Taking ice baths has been popularized, in part, due to the effects of the cold on weight loss. One of the body’s ways of responding to cold is to increase metabolism, not to produce energy in the form of adenosine triphosphate (known as ATP), but to produce heat to warm the body and, in the process, burn fat. This process is referred to as cold thermogenesis. There are two types of thermogenesis that occur as a biological response to cold exposure. The first kind of coldinduced thermogenesis occurs in muscle tissue and involves ramping up metabolism in order to produce heat. This works because metabolism is not 100% efficient and produces heat as a byproduct. This is referred to as shivering thermogenesis, because the muscle contractions are what actually increases the energy metabolism. The second type of coldinduced thermogenesis occurs in adipose tissue (fat) and does not involve shivering. It is called nonshivering thermogenesis. This type of thermogenesis is what is really responsible for the “fat burning” effect that cold exposure can have and usually happens after the body has adapted to cold exposure. Let’s talk about nonshivering thermogenesis and brown adipose tissue.This process is partly regulated by norepinephrine, which we already know is robustly induced by cold exposure by anywhere from 2 to 5fold, depending on the intensity of the cold and length of the exposure. Coldinduced norepinephrine increases the expression of protein known as uncoupling protein 1 (UCP1), which has the effect of uncoupling the mitochondria, the energyproducing
powerhouses of the cell.
But what does it mean for mitochondria to be uncoupled? When it is said that the mitochondria are coupled, we are referring to the coupling of the generation of a unit of energy (ATP) to thetransport of electrons (which have been derived from the food you eat), that create an electrochemical gradient across mitochondria which is negatively charged on the inside and positively charged on the outside. Mitochondria are a little bit like batteries in that sense. When cold exposure activates the uncoupling protein 1 (UCP1), this uncouples the electrochemical gradient, meaning there is no longer a negative or positive terminal to the mitochondria. In response, the mitochondria try and reestablish the electrochemical gradient by transporting electrons which are derived from stored fat (called fat oxidation) and producing heat as a byproduct of this process. One of the ways uncoupling protein 1 (UCP1) ramps up metabolism is by producing more mitochondria in adipose tissue, which causes a “browning effect” by converting or “transdifferentiating” the more common white adipose tissue into it’s more metabolically active counterpart, brown adipose tissue (BAT). You can think about this is simple terms: the more brown adipose tissue your body has, the more fat your body will burn. The reason it is called
brown adipose tissue is because each fat cell has more mitochondria per cell and the mitochondria make the fat appear brown when looking at it under a microscope. Cold exposure increases nonshivering thermogenesis in humans.It was thought for some time that human adults had negligible amounts of brown adipose tissue (BAT). Increasingly, however, studies are showing that adult humans do have this special type of adipose tissue that is metabolically active. The fact that we have brown adipose tissue at all in adulthood actually overturns old dogma that once stated that BAT was mostly found during infancy in humans. In fact, it’s now been shown that brown adipose tissue (BAT) shows an inverse correlation to percent body fat in an individual. Therapeutically enhancing the transdifferentiation or production of brown adipose tissue (BAT) from white adipose tissue (WAT) is a promising and active field of clinically applicable research for the treatment of obesity.
The good news is that repeated intermittent cold exposure has been shown to both increase brown adipose tissue (BAT) in humans and increase our capacity for nonshivering thermogenesis. Healthy young men and women that were exposed to air temperatures of 5961°F (1516°C) for 6 hours a day for 10 consecutive days increased their brown adipose tissue by around 37%, and after acclimating also increased nonshivering thermogenesis by 1118%. It is also interesting to note that if the BAT was sampled during the summer it was only detected in ~25% participants compared to 50% if BAT was sampled during winter. If having more brown adipose tissue, which becomes more active in cold, helps us stave off
obesity then it might reasonably be surmised that being cold would boost our metabolism. In fact, it does! One study done in a small sample of young men showed that coldwater immersion (head out) in 68°F (20°C) for one hour increased metabolic rate by 93% and 1 hour at 57°F (14°C) increased metabolic rate by 350%. I’d like to discuss one mechanism by which cold exposure may increase the concentration of brown adipose tissue. One study found that the sympathetic nervous system may be playing an intimate role in the production of brown adipose tissue in rats: experimentally blocking betaadrenergic receptors, which norepinephrine acts on, prevented the production of brown adipose tissue. This relationship is interesting, because it might imply that the greater the release of norepinephrine that we can induce from cold, the more browning of our adipose tissue we might expect to occur.
