Wim Hof breathing method to lower resting heart rate and increase blood oxygen saturation

I'd like to introduce something that's made a tremendous difference in my resting heart rate and overall feeling of well-being. It's the Wim Hof Breathing Method.

Wim (pronounced like Veem if you're North American) Hof is a Dutch man who holds many world records. His specialty is cold conditions and ice. For instance, he climbed both Mt. Everest and Mt. Kilimanjaro in shorts. He has done things that defy conventional thinking about what the human body is capable of doing. After gaining fame in the press, Dutch researchers became interested in how he was able to do these superhuman feats. Lots of studies have been done over the years. It turns out to be due in large part to his 3 part breathing method, which is a component of his 3 part training method. With the breathing method, he charges his body with oxygen and it penetrates the cells and sort of reboots the nervous system (my words). Currently, they're looking into using the method to improve things like lupus and autoimmune diseases. Both scientific and anecdotal results are very promising.

There are many, many videos on YouTube about it. Here's Wim Hof demonstrating his method on a video podcast. I have cut right to the demonstration: [youtu.be]

If you try it, I highly recommend easing into it. I started with one round for the first 3 days. The usual amount is 3 rounds. It was great using my pulse oximeter from the very start so I knew what my heart rate was and what my oxygen saturation was. Every single time I've done the technique, my resting heart rate has lowered and my oxygen saturation has gone up and stayed up.

I feel much better, and I credit Wim Hof with giving me back my quality of life. I know I'm going to do the method every day, for life.



Edited 1 time(s). Last edit at 11/02/2018 04:05PM by DojoMojo.

Sounds good! Wim has some very interesting data for those using his breathing technique, I've got his book.

Wim talks about using his breath hold swimming under ice. I do not recommend this. His technique reduces serum CO2 with hyperventilation. It will also reduce O2 as the breath hold time increases. The breathing center in the brain has two sensors that trigger the urge to breathe. The CO2 sensor is the one that usually triggers the out of breath feeling and urge to breathe. O2 has to drop pretty low for the O2 sensor to trigger. Hence shallow water blackout can happen. This can be fatal. If you aren't in water, there is no problem. Just don't play with this in water.

I do a lot of cold exposure as Wim recommends (daily 20 minute baths at 49-59 deg F, depending on the season). I've not found that I needed to precede the baths with his breathing, so I don't (I"m not knocking the breathing).

Glad it is working for you!

George

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DojoMojo
Every single time I've done the technique, my resting heart rate has lowered and my oxygen saturation has gone up and stayed up.

I feel much better, and I credit Wim Hof with giving me back my quality of life. I know I'm going to do the method every day, for life.

Thanks for this. Very noob question here. I always thought of a low resting heart rate as a result of lots of exercise, rather than a goal in itself. What is the advantage of it? Also what's the advantage of a higher oxygen saturation number? Do you feel a lot better/different?

Thanks

That was a valuable 2:24min spent, thanks Dojo! (Wim Hof)

Don't expect much from deep breathing (hyperventilation) other than reduced CO2 in the blood. However, it can help you relax if you don't over do it.

[forums.deeperblue.com]...

Mar 14, 2015 · With hyperventilation you can increase O2 saturation of the arterial blood by 1-2% depending on its basal level (checked with professional pulse oximeter). However, since arterial blood constitutes only ~25% of total blood volume this change is completely insignificant.

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Ken
However, since arterial blood constitutes only ~25% of total blood volume this change is completely insignificant.

Interesting. I'd never really considered that question so I looked it up. Sources I found say it's even less than that. At any given moment arterial blood is about 10% of the total, venous about 70%, capillaries 5%, and lungs 10%. Since blood in the lungs is going to be more or less evenly split between arteries and veins, it's more like 15% arterial and 75% venous.

Whatever it is that he and people who follow his regimen achieve is remarkable. He says it's got to do (among other factors) with increasing the alkalinity of the blood?
Not sure Ken, are you saying the benefits of the Wim Hof techniques are not worth the effort? Is there a better way?

I think it's interesting, but if you think you're going to breathe your way out of afib I think you're headed for disappointment.

One can always dream

My point is that by deep breathing or hyperventilating, you do not increase the O2 in your blood, unless you have some physiological issue and have below normal levels (95-100% is normal). Other than a couple of deep breaths to relax and focus before a race, athletes don't try to flush CO2 or increase O2 with deep breathing (swimmers, runners, etc.).

