We'll discuss what we (and much less I) know about altitude sickness, some fun facts about dolphins, and some numerical data on a limited case study with my data. I propose in this article methods for consciously controlling breath patterns to keep blood oxygen levels high and heart rate low, and training techniques. If proven effective these might be useful to limit altitude sickness, and prevent the deadly HACE and HAPE that kill people every year.
Dolphins
The first half of my vacation was freediving with dolphins and a freediving class that helped shape the rest of this post. If dolphins could hike up a mountain they wouldn't get altitude sickness (they are also smart enough not to go). We are fortunate to have both automatic breathing we don't have to think about, and manual breathing that allows us to control our respiratory rate. Unfortunately our automatic breathing is broken when we go up in the mountain and I believe is the main cause for altitude sickness. It is great we can use a manual override, but that works only when we are not asleep.
Each breath a dolphin makes is a conscious act. Conversely, dolphins in captivity or in "The Cove" can commit suicide by not taking their next breath.
* Please, please don’t buy tickets to dolphin shows to end dolphin captivity.
Dolphins shut off a half of their brain to sleep, while the other half maintains their breathing. They swim in circles with the outer eye looking for danger while the half associated with the inner eye is asleep. This is the key ability that we unfortunately don't have. I would be able to get much better sleep if I could teach my automatic breathing to quickly keep up.
Altitude sickness: AMS, HACE, HAPE
Presently we do not fully understand how hypoxia causes altitude sickness. What is certain though is that hypoventilation, and decreaseed breathing response to hypoxia are strongly correlated with it.
Partial pressure of oxygen gets exponentially lower with higher altitude. Lower partial pressure makes gas exchange in tissue and alveolar capillaries more difficult. Our short term adaptations to hypoxia (really reactions to high levels of CO_2) cause tissue vasodilation (expansion of capillaries in tissues), and in later stages pulmonary vasodilation (capillaries in alveoli). Both of these improve oxygen delivered to tissues and replenishment in the lungs. However, they come at a cost of swelling, and leaking fluids from the cell walls.
In the brain the expanded tissues putting pressure on the skull trigger even more swelling in a vicious cycle - HACE (high-altitude cerebral edema). In the lungs the expanded capillaries for gas exchange leak more fluid and usable area is depleted even more rapidly - HAPE (high-altitude pulmonary edema).
Both conditions can be fatal within hours. About 1% of people ascending above 3000m get HACE, and ~1.5% get HAPE. Milder versions of these are experienced as AMS - and affect more than 40%. Symptoms of AMS include nausea, dizziness, vomiting, headache, lethargy, fatigue, stomach illness, rapid heart rate and poor sleep.
Hydration
Leakage in blood plasma increases blood viscosity, which requires the heart to work harder and blood pressure to rise. Higher pressure further increases leakage. Good hydration lowers viscosity and cuts the vicious cycle early.
Hemoglobin binding
Oxygen is carried bound to hemoglobin and dissolved in plasma. Just having highly oxygenated hemoglobin is not enough, we want it to quickly release oxygen in the tissues. Blood acidity H+, CO2 and temperature are correlated to higher oxygen release. Hypothermia and alkaline blood (low CO2) make it harder to deliver oxygen to the tissues. That's why high in the mountain it is critical to eat and drink to keep hypothermia at bay, and make sure to not hyperventilate if you are breathing to compensate!
Every year people die from altitude sickness
A very experienced at high altitudes climber died earlier this year on an attempt to summit Mt Shasta (4,322m). They were forced to camp ~4000m in a snowstorm. HACE was just too quick and too deadly, there was little his partner could do to save him. My conjecture is that the snowstorm made all the difference - much lower barometric pressure has decreased the O_2 partial pressure. Furthermore they likely have been dehydrated if they didn't boil enough snow as they had to dig emergency shelter.
Our goals from the above research should be to maintain slightly higher blood acidity, lower blood pressure, and lower blood viscosity. I believe we can control these with conscious diet, exercise pace, and breathing choices.
Diet choices
I think a diet high in carbohydrates should be recommended, and moving at a faster pace as long as hydration is sufficient.
What you metabolize affects the Respiratory Quotient - the ratio of CO_2 produced over O_2 consumed. What you burn depends on what you eat and the pace at which you are exercising.
Carbohydrate metabolism produces 1 CO_2 for each O_2 molecule therefore R.Q. is 1.0, protein R.Q. is 0.81, and fat R.Q. is 0.7. Since the respiratory rate is mostly a function of CO_2, eating mostly carbs will either 1) accelerate the course of AMS and acclimatize or die faster, or 2) increase the respiratory rate to provide sufficient oxygenation.
