2.0 ATA vs 1.3 ATA: how much oxygen each hyperbaric pressure actually delivers

Why inspired oxygen pressure beats chamber pressure

Haemoglobin is close to saturated while you sit reading this. Around 97%, breathing ordinary air. There is almost no room left on it.

So hyperbaric medicine takes a different route. Oxygen dissolves straight into blood plasma, and the amount you carry that way rises in proportion to the pressure of the oxygen you breathe. That is Henry's law.

Which gives you the figure that matters, and it is not chamber pressure:

chamber pressure × oxygen fraction = inspired oxygen pressure

ATA means atmospheres absolute. One ATA is what you are under at sea level, so a chamber at 2.0 ATA doubles it.

A soft-shell chamber at 1.3 ATA, running on ordinary air at 21% oxygen:

1.3 × 0.21 = 0.27 ATA

A clinical chamber at 2.0 ATA, with 93% oxygen through a mask:

2.0 × 0.93 = 1.86 ATA

The depth went up by about half. The oxygen went up more than fourfold. Multiply the two and you get the sevenfold gap, which means the gas is doing more of the work than the depth.

Run the same formula across the equipment people actually encounter and the spread is wider than the labels suggest.

A fabric chamber on room air barely clears what you are breathing now. A clinical session sits almost seven times higher.

Since the gas carries most of that gap, the obvious response is to add oxygen to the small chamber. It does help. Push a concentrator into it and you might reach 40%, giving 0.52 ATA, which is nearly double what room air manages and still about a quarter of a clinical session. Even an implausible 90% inside that chamber tops out at 1.17 ATA, or 63% of a 2.0 ATA session.

So enrichment closes most of the gap but cannot close all of it, and the ceiling is set by the depth. That is the arithmetic. The practical objection lies elsewhere. Fabric chambers are cleared for air, not oxygen, and the regulators have had things to say about combining the two.

Those two numbers are all it takes to compare any two providers. A clinic that will not give you both is telling you something by declining.

What 2.0 ATA measured at the wound that 1.4 ATA did not

Arithmetic is cheap. The harder question is whether that oxygen arrives anywhere that matters.

In 2024, Ram Sack and colleagues at Rambam Health Care Campus in Haifa went and looked. They recruited patients with chronic ulcers, taped transcutaneous oxygen sensors to the skin beside the wounds, and took readings while the patients breathed pure oxygen. The clever part was what they held still. Everyone got 100% oxygen in both conditions. The only thing that changed was depth.

At 1.4 ATA, after ten minutes of oxygen breathing, tissue oxygen averaged 161 mmHg. At 2.0 ATA it averaged 333. The difference came in at p below 0.001, and every electrode site reached significance at both the five and ten minute marks. Their conclusion was unusually blunt for a journal. The data gave no evidence that treatment at 1.4 ATA would benefit a patient with a chronic ulcer.

Note where that comparison starts. The shallow arm was 1.4 ATA on pure oxygen, already far beyond anything a fabric chamber can produce. The gap to 2.0 was still that wide.

It is a small single-centre study in the field's own specialist journal, and it measured oxygen tension, which is not healing. A wound that receives more oxygen does not automatically close faster.

The variation was also enormous. Individual readings ran from 1 to 601 mmHg at the lower pressure and from 1 to 914 at the higher. Some of those wounds were barely perfused at all, and an average hides that completely.

What it establishes is the direction and rough size of the effect, measured in tissue instead of calculated on paper.

Where the 1.4 and 1.5 ATA definitions came from

Somebody had to draw a line. Three organisations drew it in three slightly different places.

The Undersea and Hyperbaric Medical Society puts the floor at near-100% oxygen in a chamber at 1.4 ATA or above. That is the floor of the definition, not of practice. The same document requires at least 2.0 ATA for every approved indication.

The European Committee for Hyperbaric Medicine regulates the gas instead of the vessel, demanding inspired oxygen above 1.5 ATA, which drags the chamber up with it. Australian and New Zealand practice defines hyperbaric oxygen loosely and then treats between 2.0 and 3.0 anyway.

In 2026, Mark Morningstar and Megan Strauchman reviewed those definitions in a paper titled, unambiguously, Hyperbaric Oxygen Therapy and Mild Hyperbaric Oxygen Therapy Are Not Synonymous. They proposed 1.5 ATA as a working threshold, and were careful about what the number is.

Nothing biological happens at exactly 1.5. Some oxygen-sensitive processes begin well below it, others sharpen above it. What the threshold marks is the lower edge of the protocols the clinical evidence was built from.

So treat 1.5 as an administrative line with real evidence behind it. It still describes a genuine difference, because a chamber at 1.5 is hard-sided and running oxygen, which a chamber at 1.3 is not.

What a 1.3 ATA soft-shell chamber actually delivers

The category has a name in the literature, even if the brochures avoid it: mild hyperbaric oxygen therapy, or mHBOT. Morningstar and Strauchman define it as exposure between 1.2 and 1.49 ATA, against 2.0 ATA and above for medical-grade hyperbaric oxygen, and argue the two are physiologically distinct treatments that happen to share a name.

Soft-shell chambers run between roughly 1.1 and 1.4 ATA. In the United States they hold a single FDA clearance, for acute mountain sickness, and they are built to be pressurised with air. Supplemental oxygen inside them falls outside that clearance, which makes the concentrator upgrade an off-label modification rather than a stronger version of the same product.

