The core challenge facing plateau travelers is the “cliff-like decline in oxygen supply” caused by low pressure, and the essence of acute altitude sickness is the body’s compensation imbalance for this “sudden drop in oxygen partial pressure”. The core of our oxygen generator to alleviate altitude sickness is to reconstruct the “effective gradient” of alveolar-blood oxygen transport by precisely replenishing oxygen concentration. Its mechanism of action can be analyzed in depth based on the physical characteristics of the plateau environment, the molecular logic of the body’s stress response and clinical intervention data:
“Oxygen Deprivation” in Plateau Environment: From Physical Laws to Physiological Impact
For every 1000 meters increase in altitude, the atmospheric pressure drops by about 12kPa, and the partial pressure of oxygen inhaled gas (PiO₂= atmospheric pressure ×21%) will decrease linearly with the atmospheric pressure – this is an inevitable physical law:
- Plain (altitude 0 meters, atmospheric pressure 101kPa): PiO₂=101×21%≈21.2kPa (about 159mmHg), alveolar oxygen partial pressure (PAO₂) is about 13.3kPa (100mmHg), arterial blood oxygen saturation (SaO₂) is stable at 97%-98%;
- Altitude 3000 meters (atmospheric pressure is about 70kPa): PiO₂=70×21%≈14.7kPa (about 110mmHg), which is only 70% of the plain; at this time, PAO₂ drops to 8-9kPa (60-68mmHg), and SaO₂ drops sharply to 85%-88%;
- Altitude 4000 meters (atmospheric pressure is about 62kPa): PiO₂=62×21%≈13.0kPa (about 98mmHg), PAO₂ further drops to 6-7kPa (45-53mmHg), and SaO₂ can be as low as 75%-80%.
This “sudden drop in oxygen partial pressure” is a “double blow” to the body:
- Gas exchange disorder: The oxygen partial pressure difference (PAO₂-PaO₂) between the alveoli and the blood narrows from 4kPa (30mmHg) in the plain to below 2kPa (15mmHg), and the diffusion efficiency of oxygen from the alveoli to the blood decreases by 50%, resulting in “insufficient oxygen supply” of the tissue;
- Compensational hyperinjury: Tissue hypoxia activates carotid body chemoreceptors and triggers sympathetic nerve excitation – the respiratory rate increases from 12-16 beats/minutes in the plain to 20-25 beats/minutes (shortness of breath), and the heart rate increases from 70 beats/minutes to 90-100 beats/minutes (accelerated heart rate). In the short term, oxygen supply is compensated by “increasing ventilation and cardiac output”, but in the long run, it will cause respiratory muscle fatigue and myocardial oxygen consumption surge, which will aggravate discomfort.
The “molecular chain” of acute altitude sickness: from HIF-1α to symptom outbreak
When SaO₂ continues to be below 85%, the body initiates the “hypoxia stress pathway”, with the core being the activation of the hypoxia-inducing factor (HIF-1α):
HIF-1α is a “molecular switch” that cells sense hypoxia. It will be degraded by proteases in a normal oxygen environment. When it is hypoxia, it will be stable and enter the nucleus, and start the downstream target genes. The most critical of these is the erythropoietin (EPO) gene. Increased secretion of EPO will stimulate the bone marrow to produce more red blood cells (it can be increased within 24 hours), trying to improve oxygen supply by “increasing oxygen carriers”.
However, this compensation has “hysteresis” and “side effects”: excessive erythrocytic hyperplasia (staying at an altitude of 4000 meters for 3 days, and the hematocrit HCT can increase from 45% to more than 50%) will cause a 20%-30% increase in blood viscosity, slowing down blood flow, which will aggravate tissue hypoxia (forming a vicious cycle of “the more hypoxia is, the more viscous, the more viscous, the less oxygen is,”); at the same time, HIF-1α will also stimulate cerebral vascular dilation (trying to increase cerebral blood flow), lead to an increase in intracranial pressure, triggering typical plateau headaches (bloating and painful on the forehead, which aggravates after activity), and affect the vomiting center through central hypoxia, inducing nausea and decreased appetite.
