What are you using for a pulse oximeter? Googling a bit, it seems most oximeters are accurate to only about 2-4%, and many factors can make it worse such as cold hands, movement etc. Seems like a reading of 97 vs 99% is basically the same. Have you noticed the same behavior since posting this a month ago?
I recently started doing this protocol in an effort to increase EPO/hemoglobin for a race I have coming up; the paper showed a 24% increase in EPO using apneas.
They did 3 sets of 5 max breath holds, but stopped the hold when about 60% SaO2 was reached (since this was a study, they had catheter O2 measurements rather than SpO2 pulse readings). I’d imagine there is probably a lag in SpO2 vs SaO2.
Protocol is:
1 minute of hyperventilation followed by a max breath hold
2 minutes rest between holds, repeat 5 times
10 minutes rest between sets of 5
Using a pulse oximeter off Amazon, I typically start off at 95%+ and get to around 50-60% at the end of a hold. It’s probably very inaccurate at the lower range, but at least O2 seems to be getting quite low.
It seems like oximeters are just not calibrated below 80%, and peripheral blood flow may be altered when more hypoxic, so all bets may be off when trying to use them below that level.
It was a one time thing. The next time and every time since my spo2 patterns were back to my normal. “Normal” doesn’t mean always the same. Some days my spo2 drops fast on every set, while other days it is resistant to falling (drops slowly and not as far). I never get the “won’t drop at all” effect except that one time with rapa, which is why I posted about it.
I’ve noticed the lag. I do a 10 second recovery (pressure breathing) between aches of the 5 30 second long sets. My spo2 recovers to 96 or 97% each time but the recovery occurs / is seen / is felt at different times.
(1) my lungs get the o2 and dump the co2 immediately
(2) my brain senses the drop in co2 after about 5-10 seconds
(3) my spo2 recovery takes 20-30 seconds to show up at my finger
Carbon monoxide (CO) produced during smoking has been proposed to be a protective factor for Parkinson’s disease (PD). In rats, increasing CO levels have recently been shown to induce hypoxic response-like pathway activation. Smoking thus may strengthen the hypoxia response systems by challenging the oxygen transport system, resulting in increased cellular resilience. Here we outline the overlaps between two novel promising approaches against PD, low-dose CO inhalations and hypoxia conditioning.
Deficits in cellular and systemic responses to altered oxygen availability are increasingly acknowledged features of PD. Various approaches can restore these responses and possibly benefit people with PD. Smoking—at least in part via increasing CO-levels and thereby repeatedly challenging the oxygen transport system—may reduce the risk for PD by “training” the hypoxia response systems and leading to increased cellular resilience and maintained adaptive capacities on the systemic levels (e.g. hypoxic ventilatory response). However, the adverse effects of tobacco smoking greatly outweigh potentially protective components of smoking or smoking behavior in PD. Smoking is associated with increased risks for many non-communicable diseases, including vascular and respiratory diseases or neoplasms, and therefore clearly is not suitable as a preventive strategy. Accordingly, although PD smokers may die from fewer neurological causes, their risk to die from smoking-related cancers has been shown to be significantly increased. Should the beneficial effects of increased CO-levels in PD be confirmed, low-dose CO inhalations may be one interesting novel strategy to target one crucial aspect of PD. If short, repeated exposures to hypoxia have similar consequences like CO, hypoxia conditioning, strategic altitude exposures or adapted breathing exercises will be important alternative approaches.
The experimental group showed periodic desaturation, with minimum and maximum oxygen saturation values of 80.19 ± 0.34% and 97.68 ± 0.31%, respectively.
After 3 hours of exposure, ABR and the spontaneous firing rate (SFR) of auditory cortical neurons were recorded.
Short-term IH induces high-frequency hearing loss, reduces ABR latency, and enhances cortical neuronal excitability, implicating both peripheral and central auditory pathways.
There’s clearly a trade-off with hypoxia @John_Hemming. I don’t have access to the whole paper to check the exact protocol.
I think it was £33 per 1-h session. But that was a discount for first-time users. And other places were way more expensive. I stopped after 3 sessions as I didn’t feel good during the third session at 15% FiO2. I wonder if the sensor had an issue. The clinic was also far from my home. I need to find one that is closer and try again.
Hypoxico is the main supplier in the US it seems, and their machines are on the order of $2000-4000. They do not appear to have the option for hyperoxia, so a separate machine would be needed if you wanted to go that route.
They also have a nice chart of oxygen percentage as a function of altitude. The spreadsheet version on their website also has values for the partial pressure of oxygen at each altitude.
It seems that inhaling low levels of carbon monoxide (CO) is much more efficient at eliciting hypoxic responses than normal hypoxia due to better binding to hemoglobin than O2. [paper].