Our diet may also be a way we can therapeutically brown our adipose tissue. One study recently showed that consumption of fish oil actually increased the metabolism of mice, reduced the fat accumulation between 15 to 25%, and was shown to likely be doing this by a brown adipose tissuemediated mechanism. Cold exposure increases activity of antioxidant enzymes.One of the side effects of ramping up fat oxidation to burn stored fat for energy is the production of those damaging reactive oxygen species (ROS) that damage nearly everything inside cells, including DNA. This is actually a normal product of energy metabolism and, in a way, is a natural part of being alive. How we respond to this damage and mitigate it is ultimately what’s important. Reactive oxygen species (ROS), by contributing to things like DNA damage and cellular senescence, are a huge component of the very process of aging. They are also a sign of mitochondrial dysfunction. Being able to prevent that damage from occurring or being able to repair it after it does occur is extremely important to staying healthy, and for one thing, cancer
free. Interestingly enough, it appears as though the exposure to cold, by functioning as a hormetic stressor, actually activates very potent genetic antioxidant systems which are exponentially more powerful than supplemental antioxidants. For example, young men exposed to cryotherapy for 3 minutes at 202°F (−130°C) everyday for 20 days doubled the activity of one of the most potent antioxidant enzyme systems in the body called glutathione reductase, and increased another potent antioxidant enzyme called superoxide dismutase by ~43%. Similarly, elite kayakers that engaged in whole body cryotherapy (248 to 284°F or 120 to 140°C) 3 minutes a day for 10 days increased the activity of superoxide dismutase by 36% and glutathione peroxidase by 68%. That is pretty stout. For those of you not familiar with superoxide dismutase, this enzyme is in your mitochondria cleaning up all that damage that is being produced every second of every day. In other words, it is awesome. It is also important to note that the increase in antioxidant enzyme activity, in this case, took multiple sessions of the whole body cryotherapy…meaning the more frequent cryotherapy was done, the more robust of an increase in activating these powerful antioxidant enzymes. You can learn more about our endogenous antioxidant systems, some of the nuance surrounding supplemental antioxidants, and the effects of reactive oxygen species in my video “Do Antioxidants Cause Cancer?” by clicking here. Cold Shock, Muscle Mass, Performance, and RecoveryWhen it comes to cold exposure in the context of exercise there are two important factors to look at…
- the type of exercise being done …and…
- the timing of the cold stress in relation to the exercise.
Let’s talk about timing. Immediately after exercise activity there is a spike in the production of proinflammatory cytokines, which are molecules that activate immune cells and are involved, importantly, in tissue repair. The production of reactive oxygen species and inflammation that occurs immediately after exercise are actually necessary to activate genetic pathways that contribute to creating more mitochondria (mitochondrial biogenesis) and also play a role in muscle hypertrophy. In fact, macrophages, a type of immune cell that can be activated in response to exerciseinduced inflammation, produce high levels of the anabolic hormone IGF1 in response to even slight injury of muscle tissue. There has been some experimental evidence that indicates that these specific immune cells are also likely involved in satellite cell migration. Satellite cells are a type of muscle stem cell that serve as precursors to actual muscle cells and www.foundmyfitness.com satellite cell numbers are actually associated very closely with the amount of actual hypertrophy that results from strength training.
Let’s get back to the exerciseinduced inflammatory response. There is an antiinflammatory response to this inflammation which begins to peak about 1 hour after exercise. At this point, some of the anabolic hormones such as IGF1 that are increased with the immune activation seem to also return to preexercise levels around 1 hour postexercise. These antiinflammatory cytokines help keep our immune system from going overboard. They modulate the activity of the
immune cells, preventing them from causing excessive tissue damage.
You might see where I’m going with this already. In the cases where cryotherapy, coldwater immersion, or perhaps even the use of ice packs are used immediately after training, it may undermine certain beneficial effects that actually come from having a small dose of inflammation. In fact, there have been some studies that seem to hint at this fact. We’ll dive back into that in a second, but the main thing to remember, for now, is that the peak antiinflammatory response occurs 1 hour after the activity, and that some inflammation and immune activation before that point is probably a good thing. Let’s talk about the variety of exercise.The other factor that may influence the outcome of studies looking for the effect of cryotherapy or coldwater immersion on athletic performance and recovery is the type of activity we’re trying to optimize for. Exercise inflicts stress upon the body, and, in response, the body activates many genes and pathways that build resilience and resistance to that stress. What is important to realize is that the type of exercise actually determines characteristics of the adaptation that occurs: the stress may be predominantly aerobic (such as endurance training), mechanical (such as resistance training) or a mixture of both (plyometric). Activities that are more characteristically aerobic place a greater demand on the cells to be able to utilize oxygen for the purposes of energy production. In other words, aerobic activities have a greater need of supporting mitochondria! Depending on the nature of the exercise (endurance vs. resistance) and the time of the cold
exposure (preexercise, immediately after exercise, or later) there may be very different and somewhat opposing outcomes. I believe that these variables can help explain some of the
conflicting evidence regarding the benefits of cold exposure in the context of exercise performance that have shown up in the scientific literature and been discussed in the media. But what does the literature actually say about cold shock and exercise performance?