We just talked a lot about strength training in the context of cold-water immersion.
In the case of endurance related activities, the consequences of coldwater immersion, and, in particular, wholebody cryotherapy are slightly more unambiguously positive. This may be characteristic of the type of adaptations that occur that are more specific to endurance activities or it could be that fact that the cold exposure was not done immediately post exercise. In addition to the effect cold can have on inflammatory processes…
Cold increases mitochondrial biogenesis. Cold stress is able to boost mitochondrial biogenesis. The reason this mechanism exists is pretty straightforward: mitochondria are able to create heat (something you need when cold) as a byproduct of energy production. As the powerhouses of the cell, it can be said that mitochondria are pretty darn useful for most of our cells, except red blood cells, which don’t have them, however, they’re especially important if we want to talk about endurance activity…
That’s because mitochondria, and the density or number of them on a per cell basis, affects our aerobic capacity. Mitochondria are what gives us the ability to use oxygen in order to produce cellular energy, and if we have more of them, it can be said we may be more adapted to aerobic activity.
Here’s how it works…
Cold exposure activates a gene called PGC1α, which makes more mitochondria in the muscle. This is referred to as mitochondrial biogenesis and PGC1α is the master regulator of this process. If mitochondrial biogenesis is the orchestra, then PGC1α is the conductor.
More mitochondria per muscle cell directly translates to aerobic capacity, and a single 15 minute exposure to cold water (50°F or 10°C) following high intensity running, increases PGC1α in muscle tissue. But even more importantly, cold exposure is actually able to increase mitochondrial biogenesis: men that were immersed in cold water at 50°F (10°C) for 15 minutes 3 times a week for four weeks after running were able to increase mitochondrial biogenesis occurring in their muscle tissue.
Exercise that is highly aerobic, such as jogging or running, has the characteristic of being very metabolically demanding and thus requiring more muscle fibers that are oxidative (oxygen using) and fatigue resistant. These types of muscle fibers mostly consist of type I (or slow twitch) muscle fibers. In contrast, muscle fibers that are specialized for bursts of short duration power mostly consist of type II (or fast twitch) muscle fibers which are muscle fibers that are more glycolytic (glycolysis is a process that produces energy that does not require oxygen).
There is a category of fast twitch muscle fibers called type IIa that are fast oxidative fibers that are more resistant to fatigue. It turns out that PGC1α, as part of or in addition to working its magic to trigger mitochondrial biogenesis, also happens to induce a switch to oxidative, fatigue resistant muscle fibers.
Remember that cold stress induces PGC1α and this induces mitochondrial biogenesis. It is interesting to note that getting rid of PGC1α in the muscle tissue of mice has been shown to shift muscle fibers from the slow twitch type I and the fast twitch type IIa muscle fibers that are both oxygen requiring and more resistant to fatigue, toward fast twitch type IIb muscle fibers, which are glycolytic fibers required for very short duration, high intensity bursts of power such
as maximal and near maximal lifts and short sprints. In line with this, genetically engineering mice to express more PGC1α in muscle tissue than they normally have, causes their muscle cells to show characteristics of type I muscle fibers, such as a greater resistance to fatigue.
In my mind, this suggests that PGC1αmediated mitochondrial biogenesis may be slightly more beneficial for endurance athletes than those focused purely on brute strength, if for no reason other than the fact that it seems to shift muscle fibers into a configuration that is more conducive to a higher aerobic capacity and more resistant to fatigue. Of course, I can’t say that this is absolutely the case because PGC1α also increase type IIa muscle fibers and type II fibers do have a higher capacity for hypertrophy.
So now that we’ve covered a little bit on why endurance activities may be a little bit less likely to experience specific deleterious consequences of mistimed cold stress, let’s talk about what the actual literature says about whole body cryotherapy, and cold water immersion in the context of performance enhancements.
Elite runners that engaged in whole body cryotherapy 1 hour, 24 hours, or 48 hours post hill sprint running had a 20% increase in speed and power up to two days later. This 20% performance enhancement post cryotherapy may be attributed to the reduction in inflammation and increase in anti inflammatory factors. Too high of levels of proinflammatory cytokines post exercise can result in acute performance deterioration and muscle damage.
