CO2 Blood Test: Causes of Low and High Results and What It Means for Athletes

Key Takeaways

A CO2 blood test measures venous total carbon dioxide, which laboratories use as a routine stand-in for serum bicarbonate.[1]
In 28,480 healthy young adults the average was 25.8 mEq/L, and the authors suggest that confirmed values outside 23–30 mEq/L may warrant further acid–base assessment.[1]
Low values are linked to higher mortality in chronic kidney disease and in older adults, but an isolated low result can be an underfilled-tube artifact.[2][3][4]
Studies have found lower blood bicarbonate after strenuous exercise and altitude exposure, while sodium bicarbonate raised blood bicarbonate by up to 12.3 mmol/L within hours in a small study of healthy men.[5][6][7][8]
If a CO2 value is measured, testing at rest and telling your doctor about bicarbonate supplements, altitude exposure, vomiting, diarrhoea or diuretics can make the result easier to interpret.
In my experience, at least in Finland, the CO2 value is generally not part of routine laboratory panels; in hospital and emergency care, a blood gas is what reveals carbon dioxide retention, which a good oxygen saturation can hide, particularly in COPD.
In my view, CO2 measurement adds little for most athletes, and VO2max or lactate testing says more about performance; bicarbonate supplementation, high-altitude sport and diving are the main exceptions.

Introduction: Why This Small Number Deserves a Closer Look

The CO2 blood test is easy to overlook on a routine panel, yet its “normal range” varies considerably between laboratories. Across clinical laboratories, reported lower reference limits range from 18 to 25 mEq/L and upper limits from 26 to 35 mEq/L, and the authors of a 2018 analysis in the American Journal of Nephrology argue that ranges this wide could hide a significant acid–base disorder.[1]

In general medicine, an abnormal value can be a clue to kidney, gut or lung problems. In sport, hard training, altitude and buffering supplements can shift it in healthy people.

Below, I cover what the CO2 blood test measures, its evidence-based normal range, the main causes of low and high results, and what the test means for athletes.

What the Test Actually Measures

Despite its name, the CO2 blood test does not measure the carbon dioxide you breathe out. Laboratories measure total CO2 in a venous sample as a routine screening substitute for serum bicarbonate.[1] Bicarbonate is one of the body’s main chemical buffers, so the result is read as a window on acid–base balance: whether the body is carrying an acid load, has lost acid or gained base, or is compensating for a breathing-related change in carbon dioxide, although pH and carbon dioxide from a blood gas are usually needed to tell these apart.

In my experience, at least in Finland, the CO2 value is usually not part of the routine laboratory panels I see, and I rarely encounter it as a screening test. In primary care or in periodic occupational health check-ups, for example, it usually does not appear at all. Certain patient groups are different: in patients with COPD, an arterial or venous blood gas is often taken, and that gives a clearer picture of carbon dioxide.

When sodium, chloride and bicarbonate are all available, clinicians can calculate the anion gap. A 2019 French expert-panel guideline defines it as sodium minus the sum of chloride and bicarbonate, with a normal value of 12 ± 4 mmol/L.[9]

When the Carbon Dioxide Level Itself Is the Problem

From a clinical perspective, carbon dioxide is not a value most clinicians think much about in routine primary care, but it comes up in specific situations, especially in hospital and emergency settings. It helps to keep two measurements apart: the routine CO2 blood test reflects bicarbonate, whereas a blood gas gives the partial pressure of carbon dioxide (PCO2), which is used to assess carbon dioxide retention. One situation where that blood gas value matters is carbon dioxide retention, which can be a deceptive finding for a less experienced clinician. A patient who, for one reason or another, does not ventilate well can drift into carbon dioxide narcosis. When someone arrives in the emergency department with respiratory failure and a falling saturation, starting supplemental oxygen is a natural first step, using a delivery method suited to how ill the patient is and to the risk of hypercapnia. If the patient’s own ventilation is weak, however, the saturation may look good while carbon dioxide clearance quietly falls and carbon dioxide starts to accumulate.

