O2 vs. CO2 Training in Freediving: What the Physiology Actually Says

Freediving coaches have split apnea training into two camps for decades: "O2 training" — long dives with long recovery, aimed at working with severely reduced blood oxygen — and "CO2 training" — short dives with short recovery, aimed at keeping carbon dioxide chronically elevated. The split is a reasonable first approximation of the two physiological stressors a breath-hold diver has to tolerate: hypoxia (falling oxygen) and hypercapnia (rising carbon dioxide). But the folk version of this model — pick a bucket, train it in isolation, argue about which bucket matters more — undersells what is actually a well-studied area of exercise and diving physiology. This article works through the mechanisms behind both stimuli, summarizes what recent peer-reviewed research on breath-hold divers shows about energy metabolism and lactate handling during apnea, and lays out a periodization framework an intermediate-to-advanced athlete can apply, with the reasoning made explicit at every step rather than asserted as opinion.

Two stressors, one dive

During any breath-hold, two things happen simultaneously: the partial pressure of oxygen in arterial blood (PaO₂) falls, and the partial pressure of carbon dioxide (PaCO₂) rises. In elite static apnea, direct arterial sampling has recorded PaO₂ dropping from a resting 14.3 ± 2.2 kPa to a critical 4.9 ± 0.5 kPa by the end of a maximal breath-hold, with the same athletes able to sustain apneas averaging 375 seconds despite operating in this range for the final portion of the dive (Perhonen et al., 2025). That number matters for two reasons: it shows how far below normal resting values (roughly 13 kPa) a trained diver's blood oxygen is allowed to fall before the dive ends, and it explains why hypoxia, not hypercapnia, is the physiological event that actually terminates most maximal-effort dives via loss of motor control (LMC) or blackout.

Hypercapnia, meanwhile, is the trigger behind the conscious urge to breathe. Rising CO₂ is detected by central chemoreceptors in the medulla and peripheral chemoreceptors in the carotid bodies, and the resulting drive to ventilate is what most beginner freedivers experience as the limiting sensation during a dive — long before oxygen has fallen anywhere near a dangerous level. A comparative review of competitive freediving physiology describes this directly: trained freedivers exhibit "a blunted ventilatory chemosensitivity to hypercapnia at rest and post-exercise that is distinct from scuba divers and controls" (Reider & Stöggl, 2024). In plain terms: part of what separates a trained diver from a beginner is not a higher pain tolerance, but a genuine downward recalibration of the CO₂ receptor's sensitivity, so the same PaCO₂ produces a weaker urge to breathe. This is the physiological target that "CO2 training" is nominally trying to hit, and it is a real, measurable adaptation — the disagreement in the community is not over whether it exists, but over how much dedicated training time it deserves relative to hypoxic and aerobic-base work.

What "O2 training" is actually training

Long, low-frequency dives with generous recovery accomplish two things that short repeated efforts cannot. First, they allow PaO₂ to fall far enough, for long enough, to drive the specific adaptation that matters for competitive performance: comfort and motor control at low blood oxygen. Second, because rest intervals are long, they do not accumulate a hypercapnic and metabolic-acidotic background from set to set the way short-rest repeats do, which keeps the primary training stimulus close to pure hypoxic tolerance rather than a blend of several stressors at once. This is consistent with the specificity principle that runs through most of exercise physiology: the adaptation you get resembles the stimulus you apply, and the terminal event in competitive apnea is overwhelmingly hypoxic, not hypercapnic (Perhonen et al., 2025).

There is also a metabolic argument for prioritizing this style of training, and it comes from some genuinely striking recent findings on how trained breath-hold divers handle lactate. A 2025 case-control study compared six elite breath-hold divers — three ranked in the world's top ten, one a world-record holder — against six aerobically trained control athletes matched for VO₂max and BMI. The divers showed roughly 30% higher cardiac and erythrocyte lactate dehydrogenase (LDH-1) activity than controls (30.3 ± 3.9% vs. 23.4 ± 3.7%, p = 0.012), and — critically — after a standardized ischemic stimulus, adding lactate to the divers' arterial blood increased p50 (the oxygen tension at which hemoglobin is 50% saturated) from 23.3 to 23.9 kPa, meaning the blood released oxygen to tissue more readily in the presence of lactate. That same effect was absent in the control athletes' blood. The trained divers also cleared venous lactate differently after the ischemic stimulus than controls did (p = 0.001), and showed a rise in venous glucose after maximal exercise that the controls did not, consistent with lactate being actively shuttled and used as fuel rather than simply accumulating (Perhonen et al., 2025). The authors describe lactate, in this hypoxia-adapted population, as functioning almost as a "cardiac super-fuel" that improves oxygen unloading rather than simply signaling fatigue. This is a genuinely different metabolic phenotype from an untrained aerobic athlete's, and it appears to be a product of sustained hypoxic exposure — the kind produced by long, low-frequency, near-maximal dives — rather than of short repeated hypercapnic efforts.