Carbon monoxide (CO) is an important endogenous molecule that can also be inhaled (Prabhakar, 1998). It has long been established that CO has an Hb binding ability greater than that of O2. Therefore, when an individual inhales CO, this can be considered to induce mild hypoxia in vivo, as carboxy-hemoglobin (HbCO) is incapable of carrying enough O2 and there is reduced amount of O2 bound to Hb and delivery to active muscle. As persistent CO inhalation reduces Hb ability to carry O2, acute exposure to small doses of CO could, in theory, induce similar performance benefits to that of altitude training. Previous research showed that increased ventilation in mild exercise rapidly removes CO from the blood in humans (Zavorsky et al., 2012). The clearance half-time in males is slower in comparison to their female counterparts due to their larger tHb (Zavorsky et al., 2014). If CO can enhance sporting performance, a sample of well-trained male individuals, who can have up to a 37% higher tHb in comparison to untrained athletes, (Kjellberg et al., 1949) is a suitable subject population as CO can remain in the blood for prolonged periods of time. Hence, it is hypothesized that an appropriate dosage of inhaled CO might have sufficient time to provoke mild hypoxia before clearance, causing similar physiological adaptive responses to that of altitude training.
For it to work, it may require combination with exercise:
Since a periodic inhalation of small amounts of CO at sea level might have potential to simulate the hypoxic effects of altitude and increase tHb mass and enhance maximal aerobic power, it is worthwhile to investigate if CO inhalation could offer a more convenient and less expensive method of improving exercise performance. In a study, by Fröscher and Uhlmann (2016) 10 days of intermittent, low-dose CO inhalation at rest did not lead to improvements in Hb mass or aerobic peak power, but to the best of our knowledge combined inhalation of CO and exercise training intervention has not been performed. Consequently, the aim of this study was to examine the effect of inhaling a small amount of CO on EPO secretion and total hemoglobin mass (tHb), running economy and maximal aerobic power in a combination with treadmill training in well trained young adults.
The protocol only requires 2 minutes (!) of breathing low-dose CO:
Twelve male college student athletes, who were well-trained soccer players, participated. They performed a 4-week treadmill-training program, five times a week. Participants were randomly assigned into an experimental group with inhaling CO (INCO) (1 mL/kg body weight for 2 min) in O2 (4 L) before all training sessions and a control group without inhaling CO (NOCO). CO and EPO concentrations in venous blood were first measured acutely at the 1st, 2nd, 4th, 6th, and 8th hour after INCO, and total hemoglobin mass (tHb), running economy and VO2max were measured before and after the 4 weeks training intervention.
They got an impressive 40% increase in EPO, and an increase in VO2 max:
HbCO% increased from 0.7 to 4.4% (P < 0.05) after 1 h of CO inhalation and EPO increased from 1.9 to 2.7 mIU/mL after 4 h post CO inhalation (P < 0.05) acutely before the intervention. After the training, the tHb and VO2max in the INCO group increased significantly by 3.7 and 2.7%, respectively, while no significant differences were observed in the NOCO condition. O2 uptake at given submaximal speeds declined by approximately 4% in the INCO group.
This paper shows similar results:
For more typical hypoxia protocols, this compares to intermittent and continuous protocols that take anywhere from 45-120 minutes to complete:
8x4 minutes hypoxia at 80% SaO2 (45% increase in EPO)
1 hours continuous hypoxia at 80% SaO2 (85% increase in EPO)
Yes, that’s why smokers have significantly lower risk of Parkinson’s disease. There is an ongoing trial of CO in PD. Some hypoxia trials also combine it to CO. What are other (healthier) ways than smoking to get 2 min of low-dose CO?
The thing about breathing CO is that it reacts with haemoglobin to create carboxyhemoglobin that leads to tissue hypoxia for a while. I am not myself a fan of hypoxia although I recognise that it has some positives. If I were to try hypoxia I would prefer to use a mask rather than disabling haemoglobin.
I recently received a 2.0 HBOT chamber and a generator capable of hypoxia and hyperoxia. I don’t have any particular condition that I’m looking to treat, mostly just looking for any improvements in athletic performance (ie VO2 max) and longevity (ie any health marker improvements, vascular improvements/maintenance, telomere length, etc). In part, I figured I’d give the hypoxia/hyperoxia a try because I can stack it with parts of my routine that I’m already doing like zone2, HIIT and sleeping. I’d be curious if anyone has thoughts on controlled experiments to run with before/after testing. I can easily test anything on the labcorp/quest test menus, and am willing to also pay for specialty testing.
Some ideas:
HBOT 5/week for 8 weeks. 60m at 2.0 pressure (75m session). Measure: telomeres, VEGF, oxidative stress markers
Zone 2 Rowing x 3/week for 8 weeks. 5m hypoxia@10-15% targeting 80% SPO2, 3m hyperoxia at 35%, repeat 8 times. Measure: VO2max, LT1, RHR
4x4s x 3/week for 8 weeks @ 100% oxygen. Measure: VO2max, LT1, RHR
Sleep in altitude tent working my way down to 12%.
Subjectively would be great to see memory improvements and/or hippocampus volume increase (as measured by neuroquant), but I’m not holding my breath. Neuroquant I get once per year, so we wouldn’t be able to pinpoint a particular intervention.
