The Global CO2 Paradox

The Global CO2 Paradox

Too Much in the Atmosphere and Too Little in the Human Body

Gerry Gajadharsingh DO

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Gerry Gajadharsingh writes

“We are repeatedly warned that the world has too much carbon dioxide. Yet in clinical practice I regularly meet patients whose breathing physiology suggests the opposite problem within their own bodies: they are breathing out more carbon dioxide than their metabolism requires.

That apparent contradiction prompted an intriguing question. If billions of people learned to breathe more efficiently and stopped losing unnecessary carbon dioxide, could they improve their physiology while also reducing atmospheric CO2? The mathematics gives us a useful answer, although not quite the one we might initially expect.

The simple answer

Breathing more efficiently may improve an individual’s physiology, but it would not directly reduce the amount of carbon dioxide in the atmosphere. The CO2 breathed out by a person is chemically the same as the CO2 released by burning coal, oil or gas. The important difference is where its carbon came from.

Most of the carbon we exhale came from food. Plants had recently taken that carbon from the atmosphere, either before we ate them or before they became food for animals. Human respiration therefore returns recently captured carbon to the biological cycle. Fossil fuels release carbon that had been stored underground for millions of years, adding it to the carbon already circulating through the atmosphere, oceans and living world.

Once the body has adjusted to a healthier breathing pattern, it must still exhale the carbon dioxide produced by metabolism. Breathing more efficiently changes the concentration of CO2 within the body far more than it changes the total quantity released over time.

The potential health benefit arises for a different reason. When someone breathes more deeply or frequently than their metabolism requires, carbon dioxide can fall too low. This may constrict blood vessels, particularly those supplying the brain, and can make haemoglobin hold on to oxygen more tightly. A pulse oximeter may still show a normal reading because it measures how much oxygen the blood is carrying, not how readily that oxygen is reaching and being released into the tissues.

The practical objective is not to retain as much carbon dioxide as possible. It is to recognise inappropriate overbreathing and, where clinically suitable, help the breathing pattern return towards a more efficient and physiologically appropriate level.

For many readers, that is the main conclusion. Those who would like to understand the physiology, the calculations and the scientific evidence can continue into the more detailed sections below.

Carbon dioxide is more than a waste gas

Carbon dioxide is produced continuously as cells generate energy. It is carried in the blood, principally as bicarbonate, and expelled through the lungs. Although excessive carbon dioxide can be dangerous in respiratory failure and other conditions, an abnormally low level can also disturb normal physiology.

The amount of carbon dioxide retained in the body is strongly influenced by alveolar ventilation. If ventilation rises out of proportion to metabolic demand, arterial carbon dioxide falls. This is hypocapnia. It may occur during obvious rapid breathing, but it can also result from breathing that is only slightly too deep, too frequent or unnecessarily driven over long periods.

In my assessments I often measure end-tidal carbon dioxide around 30 mmHg, sometimes lower, rather than the mid-to-high thirties I would generally hope to see in an otherwise suitable clinical context. End-tidal CO2 is not identical to arterial CO2, and the relationship can be altered by lung disease, ventilation-perfusion mismatch, age and measurement conditions. Nevertheless, a consistently low, well-recorded value can provide useful evidence that breathing regulation deserves closer examination.

Normal oxygen saturation does not guarantee normal oxygen delivery

A pulse oximeter tells us how much haemoglobin is carrying oxygen. It does not tell us how well blood is reaching every tissue, how readily haemoglobin releases its oxygen, or how effectively cells use it. A person can therefore have an apparently reassuring oxygen saturation while other parts of oxygen transport remain suboptimal.

Carbon dioxide influences two important parts of this process. First, hypocapnia causes vasoconstriction, most clearly demonstrated in the cerebral circulation. Reduced blood flow means reduced delivery of oxygen and glucose to the brain. Second, the respiratory alkalosis associated with hypocapnia shifts the oxyhaemoglobin dissociation curve to the left. This is the reverse side of the Bohr effect: haemoglobin holds oxygen more tightly, making its release into tissues less favourable.

The clinically relevant goal is not to create hypercapnia. It is to identify inappropriate overventilation and, where suitable, help the patient move towards more efficient breathing and physiological normocapnia.

