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Iron
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CO2 tolerance essentially determines how much CO2 your body can accumulate before it feels like inhaling.
If you have a high CO2 tolerance, you breathe more slowly, which allows your CO2 levels to rise.
This will trigger the so-called Bohr effect.
The Bohr effect is the name of hemoglobin, a protein associated with 99% oxygen, which provides oxygen to cells more efficiently.
This is why CO2 tolerance is so important. After all, with low tolerance to CO2, hemoglobin retains this oxygen.
As a result, cells lose the ability to function properly:
— ATP synthesis decreases;
— Superoxide dismutase (SOD, an antioxidant enzyme) is inhibited;
— Vasodilation weakens (tissue blood supply deteriorates);
— Collagen production is disrupted;
— Fatty acid oxidation decreases (metabolic flexibility).
Also: it increases HIF‑1a (hypoxia‑inducible factor 1 alpha).
So, what is HIF‑1a?
At low CO₂ levels, hemoglobin releases oxygen less quickly and efficiently.
This causes hypoxia, which essentially means low oxygen levels.
At low oxygen levels, HIF‑1a levels rise because it is usually hydroxylated by oxygen, and in an environment with a lack of oxygen, the level of hydroxylation is lower (strangely enough).
But this is not the only reason why it increases under conditions of low oxygen content. It increases because, as already mentioned, oxygen is critically important for ATP synthesis. If there is not enough oxygen for ATP synthesis, another compensatory mechanism is required, which is why HIF‑1a enhances glycolysis, since it is not dependent on oxygen. Now that you understand how this mechanism works, I will get to the point. HIF‑1a is also a powerful stimulator of RANKL.
RANKL is the key to osteoclastogenesis, leading to increased proliferation and activity of osteoclasts, which shifts the balance towards bone resorption instead of bone formation.
This can significantly weaken the bones.
You can see this by getting a little familiar with the relationship between bones and estrogen.
Estrogen protects bones, in particular, because it hydroxylates HIF-1a in bones, preventing HIF-1a-mediated osteoclastogenesis and, consequently, bone resorption.
pmc.ncbi.nlm.nih.gov
pmc.ncbi.nlm.nih.gov
If you have a high CO2 tolerance, you breathe more slowly, which allows your CO2 levels to rise.
This will trigger the so-called Bohr effect.
The Bohr effect is the name of hemoglobin, a protein associated with 99% oxygen, which provides oxygen to cells more efficiently.
This is why CO2 tolerance is so important. After all, with low tolerance to CO2, hemoglobin retains this oxygen.
As a result, cells lose the ability to function properly:
— ATP synthesis decreases;
— Superoxide dismutase (SOD, an antioxidant enzyme) is inhibited;
— Vasodilation weakens (tissue blood supply deteriorates);
— Collagen production is disrupted;
— Fatty acid oxidation decreases (metabolic flexibility).
Also: it increases HIF‑1a (hypoxia‑inducible factor 1 alpha).
So, what is HIF‑1a?At low CO₂ levels, hemoglobin releases oxygen less quickly and efficiently.
This causes hypoxia, which essentially means low oxygen levels.
At low oxygen levels, HIF‑1a levels rise because it is usually hydroxylated by oxygen, and in an environment with a lack of oxygen, the level of hydroxylation is lower (strangely enough).
But this is not the only reason why it increases under conditions of low oxygen content. It increases because, as already mentioned, oxygen is critically important for ATP synthesis. If there is not enough oxygen for ATP synthesis, another compensatory mechanism is required, which is why HIF‑1a enhances glycolysis, since it is not dependent on oxygen. Now that you understand how this mechanism works, I will get to the point. HIF‑1a is also a powerful stimulator of RANKL.
RANKL is the key to osteoclastogenesis, leading to increased proliferation and activity of osteoclasts, which shifts the balance towards bone resorption instead of bone formation.
This can significantly weaken the bones.
You can see this by getting a little familiar with the relationship between bones and estrogen.
Estrogen protects bones, in particular, because it hydroxylates HIF-1a in bones, preventing HIF-1a-mediated osteoclastogenesis and, consequently, bone resorption.
Hypoxia-inducible factor regulates osteoclast-mediated bone resorption: role of angiopoietin-like 4 - PMC
Hypoxia and the hypoxia-inducible factor (HIF) transcription factor regulate angiogenic-osteogenic coupling and osteoclast-mediated bone resorption. To determine how HIF might coordinate osteoclast and osteoblast function, we studied ...
pmc.ncbi.nlm.nih.gov
Hypoxia-inducible factor 1α enhances RANKL-induced osteoclast differentiation by upregulating the MAPK pathway - PMC
Hypoxia (low-oxygen tension) and excessive osteoclast activation are common conditions in many bone loss diseases, such as osteoporosis, rheumatoid arthritis (RA), and pathologic fractures. Hypoxia-inducible factor 1 alpha (HIF1α) regulates cellular ...
pmc.ncbi.nlm.nih.gov