Flushing CO2 by hyperventilating reduces/delays the single to breath from CO2 build up if trying to hold your breath for a long time, but passing out without warning is a possibility (shallow water blackout). There is less pain while holding your breath if you hyperventilate. I use to do a lot of skin diving/spear fishing while holding my breath (I am also a scuba instructor). I was also a competitive swimmer and a coach. I did a fair amount of underwater lap swimming while holding my breath swimming in my younger years. I think the best I did was 75 yards when I was in my 20's.

Those that can hold their breath for long periods do so through various physiological or mental preparations, but not by increasing O2 saturation. Normal, healthy, fit people can't go past 100% saturation, but training the body to use less O2 for a given exercise can be done. Anything that I do physically that demands a lot of O2, I focus on deep breathing as well as a regular pattern to keep O2 debt away as long as possible, which allows me to achieve a higher level of performance.



Edited 1 time(s). Last edit at 11/06/2018 03:56PM by Ken.

All true what you are mentioning, Ken. Wim is claiming a lot more in that long video.

Was wondering why seemingly the Flec brought me back into SR. Came across that in Wiki:

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pH modulation of sodium channel gating
As the cardiac sodium channel is the most pH-sensitive sodium channel, most of what is known is based on this channel. Reduction in extracellular pH has been shown to depolarize the voltage-dependence of activation and inactivation to more positive potentials. This indicates that during activities that decrease the blood pH, such as exercising, the probability of channels activating and inactivating is higher more positive membrane potentials, which can lead to potential adverse effects.[31] The sodium channels expressed in skeletal muscle fibers have evolved into relatively pH-insensitive channels. This has been suggested to be a protective mechanism against potential over- or under-excitability in skeletal muscles, as blood pH levels are highly susceptible to change during movement.[32][33] Recently, a mixed syndrome mutation that causes periodic paralysis and myotonia in the skeletal sodium channel has been shown to impart pH-sensitivity in this channel, making the gating of this channel similar to that of the cardiac subtype.[34]

Doesn't that also make sense why changing blood pH by breathing can influence the heart???? Maybe i'm confusing myself by looking too much

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Joe
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Doesn't that also make sense why changing blood pH by breathing can influence the heart???? Maybe i'm confusing myself by looking too much

In this post <[www.afibbers.org] I talked about my experience with increasing CO2 and converting an episode and I linked to a paper <[sci-hub.tw] where they tested sheep with high CO2, low O2 and normal air and their susceptibility to afib. The sheep on high CO2 were immune to afib, but had a material risk period after the high CO2 when switched back to normal air. In my post, I recount I experienced the risk period after exhaled breath holds, which will increase serum CO2. I hypothesized that I might be able to convert an episode with such a breath hold, which proved correct. I've not tested this again, as I haven't been out of rhythm since that time, 6 months ago.

My breathing exercises increase serum CO2 (hypercapnic) and can be hypoxic (low O2), depending on the length of the breath holds, Wim's approach is both hypoxic (low O2) from the breath hold, as well as hypocapnic (low CO2) from the hyperventilation.

In this paper,<[www.ncbi.nlm.nih.gov] they tested Wim;s approach on volunteers and measured various cytokines after intravenous administration of bacterial endotoxin.

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Excessive or persistent proinflammatory cytokine production plays a central role in autoimmune diseases. Acute activation of the sympathetic nervous system attenuates the innate immune response. However, both the autonomic nervous system and innate immune system are regarded as systems that cannot be voluntarily influenced. Herein, we evaluated the effects of a training program on the autonomic nervous system and innate immune response. Healthy volunteers were randomized to either the intervention (n = 12) or control group (n = 12). Subjects in the intervention group were trained for 10 d in meditation (third eye meditation), breathing techniques (i.a., cyclic hyperventilation followed by breath retention), and exposure to cold (i.a., immersions in ice cold water). The control group was not trained. Subsequently, all subjects underwent experimental endotoxemia (i.v. administration of 2 ng/kg Escherichia coli endotoxin). In the intervention group, practicing the learned techniques resulted in intermittent respiratory alkalosis and hypoxia resulting in profoundly increased plasma epinephrine levels. In the intervention group, plasma levels of the anti-inflammatory cytokine IL-10 increased more rapidly after endotoxin administration, correlated strongly with preceding epinephrine levels, and were higher. Levels of proinflammatory mediators TNF-α, IL-6, and IL-8 were lower in the intervention group and correlated negatively with IL-10 levels. Finally, flu-like symptoms were lower in the intervention group. In conclusion, we demonstrate that voluntary activation of the sympathetic nervous system results in epinephrine release and subsequent suppression of the innate immune response in humans in vivo. These results could have important implications for the treatment of conditions associated with excessive or persistent inflammation, such as autoimmune diseases.

Thanks for the reminder, George. I vaguely remembered you mentioning it but forgot the details
Will re-read it shortly.