I have seen this more than once myself: a bedridden patient who came to the emergency department with a mild drop in oxygen saturation, saturated well on oxygen, and later became unconscious or confused on the ward. In that situation, a blood gas analysis is the key test, because it can reveal that hypercapnia may be the cause.

Hypercapnia is also a risk when a hospitalised patient with COPD has their saturation corrected. A less experienced clinician may not realise that in many COPD patients saturation is low even at baseline, and giving them too much oxygen is a classic beginner’s mistake. For patients with COPD, the British Thoracic Society guideline suggests an initial target saturation of 88–92% pending blood gas results, lists nasal cannulae at 1–2 litres per minute as one possible starting option, and allows a target of 94–98% only if both pH and PCO2 are normal and the patient has neither a history of hypercapnic respiratory failure requiring ventilatory support nor a usual saturation below 94%, with blood gases repeated after 30–60 minutes.[10] The oxygen dose is therefore titrated to the target and the blood gas findings rather than kept at a fixed flow.

Sometimes, though, breathing deteriorates badly, for example in a COPD exacerbation, in heart failure with pulmonary congestion, or in another acute situation. The first impulse is often to start CPAP to improve saturation, but if the patient is too exhausted to breathe effectively, carbon dioxide can still build up. In my experience, bilevel positive airway pressure ventilation can then be a better choice for appropriately selected patients, particularly when carbon dioxide is accumulating, because the lungs are ventilated better and hypercapnia can be controlled more effectively. The right choice depends on the cause: the ERS/ATS guideline recommends bilevel noninvasive ventilation for acute respiratory failure with respiratory acidosis in COPD exacerbations, and either bilevel ventilation or CPAP for cardiogenic pulmonary oedema, and it notes that the lower the pH, the greater the risk of failure, so patients who are not improving must be very closely monitored with rapid access to intubation.[11]

Beyond these acute situations, some patients with advanced COPD who ventilate poorly have a carbon dioxide level on blood gas testing that is higher than in the general population, and some live in mild chronic hypercapnia. In my clinical experience, some of these patients may also have cognitive difficulties, although such symptoms can have several causes and should not automatically be attributed to elevated carbon dioxide. Their oxygen saturation is also often somewhat lower at baseline. In advanced COPD, patients also become breathless easily with any activity, and I often notice that they become breathless even while talking.

At the other extreme are patients who hyperventilate, such as the classic panic disorder patient who arrives in the emergency department after starting to hyperventilate as part of a panic attack. I have often heard these patients describe numbness in their hands and lips and a light-headed, dizzy feeling, which understandably makes them panic even more. They are naturally worried about these seemingly neurological symptoms. These patients still deserve the same careful assessment as anyone else, but an experienced clinician can often recognise the picture quickly and may immediately suspect a classic hyperventilation episode, in which the carbon dioxide level falls and hypocapnia develops.

In my view, a blood gas analysis can be useful in these patients too, to confirm the picture, since breathing is a vital function. Oxygen saturation often says something about how well a patient is breathing, but it does not measure carbon dioxide, whereas a blood gas analysis does.

CO2 Blood Test Normal Range

The reference interval cited by the American Association for Clinical Chemistry (AACC) and the Tietz textbook is 23–29 mEq/L, while Kraut and colleagues had previously proposed 23–30 mEq/L for venous samples at sea level.[1]

To test that range, the same group analysed 28,480 apparently healthy adults aged 18–40 who had routine outpatient blood tests and no conditions or medications likely to affect the result. Mean total CO2 was 25.8 ± 2.28 mEq/L (median 26), and 91% of values fell between 23 and 30 mEq/L.[1]

