The Beautiful Science of Cold Exposure (BAT, part 1 of 6)

Is there value to a cold morning stroll, a dip in an ice bath, a cold shower, or a river plunge? Does the struggle amount to any significance? This six-part series will examine what science says about this “masochistic” pursuit. Beware, many of the suppositions you held and the beliefs you advocated for could be false— it certainly was the case for me!

What is cold thermogenesis?

By definition, cold thermogenesis is the process of increasing heat production by exposing the body to temperatures cold or long enough to induce a physiological response. This physiological response is generally categorized as vasomotor and/or metabolic.

A vasomotor response is induced by retaining heat through peripheral vasoconstriction. During cold exposure, our bodies undergo a heat shift. This is done by limiting the movement of heat away from the core.

During peripheral vasoconstriction, there is an upregulation of sympathetic output to the inner part of the adrenals called the adrenal medulla, promoting the secretion of epinephrine and norepinephrine in the bloodstream. 

A Secretion of epinephrine is not limited to cold exposure but could also be activated through exercise, sleep, meditation, and even certain foods such as dark chocolate. Yes, nutrition can activate epinephrine by containing a dopamine precursor called tyrosine. It is important to remember that many types of sympathetic activation promote vasoconstriction. Therefore, even undesirable stress, such as heart failure, bleeding, etc., could also increase the upregulation of epinephrine in the bloodstream. The crucial difference between cold stress and heart failure is injury and vulnerability, the length of exposure (chronic versus acute), and the adaptive response to the stress.

The metabolic response, like the vasomotor response, is also heat related. However, the difference between the two is where the heat is produced. In a metabolic response, the source of heat production is generally created in the muscles through an involuntary somatic motor response. This involuntary contraction is also known as shivering or non-shivering thermogenesis. If it helps, think about shivering as ATP or energy.

According to the Canadian Journal of Anesthesia, shivering increases Vo2 because the cardiac output (the amount of blood the heart pumps through the circulatory system) increases with cold exposure. The increase in cardiac output is partly explained by a rise in stroke volume (end-diastolic volume minus end-systolic volume or SV = EDV - ESV) with little change in heart rate. You may wonder, doesn’t exercise increase cardiac output and stroke volume? Yes, it does! However, the increase in cardiac output is followed by an increase in heart rate, while cold immersion does to a lesser degree. 

In cold conditions, the body compromises by shivering. And it shivers and creates energy to the degree that many studies have shown a concomitant 2-5 fold increase in metabolic rate. This study, in particular, conducted by Andrew J. Young et al. in the “Journal of Applied Physiology” found that after ten minutes of cold air exposure at 5 degrees Celsius (41 F.), metabolic rate increased by 85% and continued to rise slowly for the ninety minutes of the cold air exposure. However, acclimation was shown to decrease the effects of metabolic rate. The key is to preserve the stimuli. 

Now that you have a background on cold exposure, in the upcoming six-part series, we will assess the validity of some of the most common claims of cold thermogenesis and why it may or may not matter. Many of these claims are one and the same with slight nuances.

These claims are:

Part 1/6: BAT activation.

Part 2/6: Increased Metabolism/Fat Loss.

Part 3/6: Uptake in Glucose Metabolism. Promotes Insulin Sensitivity. Shifts Towards Fat Utilization.

Part 4/6: Enhances Immune System. Promotes Cell Longevity. Promotes Mitochondrial Biogenesis. 

Part 5/6: Enhances Recovery. Promotes Brain Function and Mood. Reduces Depression.

Part 6/6: Increase Testosterone. Increase Human Growth Hormone (HGH).

BAT Activation

Have you ever heard a dietician or a self-pronounced health guru promise a 500% increased metabolism by activating your brown fat (BAT)? After watching their video or reading their articles, you are motivated to jump into a river and ignite your BAT. But what can you actually extract if you re-watch that video or re-read that article for substance? Usually, not much. The goal of this series is to provide enough evidence for you to become more informed on this topic and decide whether or not the evidence is convincing enough to start a cold thermo practice.

What is BAT?

