At reference
Teaching model · not a clinical calculator
Acid and CO₂ loosen hemoglobin's grip on O₂ — so it lets go where tissues need it.
| Site | Reference | Current | Δ |
|---|---|---|---|
| Tissue · PO₂ 40 | – | – | – |
| Lung · PO₂ 100 | – | – | – |
| P50 (mmHg) | – | – | – |
When on, moving PCO₂ recalculates pH at fixed HCO₃⁻ ( mM). Moving pH is treated as a metabolic (fixed-acid) change. APPROX
Lungs vs tissue
A red blood cell carrying 16 oxygen-binding sites, shown in the current capillary.
Cartoon: 4 Hb tetramers × 4 hemes = 16 sites. A real red cell holds roughly 270 million Hb molecules. CARTOON
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CO₂ is breathed off, pH rises → left shift → Hb loads O₂ more readily.
Higher PCO₂ → mostly acts by lowering pH (plus a small direct carbamino effect) → right shift. Arterial ≈ 40, mixed venous ≈ 46.
Metabolism makes CO₂, H⁺ and heat → right shift → Hb unloads more O₂ at the same PO₂.
Warmer → right shift. A related thermal effect shown alongside Bohr — not the Bohr effect itself. Working muscle runs warm.
Because the curve is flat near 100 mmHg, a shift barely changes arterial SO₂ but matters a lot on the steep part near 40 mmHg. That is where the Bohr effect pays off.
Metabolism makes CO₂, H⁺ and heat → right shift → Hb unloads more O₂ at the same PO₂.
CO₂ is breathed off, pH rises → left shift → Hb loads O₂ more readily.
Because the curve is flat near 100 mmHg, a shift barely changes arterial SO₂ but matters a lot on the steep part near 40 mmHg. That is where the Bohr effect pays off.
APPROX −0.40 is a commonly quoted fixed-acid Bohr coefficient, for a pH change at a stated PCO₂. A single factor near −0.48 is the other number classes quote, for when carbon dioxide itself caused the pH change and no separate PCO₂ term is added. This bench does not also apply −0.48. That would count carbon dioxide twice. 0.024 per °C is the commonly quoted temperature coefficient, about a 5.7% change in P50 per degree, because 10^0.024 is about 1.057. Far from ordinary blood, constant coefficients and a fixed Hill n are a poor description.
APPROX Some published formulas use the pH inside the red cell, near 7.24 when plasma pH is 7.40, with the same 0.40, 0.06, and 0.024. Moving the zero point from 7.24 to plasma 7.40 is fair only while the plasma-to-red-cell gap stays constant. It does not, exactly. This slider is plasma pH, the number on a blood-gas report. Do not type 7.24 into it as the reference.
TEXTBOOK Not oxygen content in millilitres per decilitre. The readouts are percent saturation from a Hill curve. Content needs a hemoglobin concentration. Dissolved oxygen, the usual classroom figure of about 0.003 mL per dL per mmHg, is left out. Next to ordinary hemoglobin it is a small slice of content.
TEXTBOOK Warming also shifts the curve right, because oxygen binding releases heat. Cooling shifts it left. That thermal effect is drawn here beside the Bohr effect. It is not the Bohr effect.
Model: SO₂ = PO₂ⁿ / (PO₂ⁿ + P50ⁿ), n = 2.7, P50ref = 26.8 mmHg; log P50 = log 26.8 − 0.40·(pH − 7.40) + 0.06·log(PCO₂/40) + 0.024·(T − 37). See README for details.
How the bioenergetic writer Ray Peat framed CO₂ and the Bohr–Haldane effect. This is a labeled lens set beside the textbook physiology. It does not change the model, sliders or numbers above. Quotes are verbatim from a Ray Peat archive and attributed to their archive file. Each card notes where the textbook agrees, where it differs, and what the live curve can and cannot show.
