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Hypoxic Threshold and Cerebral Capillary Density

Thread Status: Hello , There was no answer in this thread for more than 60 days.
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7BDiver

Active Member
Sep 5, 2019
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In general there are two forms of hypoxia, Acute Hypoxia and Chronic Hypoxia, and both will stimulate the body to adapt. When it comes to high altitude acclimatization to CH improvements in locomotor exercise performance are commonly observed. Diving is however in the form of AH. Hypoxia promotes vessel growth by upregulating multiple pro-angiogenic pathways that mediate key aspects of endothelial, stromal, and vascular support cell biology. Studies show that hypoxia influences additional aspects of angiogenesis, including vessel patterning, maturation, and function. Cerebral capillary density and increased O2 delivery is critical to maintaining corticospinal excitability in hypoxic conditions. Reading an interesting study about hypoxic pre-conditioning, Defining the critical hypoxic threshold that promotes vascular remodeling in the brain https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4261640/, proposes that there is a threshold where significant increase in vascular density is stimulated when subjects (mice!) are exposed to CH at an oxygen level of 12%-10%. That is a 50% increase in cerebral capillary density after a 7 day exposure to CH, results are not as significant when oxygen levels are above the threshold.

Unfortunately the study does not include regular intermittent mild hypoxia (RIMH) but further research is anticipated. Doing a little interpretation/translation of the test methods the oxygen level of 12%-10% is a simulation of an approximate 14,000 ft / 4267m altitude. This can be translated to oxygen saturation SaO2(%) for practical diving vernacular as about ~62%, see http://www.high-altitude-medicine.com/SaO2-table.html. For diving, the general SaO2 level for one to "blackout" is approximately 45%-50%.

Can anyone attest to or perhaps reference a study that may suggest intermittent breath-hold training reaching SaO2 level of ~62% will drastically improve hypoxic pre-conditioning compared to anything less?
 
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MarcinB

Well-Known Member
Oct 26, 2012
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Few years ago I did many (6 max attempts, 3x a week) empty lung breath holds during which SpO2 usually dropped <50%. I used a professional pulse oximeter which showed very consistent results. After some time I've noticed a clear drop in the SpO2 threshold for the development of signs of hypoxia. So some kind of brain adaptation to hypoxia must have developed.
 

7BDiver

Active Member
Sep 5, 2019
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I really need to get one of those, is there a clear correlation between peripheral and arterial SaO2, I imagine vasoconstriction will cause some difference?
 

MarcinB

Well-Known Member
Oct 26, 2012
263
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68
Arterial SaO2 is what is normally measured by pulse oximeter. However, even the best devices often do not show correct values during the breath hold due to vasoconstriction. Finger sensors tend to overestimate SpO2 under these conditions. When I resume breathing SpO2 drops very quickly. I've also tried an ear lobe sensor and it works much better during most of the breath hold, but the signal quality gets really poor when the contractions are very heavy. This problem remains for some time after I start breathing. Because of that the device often misses the lowest SpO2 value which is achieved at this time, and that's the only information that matters to me. I finally decided to use the finger sensor. In the finger the delay to reach the SpO2 nadir is greater, so there's enough time for the signal quality to improve when vasoconstriction ceases.
 

xristos

Well-Known Member
Sep 5, 2013
166
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25
I do think this could apply to humans. I have done same protocol as marcin Finger oximeter shows 40 % after most of those rv holds. I have tried to do same duration holds after some detraining period and I was really feeling like I was loosing it questioning if I was clean after every hold.
Reading the study makes me think we should do a solid block of such training(1month?) and then do the minimum maintance(1/week).?
 

Sorandril

Member
Jun 13, 2020
111
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40
In general there are two forms of hypoxia, Acute Hypoxia and Chronic Hypoxia, and both will stimulate the body to adapt. When it comes to high altitude acclimatization to CH improvements in locomotor exercise performance are commonly observed. Diving is however in the form of AH. Hypoxia promotes vessel growth by upregulating multiple pro-angiogenic pathways that mediate key aspects of endothelial, stromal, and vascular support cell biology. Studies show that hypoxia influences additional aspects of angiogenesis, including vessel patterning, maturation, and function. Cerebral capillary density and increased O2 delivery is critical to maintaining corticospinal excitability in hypoxic conditions. Reading an interesting study about hypoxic pre-conditioning, Defining the critical hypoxic threshold that promotes vascular remodeling in the brain https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4261640/, proposes that there is a threshold where significant increase in vascular density is stimulated when subjects (mice!) are exposed to CH at an oxygen level of 12%-10%. That is a 50% increase in cerebral capillary density after a 7 day exposure to CH, results are not as significant when oxygen levels are above the threshold.

Unfortunately the study does not include regular intermittent mild hypoxia (RIMH) but further research is anticipated. Doing a little interpretation/translation of the test methods the oxygen level of 12%-10% is a simulation of an approximate 14,000 ft / 4267m altitude. This can be translated to oxygen saturation SaO2(%) for practical diving vernacular as about ~62%, see http://www.high-altitude-medicine.com/SaO2-table.html. For diving, the general SaO2 level for one to "blackout" is approximately 45%-50%.

Can anyone attest to or perhaps reference a study that may suggest intermittent breath-hold training reaching SaO2 level of ~62% will drastically improve hypoxic pre-conditioning compared to anything less?
Correct. HIF triggers VEGF improving the perfusion of the brain. Also, and I have seen no mention of this in all the debates about brain health, there is such a thing as neuroglobin.
 
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