Sex makes a measurable difference. Men averaged 26.6 ± 2.16 mEq/L and women 25.0 ± 2.11 mEq/L, and a value below 23 mEq/L was found in 11.3% of women compared with 3% of men.[1] The authors discuss the effect of premenopausal progesterone on breathing as the likely explanation, citing earlier work in which arterial carbon dioxide (PaCO2) was about 2–4 mm Hg and bicarbonate about 1 mEq/L lower.[1]

The authors note that some low-end values are normal outliers, especially in women, and suggest that a confirmed value outside 23–30 mEq/L may warrant a venous blood gas to look for an acid–base disorder.[1] The study itself did not determine how many people outside the range actually had such a disorder. They also recommend separate reference ranges for populations living above roughly 1,500 m.[1]

Low CO2 Blood Test: Common Causes

Metabolic acidosis

The French expert-panel guideline defines metabolic acidosis as an acid–base imbalance with plasma bicarbonate below 20 mmol/L.[9] Because a low value can also reflect respiratory alkalosis, the panel suggests an arterial blood gas in patients with low bicarbonate to rule out respiratory alkalosis, confirm metabolic acidosis and look for a mixed disorder.[9]

The guideline recommends correcting the anion gap for serum albumin, because low albumin can hide a raised gap.[9] A raised gap signals accumulating acids; the guideline’s examples include lactate, the ketone bodies acetoacetate and hydroxybutyrate, salicylate, oxalate, glycolate and formate.[9] When the albumin-corrected gap is normal, causes to consider include bicarbonate lost through the gut, renal tubular acidosis, hyporeninemic hypoaldosteronism, or hyperchloremic acidosis after large volumes of chloride-rich fluids.[9]

Kidney disease and long-term risk

In 1,240 men with moderate to advanced chronic kidney disease not on dialysis (mean eGFR 37 mL/min/1.73 m²), baseline bicarbonate below 22 mmol/L was associated with higher all-cause mortality than 26–29 mmol/L (adjusted hazard ratio 1.43, 95% CI 1.10–1.87; 1.33, 95% CI 1.05–1.69, when compared with all values of 22 mmol/L or more), and in a time-dependent analysis mortality was lowest at around 26 mmol/L.[2]

A similar pattern appeared in the Health, Aging, and Body Composition Study of 2,287 well-functioning adults aged 70–79, in which bicarbonate was measured from arterialized venous blood gas samples. Over a mean follow-up of 10.3 years, bicarbonate below 23.0 mEq/L carried a fully adjusted mortality hazard ratio of 1.24 (95% CI 1.02–1.49) compared with 23.0–27.9 mEq/L.[3] Both studies are observational, so they show an association, not proof that low bicarbonate itself shortens life, and they studied older adults and people with kidney disease rather than healthy athletes.

Laboratory artifact: the underfilled tube

Not every low CO2 blood test is real. In a 2025 pilot study in the American Journal of Clinical Pathology, paired samples from 12 healthy adult volunteers were drawn into full tubes and into tubes filled to 33% (1 mL short draws). Median CO2 was 25.25 mmol/L in complete draws and 21.55 mmol/L in short draws, a median bias of −3.25 mmol/L (−13.1%), and the authors classified CO2 as not a candidate for reporting on short draws.[4] A short draw is therefore one possible explanation when an isolated low value does not fit the clinical picture.

High CO2 Blood Test: Common Causes

Metabolic alkalosis is a primary acid–base disorder that raises serum bicarbonate.[12] In a 2020 review in the Clinical Journal of the American Society of Nephrology, Emmett uses vomiting or nasogastric suction as the classic example: when hydrochloric acid is lost, bicarbonate that would normally be neutralized in the small bowel enters the extracellular fluid instead.[12] The same review notes that thiazide and loop diuretics very frequently cause low potassium together with metabolic alkalosis.[12]

In most patients, the alkalosis is maintained by increased bicarbonate reabsorption in the proximal tubule of the kidney, with reduced effective arterial blood volume and low potassium as the major drivers.[12] A urine chloride below 20 mEq/L generally indicates that the kidney is responding to reduced extracellular fluid volume, although urine chloride can vary widely with diuretic use.[12]