Same sliders, same model as above. “CO₂ retained” = tissue, pH 7.30, PCO₂ 50, 37 °C (consistent with HCO₃⁻ ≈ 24 mM). Quote cards that match the current shift are highlighted. ↑ See the curve
In Peat’s view, CO₂ is what makes hemoglobin let go of oxygen where tissues need it. Too much oxygen, or overbreathing, strips CO₂ away. Hemoglobin then holds its oxygen more tightly, vessels constrict, and lactate rises, so a fully saturated blood sample can sit next to poorly oxygenated tissue. Beyond hemoglobin, he treated CO₂ as a protector of proteins, binding amino groups so that glycation and oxidized fats can't, and as a sign of good oxidative metabolism. To him it was a product of healthy energy production, not just exhaust.
Only the hemoglobin part (CO₂/acid → right shift → more unloading) is in the model. Vessel tone, lactate, tissue PO₂ and protein protection are not simulated.
Haldane effect: Oxygen displaces carbon dioxide from hemoglobin, in proportion to its partial (specific) pressure.
chadnet/altitude-and-mortality.md (2006)TEXTBOOK Agrees: oxygenated Hb carries less CO₂ and H⁺ (the Haldane effect). The model above shows only the Bohr direction, not Haldane.
Bohr effect: Carbon dioxide (or acidity) displaces oxygen from hemoglobin.
chadnet/altitude-and-mortality.md (2006)TEXTBOOK Same direction as the sliders: raise PCO₂ or lower pH and the curve shifts right.
The Haldane-Bohr effect describes the fact that oxygen and carbon dioxide destabilize each other’s binding to hemoglobin. When oxygen pressure is high, the blood releases its carbon dioxide more easily. In stormy weather, or at high altitude, the lower oxygen pressure allows the body to retain more carbon dioxide.
chadnet/altitude-and-mortality.md (2006)TEXTBOOK The two-way coupling is standard. Contrast on altitude: the standard account is that on arrival, hypoxic drive increases breathing and lowers arterial PCO₂ (left-shifting). Over days, 2,3-BPG rises and the kidneys excrete HCO₃⁻, partly correcting pH. “Retaining more CO₂ at altitude” is Peat’s reading. Compare it with the textbook before relying on it.
The Bohr-Haldane effect describes the fact that hemoglobin releases oxygen in the presence of carbon dioxide, and releases carbon dioxide in the presence of oxygen. When oxygen is too abundant, it makes breathing more difficult, and one of its effects is to cause carbon dioxide to be lost rapidly. At high altitude, more carbon dioxide is retained, and this makes cellular respiration more efficient.
chadnet/the-transparency-of-life-cataracts-as-a-model-of-age-related-disease.mdTEXTBOOK The first sentence matches the textbook. The claims about oxygen excess, altitude and efficiency are PEAT interpretation. See the altitude contrast above. They are not modeled.
Carbon dioxide, produced in the cells, releases oxygen into the tissues, relaxes blood vessels, prevents edema, eliminates ammonia, and increases the efficiency of oxidative metabolism.
chadnet/altitude-and-mortality.md (2006)TEXTBOOK Releasing O₂ in tissue (Bohr) is textbook, and CO₂ dilates vessels in most systemic beds, notably the brain. The model shows only the O₂-release part. The claims about edema, ammonia and efficiency are PEAT and are not modeled.
At high altitude, the slight tendency toward carbon dioxide-retention acidosis decreases the blood’s affinity for oxygen, making it more available to the tissues.
chadnet/altitude-and-mortality.md (2006)TEXTBOOK The mechanism (acidosis → lower affinity → more unloading) is exactly what the pH slider does. The premise that altitude causes CO₂ retention differs from the textbook; see the altitude contrast in the “Bohr and Haldane” card.