My theory is that the body is normally calibrated to expect ~0.8 R.Q. (calculated from 70% fat, 30% carb at rest) so we should expect 2).
Anyways, theory accidentally matched well with practice. I forgot to buy nuts! I was supposed to start this hike a day later and intended to buy fresh macadamias from the farms...
I did have some fats in Cliff bars, the rest of my food was mostly carbs on the trail and lots of carb and protein at camp.
Acidity
Acidosis (low pH) limits red blood cell travel. Alkalosis (high pH) makes red blood cells 'greedy' and lowers hemoglobin exchange.
Overall I think we should try to cause mild metabolic acidosis. Protein metabolism create additional acidity from amino and organic acids. I'd assume that effect would be short lived and blood acidity is quickly buffered, but some protein is anyways good to have in the diet. Drugs or maybe extra water/proteins can be used to limiting the kidneys ability to make the blood more alkaline.
Hydration and electrolytes - I need 3-4 L a day, usually less with electrolytes. Temperature impact - from scorching sun to subfreezing temperatures, both demand additional water.
For lower CO_2 I think you want higher flow rate through the kidneys, not having enough electrolytes will force your body dump extra fluids. I'd also be worried that higher Na and water retention might increase fluid leakage. For good or bad, I also forgot to pack my electrolytes - I normally have Endurolytes capsules, and water dissolved Nuun.
Subject: me
This was the second time I was at 4000 m. 36 hours earlier I had been at 0 m.
Location: Mauna Loa Cabin
The cabin was at 4039m, where standard barometric pressure is 63 kPa (0.62 atm). This means that there is 62% of the oxygen available at sea level. Latitude impact and actual barometric pressure aren't included in the above estimate.
Weather: temperature outside -5C(23F), weather fronts.
The key factors to consider are O_2 partial pressure, and humidity. I definitely wasn't excited to wait the impending snowstorm at the summit cabin. It seemed wiser to get off the mountain before it hits.
Equipment: Pulse oximeter (Nonin GO2)
The one I have is easy to use, portable and cheap. Yet it is not officially certified accurate above 4000m (where I usually care to use it for hiking), nor under 70% SpO2 (and I get below that for freediving breathholds). We used this at the Stanford/UCSD Prevention of Altitude Illness with Non-steroidal anti-inflammatory Study (PAINS) at White Mountain.
Medications: Last time I was on Ibuprofen (administered double-blind, I didn't know if I am on placebo during PAINS), and now on Naproxen (non-blind, self-administered for ear-PAIN!). Naproxen may have suppressed headaches. NSAIDs impairment of kidney functions is considered beneficial in this case as that leaves more CO_2 in the blood and increases respiratory rate.
Symptoms: insomnia, short sleep cycles. Nothing else! This time I was feeling much better than last time at this altitude.
Signs: low SpO2, high heart rate
Physical condition:
Last time I was in much better aerobic condition as I had just peaked my Ironman training. Now I had been training for freediving, and I was in better anaerobic condition. The linked dolphin pictures and videos are from my up to minute long freedives and underwater swims with dolphins. Being conditioned to exercise in hypoxic conditions was probably beneficial to feeling great at altitude.
I can hold my breath for 6 minutes without blacking out (as I would frantically be writing down ridiculously low SpO2 values after clocking out). I had good hypoxic tolerance but probably decreased automatic response to hypoxia (low O2). Indeed I was most worried that I have a decreased automatic response to hypercapnia (high levels of CO2), e.g. later urge to breathe. I was hoping Naproxen would counteract that by keeping CO2 levels high.
Data: middle of the night
Waking up: 70% SpO2
Resumed breathing: 80% SpO2
Deep breathing: 95% SpO2, HR 70bpm - likely hyperventilating. Hyperventilated blood will not actually deliver oxygen from hemoglobin even though SpO2 is high. Needed oral intake.
Tidal breathing: 90% SpO2, 62bpm - good target for resting breathing
'Dolphin' breathing: 86% SpO2, 56bpm - low heart rate was a good way to fall asleep.
relaxed diaphragmic breathing, nasal intake, 2 second inhale, 4 second exhale
Data: at sunrise
Me 75% to 79% automatic, up to 90% conscious breathing, at 70bpm standing
Davie 80%, avg 115bpm very erratic heart rate
Further processing: these should be compared to calculator models of SaO2
Altitude sickness suggested prevention
Suggestion #1: 'Dolphin' Breathing when sleeping
If you are not sleeping well anyways, it is best to at least keep your tissues oxygenated and avoid HACE and HAPE. Get a Pulse Oxymeter. Find a good breathing rhythm and volume that allows you to keep high oxygenation, without hyperventilation and a low heart rate. From the few methods I've tried while falling asleep looked like keeping a low heart rate with no hyperventilation was more important than very rich SpO2 but still higher than autonomic.