This can be problematic for training even several days later, since there may be a greater risk of injury due to residual soreness and changes in muscle function. In fact, it has been shown that elite runners who engaged in whole body cryotherapy for 3 min at 166°F ( −110°C) performed 1 hour post exercise and 24 hours post exercise enhanced muscle recovery by decreasing the inflammatory process (IL1β and Creative protein) and increasing the anti-inflammatory process (IL1ra) at both time points.
Another study including elite tennis players also showed performance enhancements that were associated with a reduction in inflammation. Elite tennis players that engaged in whole body cryotherapy (184°F or 120°C) twice a day (in the morning and evening while training in the afternoon) for five days had a 2.5fold decrease in the potent proinflammatory cytokine TNFalpha and a 23% increase in the cytokine IL6, which has both pro and anti inflammatory properties and plays a role in muscle repair. These professional tennis players also experienced a 4% increase in “stroke effectiveness,” meaning they hit more balls in the target zone compared to the players that did not do cryotherapy. Hey, that’s what counts, right? Maybe it’s that norepinephrine helping with focus and attention.
These endurance performance enhancements from post exercise cold exposure may also be sustained over a prolonged time period. Elite cyclists engaged in 15 minutes of cold water immersion (159.5°F or 15.3°C) 30 minutes post training 4 times per week. This training lasted 39 days and consisted of a mixture of low–moderate intensity road rides and high intensity interval sessions on a exercise bike (ergometer). The cyclists that engaged in cold water immersion post training experienced a 4.4% increase in average sprint power, 3% enhancement in repeat cycling performance, and a 2.7% increased power over the 39 day training period. That sounds awesome.
Role in preventing muscle atrophy. So far we’ve covered effects of various cold exposure modalities on building muscle, but one last area of discussion that I’d like to cover that loosely fits into this area is the topic of muscle atrophy. Quite a bit earlier when we were still talking about some of the interesting brain effects of cold stress, we talked about the effect cold has on the production of a cold shock protein called RBM3. We also talked a bit about some of the studies done on hibernating animals, which, of course, have to be especially capable at resisting the effects of cold during the winter. One other interesting aspect of hibernation is the fact that animals that experience this phenomenon, at least in the case of black bears, also experience significantly less muscle atrophy than would be expected for such a long period of fasting and general inactivity. As you might imagine, this probably is pretty useful for a hibernating animal! There is evidence that black bears actually retain protein balance in their skeletal muscle during hibernation. In other words, they are not, generally degrading more proteins than they are making in their muscle tissue, which would cause muscle atrophy.
This phenomenon is not limited to bears. It’s been shown that hibernating squirrels also experience an increase in RBM3 in the brain, cardiac, and skeletal muscle. Skeletal muscle cells from mice that have been engineered to have increased levels RBM3 have improved muscle cell survival, and even a larger muscle cell size after being exposed to cold shock. RBM3 is clearly playing an important role in the muscle in multiple organisms and may be serving as a generalized mechanism for decreasing atrophy.
This would also explain why RBM3 is the most highly elevated gene in the muscle tissue of black bears that is in concordance with protein synthesis during their hibernation. RBM3 isn’t the only cold inducible protein that is associated, at least in animal studies, with a reduction in muscle atrophy. PGC1α, the master regulator of mitochondrial biogenesis that we talked about earlier, like RBM3, has also been shown to be increased in humans under conditions of cold stress. It has been shown to protect against sarcopenia (age related muscle loss) and metabolic disease in mice that were genetically engineered to express more of the protein.
While it’s important to note that all of these studies that I’ve discussed in the context of muscle atrophy are animal studies, it shows promise when you see a similar effect conserved across multiple different species of animal, because it hints at the fact that this mechanism might extend to us as well, and is probably not a point of specialization… at least not for one specific species.
Finally, one last note on this subject: heat shock proteins, otherwise known as HSPs, can also be induced to some extent by cold, and I’ve discussed in a previous video on the science of sauna use, how heat stress and the concomitant elevation of heat shock proteins has been demonstrated to greatly increase muscle regrowth by 30% in rats during the two week “reloading phase” that followed a week of forced immobilization (atrophy).