The loss of carbon dioxide from the lungs in the presence of high oxygen pressure, the shift toward alkalosis, by the Bohr-Haldane effect increases the blood’s affinity for oxygen, and restricts its delivery to the tissues, but because of the abundance of oxygen in the lungs, the blood is almost completely saturated with oxygen.
chadnet/altitude-and-mortality.md (2006)TEXTBOOK The model shows this directly. Press Overbreathing: SO₂ at PO₂ 100 barely moves because the curve is flat there, but at PO₂ 40 Hb keeps noticeably more O₂.
Breathing pure oxygen lowers the oxygen content of tissues; breathing rarefied air, or air with carbon dioxide, oxygenates and energizes the tissues; if this seems upside down, it's because medical physiology has been taught upside down.
chadnet/altitude-and-mortality.md (2006) · article headlineTEXTBOOK contrast: mainstream physiology holds that breathing O₂ usually raises tissue PO₂, while noting that hyperoxia and hypocapnia can constrict some vessels. The blanket claim is Peat’s and goes against the consensus. The model cannot test it, because it has no tissue PO₂ or blood flow.
If you're not using the oxygen, it doesn't do you any good to have your hemoglobin saturated if you're not using it.
interviews/kmud-100716-altitude.md [Dr. Peat], on oximetersTEXTBOOK A pulse oximeter reports arterial SO₂ only. It does not measure O₂ delivery to tissue or O₂ use.
Hyperventilation, breathing excessively and causing too much carbon dioxide to be lost, is similar to being in the presence of too much oxygen…
chadnet/altitude-and-mortality.md (2006)TEXTBOOK Hyperventilation → low PCO₂ → alkalosis → left shift. Try Overbreathing (pH 7.60, PCO₂ 25). Equating it with “too much oxygen” is PEAT framing.
Carbon dioxide inhibits the production of lactic acid, and lactic acid lowers carbon dioxide's concentration in a variety of ways.
chadnet/altitude-and-mortality.md (2006)APPROX Not modeled. Note that in this model any fall in pH, including one from lactic acid, shifts the curve right. With the link on, moving the pH slider is treated as exactly that kind of metabolic acid change.
CO₂ binding to the N-terminal amino groups of hemoglobin (carbamino) is TEXTBOOK. Extending that binding to proteins in general, and its role against glycation, oxidized fats and aging, is PEAT and is not established physiology.
The Haldane-Borre effect applies to proteins in general. When there's a lot of carbon dioxide, it basically changes the pH or the isoelectric point of the protein, making it less accessible to oxygen. And that in itself is a protection against the attack of oxygen against proteins.
interviews/kmud-100716-altitude.md [Dr. Peat]any amino group in your body, whether it's on your DNA or your enzymes or the so-called hormone receptors… when there's enough carbon dioxide, it will stick to those groups. And in the absence of carbon dioxide, other stuff will stick to those, such as glycation… So everything in your body is different when it's well saturated with CO2.
interviews/kmud-100716-altitude.md [Dr. Peat]On the heart, CO₂
makes the oxygen go to the right places in the heart… the electrons go directly to the oxygen down the electron transport chain, and the electrons are prevented from deviating and getting off and attacking the polyunsaturated fats.
interviews/kmud-100716-altitude.md [Dr. Peat]very few biologists recognize its role as a fundamental, universal protective factor.
chadnet/protective-co2-and-aging.md (2012)Carbon dioxide has antioxidant effects, and many other stabilizing actions, including protection against hypoxia and the excitatory effects of intracellular calcium and inflammation.
chadnet/protective-co2-and-aging.md (2012)Carbon dioxide is commonly thought of as a toxin, because an excess can cause unconsciousness and acidosis. But increasing carbon dioxide doesn’t necessarily cause acidosis, and acidosis caused by carbon dioxide isn’t as harmful as lactic acidosis.
chadnet/protective-co2-and-aging.md (2012)TEXTBOOK Hypercapnia is dangerous in excess, as the quote itself says. With fixed HCO₃⁻ (link on), raising PCO₂ in this model does lower pH. Renal compensation, which would raise HCO₃⁻ over days, is not modeled.