Where energy-system training and CO2-style work fit in

None of this means hypercapnic or anaerobic-leaning work is worthless — it means it plays a supporting role rather than the leading one for most of a training cycle. Dynamic apnea, in particular, is not a purely aerobic event: research on monofin swimming in trained breath-hold divers has examined the relative contribution of aerobic and anaerobic metabolic pathways across a dive, and the working consensus in this literature is that both systems are engaged simultaneously, with the balance shifting toward anaerobic glycolysis as pace, distance, and swim duration increase (Ivančić et al., 2025). A separate controlled-training study comparing aerobic-emphasis and anaerobic-emphasis programs in freedivers reported measurable performance effects from both approaches, supporting the idea that a well-built program uses both energy systems deliberately rather than defaulting to one (effects of aerobic and anaerobic training on freedivers' performance, 2024). A systematic review and meta-analysis of apnea-training interventions likewise found that structured breath-hold training produces measurable gains in both aerobic and anaerobic performance markers, reinforcing that these are not mutually exclusive training effects competing for the same adaptive budget (Frontiers in Physiology, 2022).

Finning style changes this balance further. Lactate sampling across disciplines shows monofin efforts — which recruit large, coordinated muscle groups (core, glutes, hamstrings) — producing substantial but comparatively efficient lactate accumulation, around 5.9 mmol/L post-dive in elite divers. Bifins, which isolate the quadriceps and calves with minimal glide phase, produce faster local muscle desaturation and some of the highest lactate readings of any discipline. No-fins swimming, which recruits the arms, shoulders, and trunk simultaneously with no propulsive assist, produces the highest metabolic cost of all — post-dive lactate figures exceeding 7 mmol/L have been reported, against roughly 0.7 mmol/L for static apnea (Alchemy Freediving, 2024). This is a useful, concrete argument for why a no-fins or bifins-focused athlete has more to gain from targeted lactate-tolerance and buffering work than a monofin specialist does — the disciplines are not metabolically interchangeable, and training should reflect that.

A periodization framework

Putting the physiology together, a defensible structure for an intermediate-to-advanced athlete's macrocycle looks like this:

Off-season / general preparation. This is the appropriate window for higher-volume, shorter-rest, hypercapnia-forward work, alongside general strength and conditioning. The goal here is to build the blunted CO₂-chemosensitivity response described above, and to build a broad aerobic and muscular base, without that stimulus competing for recovery resources with peak-specificity hypoxic work later in the cycle.

Main preparation phase. The primary stimulus shifts toward long, low-frequency, high-quality dives at 85–95% of confident maximum distance or time, with full recovery between efforts (a common guideline is at least a full day, often up to a week, between maximal-effort sessions targeting the same discipline). This is where the hypoxic-tolerance and lactate-shuttling adaptations described above are built. CO2-style work is not eliminated, but it is reduced to a minor, maintenance-level component — for example, one lower-intensity hypercapnic session for every three to four hypoxic-priority sessions — so it does not blunt recovery from the sessions doing the primary work.

Discipline-specific lactate work. For no-fins and bifins athletes especially, targeted sets that intentionally push into moderate-to-high lactate accumulation (for example, a controlled pace increase over the final third of a sub-maximal dive) are a reasonable, evidence-consistent way to build tolerance to the specific metabolic environment of that discipline. Monofin athletes, whose technique is more efficient per unit of lactate produced, generally need less of this work.

Taper. Volume drops, hypoxic-priority dives are reduced in frequency but not eliminated entirely, and the final one to two weeks before a competition emphasize recovery over any new training stimulus.

The throughline across all of this is that "O2" and "CO2" training are not competing philosophies to pick a side on — they are two distinct physiological stimuli, engaged to different degrees by different disciplines and different phases of a training year, and current apnea-specific research gives a reasonably clear picture of when each one earns its place in a program.

Frequently Asked Questions

Is CO2 training useless, then?
No. It targets a real, documented adaptation — reduced ventilatory sensitivity to rising CO₂ — that genuinely helps a diver tolerate the urge to breathe. The research summarized above argues for de-prioritizing it relative to hypoxic and aerobic work during the main competitive phase, not for eliminating it from the yearly plan.

Why does hypoxia matter more than hypercapnia if the urge to breathe comes from CO2?
Because the urge to breathe and the event that actually ends a maximal dive are two different things. Arterial sampling shows trained divers pushing PaO₂ down to roughly 4.9 kPa by the end of a maximal apnea — that is the physiological territory where loss of motor control and blackout occur, and it is a hypoxic event, not a hypercapnic one (Perhonen et al., 2025).

Does finning style really change how I should train?
Based on discipline-specific lactate sampling, yes. No-fins and bifins efforts generate substantially higher post-dive lactate than monofin efforts at a comparable relative intensity, which is a reasonable basis for giving those disciplines more dedicated lactate-tolerance work (Alchemy Freediving, 2024).

How much rest do I actually need between maximal-effort O2 sessions?
There is no single validated number, but the periodization logic above — full recovery, often a week for the same discipline at near-maximal effort — reflects the fact that this type of session is targeting deep hypoxic and metabolic adaptations that need time to consolidate, not a repeatable daily stimulus.

Can I do CO2 and O2 training in the same session?
You can, but you are then training a blended stimulus rather than either one cleanly, which makes it harder to know which adaptation you are actually driving. Most of the research cited here studied these as distinguishable stimuli; if your goal is to reason clearly about your own progress, separating them across sessions or phases makes the data easier to interpret.

Where can I read the primary research myself?
Links to every study cited in this article are provided inline above. As with any training article, treat this as a framework to apply and test against your own logbook, not a substitute for coaching supervision — always train hypoxic and hypercapnic work with a trained buddy and proper safety protocols.