The unnaturally high PO2 usually occurs when blood cannot reach
tissues due to endothelial capillary inflammation. The endothelial inflammation reduces below the passable diameter of a red
blood cell (RBC). When this occurs, only plasma can flow through the
capillaries, limiting energy production to anaerobic fueled by
glucose absent oxygen.
The reduced capillary cross section causes RBCs to go around narrowed
capillaries. RBCs that don’t pass through capillaries do not release
oxygen much like a vehicle that cannot release a payload — it
just remains full. This shows up as an unnaturally high starting
PO2 and a tendency NOT to desaturate during hypoxic
This pattern has been observed:
For comparison a starting saturation level of about 97%, with
rapid desaturation to 87%, is normal (sea level).
This pattern contradicts the typical medical conclusion that a high
hemoglobin saturation indicates good tissue oxygenation. The medical
interpretation presumes, usually incorrectly, that oxygen can always
move from the RBC to tissue. By the time this saturation pattern,
99-100%, occurs when the person’s body has a large percentage of
The severity of systemic hypoxia is indicated by how long it takes
them to resaturate after the inflammation is reversed. On the pulse
oximeter, how many minutes does it take them to saturate to 99% after
they reperfuse dip? The longer the time, the greater the accumulated
oxygen tissue debt.
The degree of systemic hypoxia is indicated by how long it takes the
person to resaturate afterwards (the amount of time the person spends
on oxygen with a low oxygen level).
The problem is that the oxygen bound to hemoglobin cannot dissociate
because it never passes through the capillaries where it can release
oxygen. In this case, unnaturally high hemoglobin saturation means
poor tissue oxygenation.
The telltale for resolution of this pattern is a dramatic drop in
PO2 late in the session while on oxygen. Here is a model
for what happens:
Started abnormally high 99% PO2 on start and then desaturated to 80% after hypoxic challenge about 9 minutes into the session. User remained at 80% PO2 for 2 minutes while breathing oxygen. Normal resaturation time is 5 seconds.
The telltale for resolution of this pattern is a dramatic drop in PO2 late in the session while on oxygen. Here is a model for what happens:
This is the typical chronic-fatigue pattern. It usually includes persistent muscle touch sensitivity from regional tissue acidosis. Over time this condition can progress to multiple local and systemic disease states:
Normally this pattern only occurs once during early use. Re-perfusion is durable until conditions that caused endothelial inflammation recur.
LiveO2 Adaptive Contrast appears to be a requirement to provoke resaturation. It seems the reason for this is that reduced-oxygen air creates vasodilation and increases arterial pulse pressure, which maximizes pulse pressure at the capillary entrance. This re-perfusion effect has not been observed with LiveO2 Standard.
If you experienced this pattern, you will likely: