Carbon Dioxide Transport
Authors: GJ Arthurs, M Sudhakar
DOI / Source: https://doi.org/10.1093/bjaceaccp/mki050
Date: 14 October 2005
Reading level: Beginner
Why This Matters for Freedivers
This paper helps freedivers understand why CO₂ “build-up” doesn’t behave like a simple balloon filling up: the blood buffers and transports CO₂ extremely efficiently, which affects how fast CO₂ pressure rises and how the urge to breathe develops. It also reinforces a key safety idea: discomfort is mainly a CO₂ signal, not an oxygen safety gauge—so training should prioritize good decision-making and conservative dive practice, not just learning to tolerate suffering.
Synopsis
Freedivers often talk about CO₂ like it’s just “the gas that makes you uncomfortable.” This paper explains something more interesting: your body can store and move huge amounts of CO₂ without a massive jump in CO₂ pressure, and that’s one reason breath-holds don’t always “feel” as dangerous as they truly are. It breaks CO₂ transport into three main forms in blood: a small amount is dissolved directly in the blood, a large amount is converted into bicarbonate (HCO₃⁻) inside red blood cells (using the enzyme carbonic anhydrase), and some binds to proteins—especially haemoglobin—as carbamino compounds. 
The clever part is how red blood cells manage this without “breaking.” When CO₂ enters the red cell, it’s rapidly turned into bicarbonate plus hydrogen ions. The hydrogen ions would make the cell too acidic, but they get buffered by haemoglobin—especially when haemoglobin has released oxygen (this is tied to the Haldane effect, which helps deoxygenated blood carry more CO₂). Meanwhile, bicarbonate moves out into plasma in exchange for chloride (the chloride shift), which is why venous blood chemistry is a bit different from arterial blood. The article also describes how CO₂ content rises fairly steadily with CO₂ pressure (the CO₂ dissociation curve is more linear than oxygen’s), and it gives useful “ballpark” numbers: mixed venous blood carries a bit more total CO₂ than arterial blood. 
For breath-hold diving, the most relevant section is the “effect of apnoea”: the body contains vastly more CO₂ “capacity” than oxygen, so during apnea CO₂ pressure rises gradually (they give a rough rise per minute), while oxygen can drop quickly unless you start with a large oxygen reserve. The bigger message is that CO₂ is not just waste gas—it’s part of a tightly managed system involving blood chemistry, haemoglobin, and ventilation control. Understanding that system helps explain why the urge to breathe can be intense even when oxygen is still okay, and also why oxygen can become critically low without dramatic warning symptoms.
Abstract
Carbon dioxide is produced by cell metabolism in the mitochondria. The amount produced depends on the rate of metabolism and the relative amounts of carbohydrate, fat and protein metabolized. The amount is about 200 ml min 1 when at rest and eating a mixed diet; this utilises 80% of the oxygen consumed, giving a respiratory quotient of 0.8 (respiratory quotient¼ rate of carbon dioxide production divided by rate of oxygen consumption). A carbohydrate diet gives a quotient of 1 and a fat diet 0.7.
Key points Carbon dioxide is transported in the blood in three ways: (i) dissolved in solution; (ii) buffered with water as carbonic acid; (iii) bound to proteins, particularly haemoglobin. At a haemoglobin concentration of 15 g dl–1, mixed venous PCO2 6.1 kPa contains 52 ml dl–1 of carbon dioxide; arterial blood PCO2 5.3 kPa contains 48 ml dl–1. The effects of carbon dioxide production in the tissues include: increased plasma Cl–; increased red blood cell mean corpuscular volume; and haemoglobin becoming less acidotic than oxygenated haemoglobin.