accumulation and its metabolic benefits

The systemic effect of cold exposure, leading to hormone-regulated adaptations, is classic example of hormesis!

A 2013 article by Piya et al in Endocrine Abstracts, describes evidence for Irisin as a central regulator in energy homeostasis. The authors identified irisin in human cerebrospinal fluid (CSF) and found that brain levels of irisin were significantly lower in obese pregnant women than in their lean counterparts

The suggestion here is that irisin could be acting to inhibit NPY receptors, thereby reducing appetite and increasing metabolism

While what we’ve learned about irisin is promising, it should be noted that this is cutting edge science. It’s early days, and the precise role that irisin plays is not fully understood. It could be a major player or — as Peter Attia (whom I respect) suggests — a relatively minor one