Definitely needs more research. The key question is can the automatic system maintain the manual style after you fall asleep.
Suggestion #2: Breathe consciously when moving
Find a good rhythm and just like each step has to be conscious until you get in the 'zone' same should be each breath. Breathe through your nose to keep moisture in. Continuous breathing is easiest to maintain.
Suggestion #3: Breathing or hyperventilation when stopping
Don't forget to breathe when you stop! In fact, after heavy exertion if I stop to eat or drink, I'd sometimes get a headache in the back of the head. That is likely due to high CO2 - e.g. as heart rate stays high for a while. The easiest way to reduce that is with controlled hyperventilation (upper chest) to remove extra CO2.
Training #1: Low oxygen tolerance tables
This is training you can safely do at home in your bedroom, by gradually increasing the time you can hold your breath to accustom the body to extremely low levels of oxygen.
For freediving training this is alternated with high carbon dioxide CO_2 tolerance tables. Learn more at a freediving class
To avoid any risk of reduced urge to breathe, if you are only interested in high altitudes, I'd stick only to O2 tables.
Altitude sickness prevention
My take is that the critical time to check for HACE and HAPE progression is in the morning. Never leave someone behind early on. HAPE gets worse with exercise, and victims will need support for safe descent.
Having a partner is not always of much help once HACE and HAPE hit.
It's always best to be self-sufficient and track early symptoms, prevent, and act conservatively.
It's still better to have others as poor judgment due to HACE will prevent proper action (e.g. descent), and you can't exert yourself with HAPE. Share your symptoms with your partners.
Don't ascend with worsening AMS when others go up, while you should be descending.
Don't treat insomnia - not waking up to breathe will only make things worse!
I think having a good sleep in the early days in the mountain may be dangerous.
Overall tiredness may make one less capable of manual ventilations.
* Avoid alcohol
* Avoid Diphenhedramine, e.g. for ear problems, or poison ivy
"Climb high, sleep low" should make acclimatization faster. In this case the summit was not that much higher than camp.
Ascend slowly. Above 3000m the recommended daily gain is 300m (1000ft) for safe acclimatization. This is the advice most ignore and pay for. The Mauna Loa route required three times faster than prudent ascent. It is probably better to stay two nights at the first cabin. Although for maximum acclimatization to living on Mauna Loa one would need 48 days.
Acetazolamide helps improve acclimatization.
I haven't taken it, but I carry in case of need for treatment to help descent, or in case of delay at altitude (e.g. snowstorm, or injury) with worsening AMS.
I haven't had a severe AMS before, and while side effects are mild I'd rather not use drugs for helping ascent. If you do know you get AMS it definitely sounds like a good choice for a preventative drug.
Freediving and Mountaineering
After further research, I overall think that freediving conditioning and high altitude climbing are very complementary activities with great cross-training potential. Awareness to one's breathing, and
knowledge of effective breathing patterns to increase oxygenation and lower heart rate, I believe are critical for one's performance and enjoyment whether deep in the ocean, or high up in the mountains. I think we need to take a lesson from the dolphin's playbook and take over our breathing. All medical studies have been too interested in prevention via drugs and analysis of automatic breathing patterns. I'd be very interested in what, if any, breathing techniques have been studied.
Further research
High carb diet was found protective in one study but not in others
Endurance training may reduce AMS, but others find high VO_2 max uncorrelated to AMS.
* Peter Bärtsch, Erik R. Swenson, André Paul, Bernhard Jülg, Elke Hohenhaus. High Altitude Medicine & Biology. December 2002, 3(4): 361-376. doi:10.1089/15270290260512846.
http://www.liebertonline.com/doi/abs/10.1089/15270290260512846
Study showing that without any difference in hypoxic and hypercapnic responses at sea level some hikers do get AMS while others do not, which implies no correlation. I'd still suggest not overtraining hypercapnic (high CO_2) tolerance training.
* West, et al. http://jap.physiology.org/content/61/1/280.extract
Research of periodic breathing at an Everest expedition high camp (8050m) showed cycles of (20s breathing and 8s not-breathing). Subjects weren't able to distinguish breathing patterns in sleep vs nonsleep!
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