For long-term risk, high values look less clear-cut than low ones. In the Health ABC cohort, bicarbonate of 28.0 mEq/L or more was not significantly associated with mortality after full adjustment (HR 1.03, 95% CI 0.84–1.26), although spline analysis showed significantly higher mortality above about 32 mEq/L.[3] In the kidney-disease cohort, values above 29 mmol/L had a hazard ratio of 1.24 that did not reach statistical significance (95% CI 0.94–1.64).[2]

CO2 Blood Test: What It Means for Athletes

Personally, I do not see CO2 measurement as particularly useful in athletes, because I am not sure what one would try to improve based on it. When the goal is to assess an athlete’s performance, VO2max testing or lactate measurement are more useful tests. One possible exception is bicarbonate supplementation, and in that situation I understand that measuring blood CO2 may be wanted in some cases. Unless supplementation, high-altitude sport, diving or another situation that directly affects blood gases is involved, however, I do not see a particular benefit in measuring it in an ordinary athlete. Divers are one group in whom carbon dioxide can matter, but I would keep diving separate from other sports. Otherwise, the CO2 value matters for athletes mainly when it has already been measured for another reason and needs to be interpreted, which is what the sections below cover.

One caveat applies to the studies below: several measured bicarbonate with blood gas analysis, for example capillary samples in the race-walker and simulated-altitude studies and arterial samples in the 3,800 m study,[5][8][13] rather than with a routine venous total CO2 test. The two measurements are closely related but not interchangeable, so the numbers describe the direction and rough size of change rather than exact lab values.

Hard exercise lowers it

In a study of 24 elite race walkers, capillary bicarbonate fell significantly between the pre-exercise sample and samples taken 2, 4 and 6 minutes after a graded maximal treadmill test, in every dietary group.[5]

Long efforts can produce a drop too. Among 22 elite male mountain runners who completed a 105 km ultramarathon, mean bicarbonate was 26.16 ± 1.77 mmol/L before the race and 21.77 ± 1.52 mmol/L after it, while pCO2 went from 40.05 to 33.36 mmHg and mean pH stayed at 7.42.[6] Here the group’s mean post-race bicarbonate fell below the usual reference interval while mean pH stayed the same, which illustrates why recent strenuous exercise may be relevant when interpreting an athlete’s bicarbonate-related blood results.

Sodium bicarbonate supplements raise it

Sodium bicarbonate has its own International Society of Sports Nutrition (ISSN) position stand, which concludes that doses of 0.2–0.5 g/kg body mass improve performance, with benefits mostly established for high-intensity tasks lasting between 30 seconds and 12 minutes.[14] The optimal single dose appears to be 0.3 g/kg, taken 60–180 minutes before exercise, and multi-day protocols use a total of 0.4–0.5 g/kg per day, split into smaller doses, for 3–7 days before competition.[14] The most common side effects are bloating, nausea, vomiting and abdominal pain.[14]

It produces a dose-dependent rise in plasma bicarbonate, with higher pH and base excess, which the position stand describes as metabolic alkalosis.[14] In 16 healthy men, 0.3 g/kg increased blood bicarbonate by between 6.0 and 12.3 mmol/L, peaking 75–180 minutes after ingestion, with large individual differences in both the size and timing of the peak that dosing by body mass did not remove.[7]

Because the routine CO2 blood test is used as a stand-in for bicarbonate, an increase of that size could also push the routine result above the 23–29 or 23–30 mEq/L ranges discussed earlier, although the cited study did not measure venous total CO2 directly. A high result taken within hours of a dose, or during a multi-day loading protocol, may reflect the supplement rather than kidney or gut disease, which is why your doctor needs to know about it.

