Why can people living on the plateau adapt to the hypobaric and hypoxic environment?

Many times, the people we live in on the plains are very distressed. It is clear that our physical fitness is good, but when we go hiking, we have a high level of rebellion. If you are physically better then you are not good at anything, you can only look at the ocean and get helpless, but there are so many in the world. People, they just live on the plateau and have no trouble. How do they adapt to the low-pressure, hypoxic, and cold conditions and adapt the plateau environment through what mechanism?

The non-adapted ethnic groups are similar, but the adapted ethnic groups have their own adaptations. The Tibetans, Andeans, and Ethiopians are the three major plateau nations in the world. Their ability to adapt to the plateau environment has evolved independently and the mechanisms are different.

Common incompatibility:

Highland disease and plateau habitation (lived in the hypoxic environment for a period of time, will produce a certain adaptation to hypoxia, the symptoms of early hypoxia can be significantly reduced, this situation is called plateau habitat.):

The biggest problem in the plateau is lack of oxygen. At an altitude of 3,000 meters, discomfort may occur. The most important symptoms are headaches, sometimes accompanied by loss of appetite, vomiting, and fatigue. If you continue to ascend, it may lead to fatal pulmonary edema and cerebral edema.

At present, the principle of altitude sickness is still not very clear. The main assumption is that when people enter the plateau, compensatory angiogenesis results from insufficient oxygen supply. The blood vessels of newborns are relatively weak, and the connection of vascular epithelial cells is loose. The immune cells and immune factors in the blood can easily penetrate into the blood-brain barrier and eventually lead to inflammation and edema of the brain tissue.

In addition, hypoxia can also damage the function of mitochondria, causing mitochondria to release a large amount of reactive oxygen species (oxygen radicals, peroxide radicals, etc.). These reactive oxygen species can cause great damage to cells and cause tissue damage.

Since the brain is the most oxygen-depleting organ, plateau has the greatest impact on brain tissue. After all, although the brain occupies only 2% of body weight, it takes up 15% of cardiac output and consumes 20% of total body oxygen and 25% of whole body glucose.

On the other hand, if the plains population lives on the plateau for a long time, the body will adapt to the plateau environment through some compensatory measures (enhanced altitude cultivation). The most important compensatory change in the body is to increase the concentration of red blood cells in the blood and increase the body's ability to transport oxygen.

In addition, increased myoglobin content in angiogenesis and muscle tissue also contributes to the adoption of the plateau.

However, altitude cultivation is costly. An increase in the concentration of red blood cells increases the probability of occurrence of cardiovascular and cerebrovascular diseases such as thrombotic cerebral infarction, and damaged red blood cells release a large amount of free hemoglobin and hematoporphyrin. These are comparative Strong inflammatory factors can cause confusion throughout the body.

Regardless of hypoxia response, plateau disease, or plateau adaptation, their central regulatory proteins are the HIF protein family (Hypoxia-inducible factors; hypoxia inducible factor).

The HIF family of proteins includes three members, HIF1, HIF2, and HIF3. Each member has two subunits. Only the combination of these two subunits will have an effect. HIF proteins are nuclear transcription factors, and most of the downstream are important genes related to hypoxia, including angiogenic factors (such as VEGFA that promote the formation of new blood vessels), erythropoiesis (EPO, promote erythropoiesis), and nitric oxide. Enzymes (synthesis of nitric oxide, promote vascular function), and a series of enzymes related to anaerobic respiration and glucose transport. In the HIF family, the most critical and most potent function is the HIF1 protein.

Tibetan adaptation:

Tibetans mainly live on the Tibetan Plateau, 53% of whom live at altitudes above 3,500m, and have adapted to high altitudes for tens of thousands of years.

By comparing Tibetan and Han people, the researchers found that in high-altitude environments, Tibetans' red blood cell concentration and hemoglobin concentration were significantly lower than those of Han nationals in a high-altitude plateau environment, which is basically comparable to that of Han people on the plains. In other words, Tibetans do not adapt to the plateau environment by increasing the concentration of red blood cells and the representative concentration of red blood. At the same time, the study found that Tibetans have faster blood circulation, and Tibetans exhale very high concentrations of nitric oxide. The main function of nitric oxide is vasodilation and blood circulation. This shows that the main mechanism for Tibetans to adapt to the plateau is to change the regulation of nitric oxide.

Genetic studies have found that compared with the most recent Han relatives, Tibetans have mutations in three genes: EPAS1, EGLN1, and PPARA.

Among them, EPAS1 is the gene encoding the first subunit of HIF2; EGLN1 is responsible for sensing the intracellular oxygen concentration. If the intracellular oxygen concentration changes, EGLN1 regulates the degradation rate of HIF protein and then regulates the intracellular HIF protein content; PPARA is mainly involved in lipids. Metabolism and storage of respiratory enzymes are related. Of course, the most important thing is EPAS1, which directly regulates hypoxia reactions.

The source of mutations in EPAS1 is also very interesting. By comparing the EPAS1 haplotypes, scientists believe that mutations in the Tibetan EPAS1 gene are from Denisovans. Before the modern Homo sapiens walked out of Africa, Eurasia lived in a happy Neanderthal and Denisova. The Neanderthals lived in Europe and West Asia, and the Denisovans lived in it. East Asia, South Asia and Central Asia.

The Maba people and the Xujiayao found in China belong to Denisova. The modern Homo sapiens who came out of Africa met the Neanderthals first. After a period of coexistence, the Neanderthals became extinct, but modern Homo sapiens blended in with some Neanderthal genes. Some modern Homo sapiens settled in Europe and West Asia, forming the ancestors of Europeans; another part of modern Homo sapiens continued east and met the Denisovan people. After a period of coexistence, Denisovans also became extinct. However, some genes have also been incorporated into the modern Homo sapiens gene bank, including the EPAS1 gene.

For the modern Homo sapiens who live on the plains (they eventually evolved into modern Han), the Denisova's EPAS1 genotype is not of much use, so Denisova's EPAS1 genotype has been at a very low frequency. Appeared in the Han nationality. For modern Homo sapiens who entered the plateau (they eventually evolved into modern Tibetans), Denisova's EPAS1 genotype favors plateau adaptation and will gradually phase out other EPAS1 genotypes, eventually taking the advantage.

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