Clinical data show that: above 3,000 meters above sea level, about 60% of the plain population will experience acute altitude sickness, of which 20% affect activity due to headache and nausea, and 5% develop plateau pulmonary edema due to SaO₂ continues to be less than 80% of the progression to plateau pulmonary edema (alveolar effusion, further worsening oxygen exchange).
“Precise Breakthrough” of Concentration Oxygen Therapy: From oxygen partial pressure reconstruction to symptoms relief
This oxygen generator provides 30%-40% oxygen-rich gases, and achieves “targeted intervention” through the following mechanisms:
1.Reconstruct the oxygen partial pressure gradient to quickly correct tissue hypoxia
When 30% oxygen is inhaled, PiO₂ in plateau environments can be significantly improved:
- Altitude 3000 meters: PiO₂=70kPa×30%≈21kPa (about 158mmHg), close to the plain level; at this time, PAO₂ rises to 11-12kPa (83-90mmHg), and SaO₂ rises from 85% to 92%-94% – this level is enough to meet the basic oxygen demand of the tissue and terminate the “hypoxia signal”.
- Altitude 4000 meters: PiO₂=62kPa×40%≈24.8kPa (about 186mmHg), PAO₂ rises to 9-10kPa (68-75mmHg), and SaO₂ rises from 75% to 88%-90%, avoiding organ damage caused by severe hypoxia.
2.Inhibiting HIF-1α overactivation and blocking compensatory side effects
When SaO₂ is stable at more than 90%, the degradation pathway of HIF-1α restarts, its intranuclear activity decreases by 40%-50%, EPO secretion decreases by 30%, and the erythrocyte production slows down. Research shows that continuous oxygen supplementation (30% concentration, 2L/min) can control the HCT increase of travelers at an altitude of 3,000 meters from 5% to 2%, maintain normal blood viscosity, and avoid the risk of thrombosis.
3.Rapidly relieve acute symptoms and reduce risk of progress
- Heath: Excessive dilation of cerebral blood flow due to hypoxia (20% increase in cerebral blood flow) can be relieved within 30 minutes of oxygen replenishment, with 10%-15% reduction in intracranial pressure, and the degree of headache (VAS score) dropped from 6-7 to 2-3 points;
- Nache: The hypoxia stimulation in the central vomiting center disappears, gastrointestinal motility recovers, and appetite can improve within 1 hour;
- More importantly, oxygen supplementation can reduce shortness of breath (respiratory rate drops from 25 beats/minute to 18-20 beats/minute) and accelerated heart rate (reduced from 90 beats/minute to 75-80 beats/minute), reduce fatigue caused by excessive cardiopulmonary compensation, and buy time for the body to adapt to the plateau (usually after 3-5 days of adaptation, oxygen supplementation can be gradually reduced).
Safety and adaptability: Why 30%-40% is the “gold concentration” of plateau travel
The core of oxygen supplementation on the plateau is to “fill gaps rather than excessive intervention”:
- 30%-40% concentrations are “physiological compensation”, which will not inhibit the body’s natural adaptation to the plateau (such as moderate red blood cell hyperplasia), and will only block “overcompensated damage”;
- Far below the oxygen poisoning threshold (FiO₂>60% and lasts for more than 24 hours, it will induce oxygen poisoning), and there is no safety risk even if used for 8-10 hours a day;
- 2L/min flow adapts to portable needs, weighing only 0.6kg, can be carried with luggage, meeting the oxygen replenishment at any time in hiking, self-driving and other scenarios.
Several altitude medical studies have confirmed that at an altitude of 3000-5000 meters, using oxygen concentrations of 30%-40% (2L/min) can reduce the incidence of acute altitude sickness by 50%, and reduce the risk of severe complications (pulmonary edema) by 80% – This is precisely the professionalism based on the metabolic law of altitude oxygen.
In short, our oxygen generator is not “to fight against the plateau environment”, but by precisely replenishing oxygen concentration, it helps the body maintain the “oxygen supply-oxygen consumption” balance under low pressure, which not only relieves current discomfort, but also creates conditions for natural adaptation, making plateau travel safer and more comfortable.