Altitude lowers it

At altitude, blood carbon dioxide falls and bicarbonate follows as the kidneys compensate.[8][13] After 12 hours at a simulated altitude of 3,000 m, capillary bicarbonate in 16 participants fell by 1.35 ± 0.29 mmol/L to 23.3 ± 1.3 mmol/L, with lower carbon dioxide and higher pH; the authors describe this as uncompensated respiratory alkalosis.[8]

In 16 lowlanders who ascended rapidly to 3,800 m, arterial bicarbonate and carbon dioxide were both lower on day 2 and day 9 than at the 1,045 m baseline, and the authors concluded that renal acid–base compensation occurred within 24 hours.[13] Kraut and colleagues also recommend separate reference ranges for populations living above roughly 1,500 m.[1] The studies summarized here do not show how quickly values return to sea-level norms after descent, so a test taken during or soon after an altitude camp should be read with that exposure in mind.

For an athlete at an altitude training camp, or one who competes at high altitude, CO2 or bicarbonate measurements may be relevant when there is a specific clinical indication. In my view, the indications are much the same as for the general, non-athletic population, for example when altitude sickness is being investigated, although the studies cited here describe adaptation to low oxygen rather than a routine diagnostic role for these tests.

A ketogenic diet changed little in one small study

In the same race-walker study, three weeks of a ketogenic low-carbohydrate, high-fat diet (under 50 g carbohydrate per day, about 75–80% of energy from fat) produced no significant group differences in blood bicarbonate after the intervention.[5] The authors concluded that chronic dietary interventions are unlikely to influence acid–base status in elite athletes, possibly reflecting pre-existing training adaptations such as enhanced buffering capacity.[5] The study was small and non-randomized (9 athletes in the diet group, 3 weeks), so it does not show that a ketogenic diet has no effect in other athletes or over longer periods.

Weight cutting, vomiting and diuretics raise it

Vomiting and thiazide or loop diuretics are established routes to metabolic alkalosis, often with low potassium.[12] An athlete who has been vomiting from illness, or who has used diuretics or vomiting to make weight, may therefore show a raised CO2 blood test for reasons that have nothing to do with fitness.

Does a higher value mean better fitness?

In 2,714 US adults aged 20–49, each 2.16 mEq/L (one standard deviation) higher serum bicarbonate was associated with a 1.46 mL/kg/min higher estimated VO2max before adjustment, and the association remained significant, though smaller, after full adjustment.[15] The analysis was cross-sectional, and after adjusting for lean body mass the link with low fitness was no longer significant, so the authors suggest lean mass may explain part of the association.[15]

The sex difference described earlier is worth remembering for female athletes: in the young-adult population studied, the authors note that some low-end values are normal outliers, especially in women.[1]

Conclusion: Reading Your CO2 Blood Test in Context

The CO2 blood test is a stand-in for bicarbonate, and in healthy young adults it averages 25.8 mEq/L, with most values between 23 and 30 mEq/L.[1] A persistently low result deserves attention in clinical context: it has been associated with higher mortality in cohorts of people with chronic kidney disease and older adults, and the anion gap helps identify its cause.[2][3][9] A high result can point toward metabolic alkalosis, for example after vomiting or diuretic use, often with low potassium.[12]

In hospital and emergency settings, the value that often matters most is the partial pressure of carbon dioxide (PCO2) on a blood gas. In my experience, a patient who saturates well on oxygen can still be quietly retaining carbon dioxide, especially in COPD, while a patient hyperventilating during a panic attack shows the opposite, hypocapnia.

For athletes, context comes first. In my view, CO2 measurement adds little for most athletes, and VO2max or lactate testing says more about performance, with bicarbonate supplementation, high-altitude sport and diving as the main exceptions.

If a CO2 value has been measured anyway, hard exercise and altitude can lower it, sodium bicarbonate can raise it by several mmol/L, and one small study found little change with a ketogenic diet. Testing at rest and being open about supplements, altitude and weight cutting can make the result easier to interpret.