You mean, forcing your body into a situation where it needs more oxygen than is available is ... good for you? That sure sounds like cardio-aerobic exercise, doesn't it?
Not to be confused with professional work where the only feasible way to complete the job is to spend hours wearing respirators clogged with particulate, having only one free hand to move heavy/bulky equipment through tight spaces, where getting a full breath of air is anatomically impossible. Extended periods of hypoxia are taxing on the body and require periods of recovery.
Generally, you don't get hypoxic while using a clogged respirator. The problem in such cases is mild hypercapnia and increased work of breathing (Respiratory loading). Hypercapnia in general can cause short term cognitive issues but not long lasting issues. Respiratory loading can cause temporary pulmonary edema.
However, the respiratory loading and hypercapnia are extremely mild in the case of clogged respirators. Especially when compared to divers and snorkelers. The usual problem is that the respirator stops preventing contaminated air from reaching your lungs. As the filters become clogged, the air bypasses the seal around your face.
This is why I prefer a powered respirator. Zero work of breathing and positive pressure at the seals.
Erotic asphyxiation is way different from intermittent hypoxia. Typically erotic asphyxiation is cutting off the flow of blood to the brain by constricting the veins and/or arteries in the neck. Intermittent hypoxia in the case of divers and Wim Hof enthusiasts is a breath hold. This doesn't cause a spike or decrease of blood pressure in the brain.
> Intermittent hypoxia (IH) entails alternating between intervals (typically 2–6 min in duration) of breathing normoxic (i.e., room air) and hypoxic (i.e., FiO2 of 10%–13%) gas mixtures and is a protocol that increases CBF and has been identified as a potential intervention to improve brain health (Panza et al. 2023). The onset of a hypoxia interval elicits an acute response wherein a rapid chemoreceptor-identified reduction in arterial (SaO2) and cerebral tissue (ScO2) O2 saturation stimulates increased ventilation and heart rate (HR) to maintain homeostatic O2 delivery
I am wondering if this related to hypoxia inducible factor (HIF) activation.
Seem to recall the nootropic Noopept allegedly acts as an activator for HIF-1. Maybe there are others. Could possibly be a therapeutic target, maybe not. This is not my area of study, I'm just reiterating some of what I've read in the past.
The main effect of a reaction time reduction looks incredibly small and is all the way in Fig 6. I would not over interpret this result without higher N and some discussion of effect size.
There is overall no health benefit since the hypoxic phase is quite long and creates stress during a time when the body is supposed to rest and recover. And that compounds with the underlying issue, usually mouth breathing, bad pillow, bad sleeping position, or a combination of these.
Mouth breathing is not a cause of sleep apnea, but it can be a consequence. Bad pillows and bad sleeping positions aren't causes of sleep apnea either, but some people do have "positional sleep apnea" where the apnea is (usually) much worse on the back and much better on the side.
One can also have sleep apnea without ever experiencing hypoxia. Drops in oxygen saturation during hypopneas are very minimal, and pretty much nonexistent with respiratory effort related arousals (RERAs). Not breathing is bad, but for many people with sleep apnea, the problem is the constant arousals and the lack of decent sleep, not a lack of oxygen.
I wonder how this might figure in relation to PoTS (postural orthostatic tachycardia syndrome), either way
PoTs being where the autonomic system doesn't equalise blood pressure, especially when standing up n still for several minutes, this the brain doesn't get enough oxygen, so brain fog, head rushes, grayouts (and fatigue, temperature dysregulation + intolerance)
(I've the hyper-adrenergic variety, hyper-PoTS, where the brain tries to generate pressure in a way that will never generate pressure, leaving it so frustratingly easy to have adrenaline rushes that can last for hours)
I've seen a PoTS professional describe the effects as like kind of a mini stroke
it's getting more attention now due to the long COVID relation, and it seems that maybe microclots have become a prime suspect as a possible cause to many symptoms, though there's so many jigsaw pieces, and discerning correlation n cause n effect etc..
obviously there's many contextual tipping points between that and this study (if generalisable)
apparently I have a strong heart. idk
related;
I've nostrils with the collapsing innner valve, so I can't get deep breaths through my nose (and got getting enough air whilst sorry l asleep is a cause of bruxism)
rhinoplasty then turbinate reduction helped mildly, but apparently having some cartridge inserted would help prop the path open for a more normal use.
so,
both of these leave me feeling out of breath a lot
and it's why I'm a month breather. hopefully a third bit of surgery will finally properly help
some kinda vague anecdata there, some kind of a lens anyway!