Where the two percent figure comes from

For many years I have used the practical teaching statement that every 1 mmHg fall in carbon dioxide may reduce cellular oxygenation by approximately 2%. On reviewing the literature more closely, the underlying principle remains sound but the endpoint needs correcting.

Human studies and reviews commonly report a change of approximately 2% to 4% in cerebral blood flow or middle cerebral artery velocity for each 1 mmHg change in arterial CO2 across much of the physiological range. The response varies between people and is not perfectly linear. It should not be translated directly into a universal percentage change in cellular oxygenation throughout the body.

The more accurate teaching statement is therefore that cerebral blood flow commonly changes by around 2% to 4% per 1 mmHg change in arterial CO2, while hypocapnia may further impair tissue oxygen availability through its effect on oxygen unloading from haemoglobin.

What happens when CO2 rises from 30 to 35 mmHg

The alveolar ventilation equation shows that arterial CO2 varies inversely with alveolar ventilation when metabolic CO2 production is unchanged. Moving from 30 to 35 mmHg would therefore correspond to alveolar ventilation falling to 30 divided by 35, or approximately 85.7% of its previous value. That is a reduction of about 14.3%.

For illustration, someone producing 200 mL of CO2 per minute might require approximately 5.75 litres of alveolar ventilation per minute at 30 mmHg, compared with approximately 4.93 litres at 35 mmHg. The person would move less air, but the expired air would contain a higher concentration of CO2.

If cerebral CO2 reactivity were within the commonly reported range, a 5 mmHg rise could be associated with a sizeable change in cerebral blood flow. It would be tempting to calculate 10% to 20%, but this remains an estimate rather than a promise: cerebrovascular responses are nonlinear and depend on the starting CO2, vascular health, blood pressure, posture, medication and individual physiology.

The clinical relevance is illustrated by research into orthostatic intolerance. In one study, patients with orthostatic hypocapnia had end-tidal CO2 values averaging about 26 mmHg and cerebral blood-flow velocity fell by approximately 22% during tilt, despite the absence of orthostatic hypotension. This does not prove that every symptomatic patient with a low end-tidal reading has the same mechanism, but it demonstrates why CO2 can matter even when blood pressure and oxygen saturation appear acceptable.

Would better breathing reduce atmospheric CO2

This is where the paradox resolves. If someone reduces excessive ventilation, the body initially retains a small amount of carbon dioxide while a new equilibrium is established. Once that steady state is reached, the carbon dioxide produced by metabolism must still be excreted. The person breathes a smaller volume of air containing a slightly higher concentration of CO2, but does not continuously store a large share of metabolic carbon dioxide.

The same molecule with a different carbon history

A molecule of carbon dioxide contains one carbon atom and two oxygen atoms, regardless of whether it came from human respiration, a forest fire or a power station. Fossil CO2 is not a chemically different gas. The climate distinction concerns the origin of the carbon and whether its release increases the quantity circulating within the active carbon cycle.

The carbon in exhaled breath came mainly from carbohydrates, fats and proteins. Those nutrients ultimately trace back to photosynthesis, through which plants removed CO2 from the atmosphere. When we metabolise food and breathe out CO2, we return carbon that entered the biological cycle comparatively recently. The interval may range from days to years, but respiration mainly moves carbon around a cycle that is already active.

Coal, oil and natural gas also originated from organic matter, but their carbon became isolated in geological deposits for millions of years. Combustion moves this ancient carbon from a long-term underground store into the atmosphere. Unless an equivalent amount is removed and stored again, the active atmospheric carbon stock rises.

Scientists can also detect this history through carbon isotopes. Carbon-14 is radioactive and decays over time, so fossil fuels are so old that they contain virtually no remaining carbon-14. Fossil carbon is also relatively depleted in carbon-13. Its addition therefore changes the proportions of carbon-12, carbon-13 and carbon-14 in atmospheric CO2. This measurable fossil-fuel signature is known as the Suess effect.

An average resting adult producing around 200 mL of CO2 per minute would exhale roughly 288 litres per day, equivalent to about 0.56 kg. Multiplied across the present global population, human respiration is substantial, but its carbon largely belongs to the short biological carbon cycle.

