1) Fill the oxygen reservoir
2) Put on the mask and connect
3) Set the system to +O2
4)Exercise for 6–8 minutes at sustainable but aerobic pace (solidly aerobic)
• Note exertion challenges — discomfort that occurs at about 1 minute intervals
• Mentally note the first challenge intensity
• Reduce effort moderately during challenges
• Continue on oxygen until challenges become unnoticeable and exertion is easy
• Usually 6–8 minutes
5) After exertion challenges end — Begin Sprint Sequence
• Switch to -O2
• Sprint for 15 seconds at maximum output
• Switch to high oxygen and continue sprint 15 more seconds on +O2
• Recover on +O2 until detox clears
6) Repeat 3–6 times
7) Stop exertion at 15 minutes
8) Continue breathing oxygen until pulse drops 100 BPM.
• Magnesium Orotate/Aspartate 500 mg
• Thiamine 100 mg
• Vitamin C 500 mg
• 500 mg Arginine Alpha-ketoglutarate
** Supplemental nutrients are not usually necessary to achieve the documented usage guide effect.
This method is the preferred beginner’s usage guide. The whole-body effect is enough to create a clear and compelling improvement in sense of well being, and a noticeable improvement in most symptoms relating to systemic or regional hypoxia.
Generally the High Oxygen Phase improves symptoms relating to body-wide low oxygen, while the hypoxic sprint process tends to penetrate more acute areas with a longer history of reduced oxygen.
The 99er Pattern
The telltale for this pattern is an abnormally high 99% PO2 at start. After a few minutes of challenge the users will desaturate to an unusually low PO2 80% or lower provoked by brief hypoxic challenge. Users will dwell at the reduced PO2 for several minutes after returning to oxygen. The re-saturation pattern often occurs 9 minutes into the session. For comparison, a normal user will re-saturate to 99% within time is 5 seconds of switching to oxygen regardless of how long they remained on low oxygen.
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 exertion challenge.
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 under-oxygenated tissue.
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:
Capillary pulse pressure reaches the penetration threshold as arterial blood pressure and hypoxia-induced vasodilation deliver more pressure to capillary bed. This takes effort and some time. It does not happen instantly, and takes 5–10 minutes of effort.
Endothelial cells switch back to normal metabolism and pump out sodium and quickly shrink back to normal size
Capillary opens to red blood cell passage and tissue reoxygenation begins
PO2 drops as tissues absorb large amount of oxygen until reperfusion is complete, usually in 2–4 minutes.
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:
Hypoglycemia as under-oxygenated tissues use excessive glucose. If the liver fails to keep up with demand, then blood sugar falls to hypoglycemic levels and causes systemic fatigue.
Gall bladder conditions including discomfort and gallstones. When the cori cycle depletes lactic acid reacts with bile in the gall bladder to precipitate solids which often form gallstones and cause discomfort.
This author suggests that tissues that retain excess lactic acid for a long time become hypersensitive as with fibromyalgia.
Normally this pattern only occurs once during early use. Reperfusion 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 reperfusion effect has not been observed with LiveO2 Standard.
What to Expect
If you experienced this pattern, you will likely:
Feel stronger and have increased endurance
Reduced cravings for sweets and simple carbohydrates
Reduced tendency for muscle soreness
Greater strength in major muscles
Reduced tendency for loose stools
Improved fat digestion from improved bile availability
Have an increased respiration rate at rest
There are no common questions about this usage guide yet.
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