Brown adipose tissue, also known as BAT, has many functions. Chiefly, BAT’s purpose is to convert food or food storage into body heat; this is why the activation of brown fat is promoted and associated with well-being and health. The Journal of Gerontology contrasts the two adipose tissues: WAT stores excess energy as triglycerides, and BAT specializes in energy dissipation through heat production (Shung et al., 2020). This short sentence does an excellent job of portraying the antagonistic functions of white and brown adipose tissue.

But why does BAT use more energy? 

I will answer this question in more detail toward the end of this section. For now, know that browning or BAT usually means more mitochondria. In comparison, white adiposity represents fewer mitochondria, and the mitochondria generate most of our energy (calories). 

Although this may seem simple enough, there is still much to understand and learn! For example, it was presumed that BAT wasn’t preserved with age but decreased after infancy. Only recently, in 2003, scientists discovered BAT formation in adults, and cold played a significant role in this activation. Who knows what else scientists will dig up and uncover on BAT in the future?

How does the cold increase BAT?

I touched on this question during my introductory, but if you want to learn more, continue reading. 

In response to cold, norepinephrine gets secreted from the adrenals and binds to the b3 adrenergic receptor in the adipose tissue. The activation of these receptors sends an intracellular signal to break down Triglycerides to FFA (free fatty acids). These fats interact with UCP1 (uncoupling protein 1), a mitochondrial carrier protein found in brown adipose tissue, affecting energy synthesis. This energy can be derived from recent ingestion of food or stored energy such as white adipose tissue (WAT). 

Aside from promoting the conversion of white adipose tissue to brown adipose tissue, BAT also seems to have an affinity for insulin. This affinity, most likely due to the expression of GLUT4 (a glucose transporter), has been hypothesized to increase or upregulate glucose metabolism in BAT without needing insulin secretion. In other words, BAT requires energy in the form of glucose, and this glucose uptake doesn’t require the central glucose metabolizer insulin. 

Does this then mean that cold exposure decreases plasma glucose? Maybe! But our bodies are efficient and can make up for potential plasma glucose reductions. Another question commonly arises: can I get away with eating more carbohydrates? That depends on what you mean when you say, “Get away.” In theory, yes. Though to what extent is still yet to be determined. Suppose you want to know this for yourself. In that case, I recommend purchasing a keto mojo, or better, a continuous glucose monitor and checking 20, 40, 60 minutes, and 2 hrs after eating if glucose is affected after a cold shower, ice bath, etc. do this a few times with the same foods and portions.

Does BAT use fat as its primary energy source?

The answer wasn’t as easy to uncover as I thought it would be. For example, a study in The Journal of Applied Physiology and Occupational Physiology found one result, and a different study found another. Let's look at the first. This study had seven healthy men fast for 14 hrs overnight and then undergo 2 hours of cold air exposure at 10 degrees Celsius (50F). Measuring their energy oxidation during this time through indirect calorimetry, the results showed a 63% increase in fat oxidation and a 588% increase in carbohydrate oxidation. The study showed a far more favorable carbohydrate utilization. However, a different research paper with a similar design showed the opposite effects: fat oxidation was higher (376%) than plasma glucose and muscle glycogen combined (247%). 

What accounted for the difference? The first group used air to induce stress, while the second used liquid suits. Interesting! The utilization of energy may be due to differences in cold exposure. Maybe the severity or type of cold stress affects different outcomes. Other studies that had participants run or walk in cold air conditions also showed increased fat oxidation (measured using a respiratory quotient). 

Some experiments explain energy substrate utilization in terms of shivering. In short, more shivering increases carbohydrate metabolism while less induces fat oxidation. Nevertheless, I would love to see more studies testing this hypothesis.

This only scratches how BAT is activated and used as energy: how it might be associated with much more such as insulin sensitivity, fatty acid utilization, and glucose uptake. Although more research needs to be conducted regarding cold thermogenesis on fuel substrate utilization during different macronutrient adherence, such as the keto or high carbohydrate diet. To learn more about the science of cold and BAT, I highly recommend the Effects of cold exposure on metabolites in brown adipose tissue of rats, found in the Molecular Genetics and Metabolism Reports. This research paper can be downloaded in PDF. 

In the next article, I will discuss the claims of increased metabolism and fat loss. I chose this as the second topic because it goes “hand in glove” with BAT activation— or take the glove off if you want to provoke your inner BAT.

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