This does not make the entire food system carbon-neutral. Agriculture, fertiliser production, land clearance, refrigeration and transport may all generate additional greenhouse-gas emissions. The narrower point is that the carbon in the CO2 produced by metabolising food has usually been captured recently from the active atmosphere, whereas fossil-fuel combustion introduces carbon from a long-term geological store.

Teaching the world to breathe better would therefore not directly solve climate change. The possible environmental effects would be indirect: healthier people might require fewer healthcare resources, travel less for illness and function more efficiently. Those are plausible downstream benefits, but they should not be confused with a direct reduction in atmospheric CO2.

Breathing within an integrated regulatory system

Breathing regulation cannot be separated from the rest of human physiology. Within the Integrated Regulatory Systems Framework, the respiratory system interacts continuously with the neural, circulatory, endocrine, immune and inflammatory, metabolic and musculoskeletal systems. Pain, anxiety, infection, metabolic disturbance, posture, medication, sleep and physical conditioning can all alter ventilation. In turn, changes in breathing and CO2 can influence cerebral perfusion, pH regulation, symptoms and the individual’s capacity to adapt.

This is why a low end-tidal CO2 measurement should neither be ignored nor treated as a diagnosis by itself. It is one piece of physiological information. It must be interpreted alongside the history, examination, respiratory pattern, spirometry where appropriate, cardiovascular findings, medication, metabolic health and the possibility of pulmonary or systemic disease.

Breathing retraining also needs to be proportionate. The aim is generally quiet nasal breathing with less unnecessary depth and effort, not forced breath-holding or a pursuit of the highest possible CO2 reading. I often encourage suitable patients to spend one or two minutes each hour observing and settling their breathing, with gentle end-in and end-out pauses where clinically appropriate. Anyone with significant respiratory, cardiovascular or neurological disease requires individual assessment rather than generic online instruction.

The real global opportunity

The world may have too much carbon dioxide in its atmosphere while many individuals intermittently maintain too little within their arterial physiology. These statements are compatible because they describe different systems, timescales and carbon cycles.

Better breathing will not remove fossil carbon from the atmosphere. It may, however, help some people make better use of the oxygen already present in their blood by supporting cerebral perfusion, acid-base regulation and oxygen unloading. That is a more modest claim than the original thought experiment, but it is also more clinically meaningful.

Perhaps the most useful conclusion is that more breathing is not always better breathing. As with so much in physiology, effective regulation depends on the right amount, at the right time, for the needs of the individual.”

 Clinical Disclaimer

This article is intended for educational and informational purposes only. It does not constitute medical advice and should not replace individual consultation with a qualified healthcare professional. Breathing exercises and carbon dioxide measurements require appropriate clinical interpretation, particularly in people with respiratory, cardiovascular or neurological conditions.

Selected References

1. Ainslie PN, Duffin J. Integration of cerebrovascular CO2 reactivity and chemoreflex control of breathing: mechanisms of regulation, measurement and interpretation. American Journal of Physiology Regulatory Integrative and Comparative Physiology. 2009;296:R1473-R1495. doi:10.1152/ajpregu.91008.2008.
2. Battisti-Charbonney A, Fisher J, Duffin J. The cerebrovascular response to carbon dioxide in humans. Journal of Physiology. 2011;589:3039-3048. doi:10.1113/jphysiol.2011.206052.
3. Hoiland RL, Fisher JA, Ainslie PN. Regulation of the cerebral circulation by arterial carbon dioxide. Comprehensive Physiology. 2019;9:1101-1154. doi:10.1002/cphy.c180021.
4. Novak P. Hypocapnic cerebral hypoperfusion: a biomarker of orthostatic intolerance. PLoS One. 2018;13:e0204419. doi:10.1371/journal.pone.0204419.
5. Malte H, Lykkeboe G. The Bohr/Haldane effect: a model-based uncovering of the full extent of its impact on O2 delivery to and CO2 removal from tissues. Journal of Applied Physiology. 2018;125:916-922. doi:10.1152/japplphysiol.00140.2018.
6. Suess HE. Radiocarbon concentration in modern wood. Science. 1955;122:415-417. doi:10.1126/science.122.3166.415-a.