Readit News
Not to be confused with professional work where the only feasible way to complete the job is to spend hours wearing respirators clogged with particulate, having only one free hand to move heavy/bulky equipment through tight spaces, where getting a full breath of air is anatomically impossible. Extended periods of hypoxia are taxing on the body and require periods of recovery.
However, the respiratory loading and hypercapnia are extremely mild in the case of clogged respirators. Especially when compared to divers and snorkelers. The usual problem is that the respirator stops preventing contaminated air from reaching your lungs. As the filters become clogged, the air bypasses the seal around your face.
This is why I prefer a powered respirator. Zero work of breathing and positive pressure at the seals.
> Intermittent hypoxia (IH) entails alternating between intervals (typically 2–6 min in duration) of breathing normoxic (i.e., room air) and hypoxic (i.e., FiO2 of 10%–13%) gas mixtures and is a protocol that increases CBF and has been identified as a potential intervention to improve brain health (Panza et al. 2023). The onset of a hypoxia interval elicits an acute response wherein a rapid chemoreceptor-identified reduction in arterial (SaO2) and cerebral tissue (ScO2) O2 saturation stimulates increased ventilation and heart rate (HR) to maintain homeostatic O2 delivery
Anyways, erotic asphyxiation is such a bad idea.
Seem to recall the nootropic Noopept allegedly acts as an activator for HIF-1. Maybe there are others. Could possibly be a therapeutic target, maybe not. This is not my area of study, I'm just reiterating some of what I've read in the past.
Mouth breathing is not a cause of sleep apnea, but it can be a consequence. Bad pillows and bad sleeping positions aren't causes of sleep apnea either, but some people do have "positional sleep apnea" where the apnea is (usually) much worse on the back and much better on the side.
One can also have sleep apnea without ever experiencing hypoxia. Drops in oxygen saturation during hypopneas are very minimal, and pretty much nonexistent with respiratory effort related arousals (RERAs). Not breathing is bad, but for many people with sleep apnea, the problem is the constant arousals and the lack of decent sleep, not a lack of oxygen.
PoTs being where the autonomic system doesn't equalise blood pressure, especially when standing up n still for several minutes, this the brain doesn't get enough oxygen, so brain fog, head rushes, grayouts (and fatigue, temperature dysregulation + intolerance)
(I've the hyper-adrenergic variety, hyper-PoTS, where the brain tries to generate pressure in a way that will never generate pressure, leaving it so frustratingly easy to have adrenaline rushes that can last for hours)
I've seen a PoTS professional describe the effects as like kind of a mini stroke
it's getting more attention now due to the long COVID relation, and it seems that maybe microclots have become a prime suspect as a possible cause to many symptoms, though there's so many jigsaw pieces, and discerning correlation n cause n effect etc..
obviously there's many contextual tipping points between that and this study (if generalisable)
apparently I have a strong heart. idk
related;
I've nostrils with the collapsing innner valve, so I can't get deep breaths through my nose (and got getting enough air whilst sorry l asleep is a cause of bruxism)
rhinoplasty then turbinate reduction helped mildly, but apparently having some cartridge inserted would help prop the path open for a more normal use.
so,
both of these leave me feeling out of breath a lot
and it's why I'm a month breather. hopefully a third bit of surgery will finally properly help
some kinda vague anecdata there, some kind of a lens anyway!
https://en.wikipedia.org/wiki/Professional_diving
I'd say most professional athletes are less intelligent than average…