The UHMS is uncomfortably direct about what this delivers. Breathing air in one of these chambers, it says, provides no more oxygen to the body than breathing supplemental oxygen through a mask at sea level. It adds that it knows of no reliable clinical evidence for any therapeutic effect from compression below 1.4 ATA outside altitude illness.

Health Canada came at it from a different angle and warned about safety instead. It classes consumer soft-shell chambers as unlicensed medical devices, and lists fire, cross-contamination between users, and barotrauma to ears, sinuses, lungs and teeth. One line in that advisory matters more than the rest. Fire risk rises substantially when a chamber is combined with an oxygen concentrator. That is precisely the modification sold as the route to clinical doses.

None of which proves that mild pressure does nothing. In persistent post-concussion symptoms the evidence that it does something is stronger than the rest of the field usually admits, and that section comes next but one. What the regulatory picture establishes is narrower. The clinical effects have not been demonstrated, and the studies quoted in support of these chambers were run somewhere else.

The 2.0 ATA studies behind the stem cell and telomere claims

Almost every conversation about hyperbaric oxygen and healthy physiology runs through the same two studies. Both were conducted at 2.0 ATA.

The first came from Stephen Thom's group at the University of Pennsylvania in 2006. Circulating CD34+ stem cells roughly doubled after a single two-hour exposure and rose about eightfold across twenty treatments, with no matching rise in overall white cell count. The team traced the mechanism to nitric oxide signalling in bone marrow.

Buried in that paper is an accidental experiment. Three chamber attendants sat at 2.0 ATA beside the patients for the full two hours, breathing chamber air instead of oxygen. They were, in effect, pressure without hyperoxia. Their stem cell counts did not move.

Three unblinded people is not a control group. It is still the clearest hint available that pressure matters for what it does to the oxygen you breathe, and not for its own sake.

The second is the telomere study from Shai Efrati's group at the Sagol Center in Israel, published under Yafit Hachmo as first author, published in Aging in 2020. Thirty-five healthy adults aged 64 and over completed sixty daily sessions of ninety minutes on 100% oxygen at 2.0 ATA, with three air breaks inside each session. Telomere length rose by more than 20% across four lymphocyte subsets, and several senescent cell populations fell.

That study is routinely described as a randomised controlled trial. It was not. It was single-arm, with no control group, measuring laboratory markers in a small older cohort. Both things are true at once: the finding is real, and it is preliminary. Nobody has shown that longer telomeres in circulating lymphocytes translate into a longer or healthier life, and the same caution applies to progenitor cell counts. These are plausible proxies standing in for outcomes nobody has measured yet.

One detail of the Israeli setup is routinely misunderstood. They pressurised a multiplace vessel and delivered oxygen to each participant by individual mask, so the chamber itself never held pure oxygen. Filling a chamber with oxygen is not the standard research arrangement. Masks are.

And neither study tested 1.3 or 1.5 ATA. Neither can tell you what those pressures would have produced, because that experiment has not been run for either endpoint.

Why Age Back Clinic runs at 2.0 ATA

Because that is where the evidence was generated. Thom's stem cell counts, the Sagol telomere study, the deep arm of the Haifa measurements and every indication the UHMS currently approves all sit at 2.0 ATA or above. Treat below it and you are extrapolating downward from research that never tested those pressures. Treat above it and you buy more of some markers along with more oxygen toxicity risk.

That is a reason and not a proof. No dose-response trial has established 2.0 as the optimum for cognition or longevity, and nobody should claim otherwise.

The setup. Two CE-certified hard-shell multiplace chambers, seven seats between them. Oxygen by individual mask at approximately 93%, which gives 1.86 ATA inspired. Compression and decompression take about ten minutes at each end, so a 65-minute booking gives roughly 45 minutes at pressure, and a 95-minute session matches the exposure time used in the Sagol telomere protocol. Oxygen, pressure, temperature and humidity are logged continuously, with automatic switchover to air if a reading leaves range.

Ask any other provider for the same two figures and you can place them on the table above.

The case for low pressure in post-concussion symptoms

In one clinical area the evidence points the other way, and it is the area where low-pressure chambers have their strongest claim.

In 2022, Paul Harch sorted eleven studies of persistent symptoms after mild traumatic brain injury by pressure dose and oxygen dose, and published the analysis in Frontiers in Neurology.

He found significant symptomatic or cognitive improvement at 40 sessions of 1.5 ATA, and at 30 sessions of 1.3 ATA on air. Results at 1.2 ATA conflicted. Trials at 2.4 ATA oxygen came back negative. He argues this meets Level I criteria for the indication, a view not everyone shares.

The argument exists at all because of a design choice made years earlier. In the major military trials, mildly pressurised air was selected as the placebo, on the assumption that it was inert.

George Wolf's Air Force trial gave 50 service members thirty sessions of either 2.4 ATA oxygen or room air at 1.3 ATA. The groups did not separate. Both improved, on post-concussion and post-traumatic stress measures alike.

David Cifu's Pensacola trial went further. All sixty participants were compressed to 2.0 ATA, and only the gas varied, at 10.5%, 75% or 100% oxygen. Again nothing separated.

Robert Miller's multicentre trial added the arm the others lacked: a group that received no chamber at all. Both chamber groups improved against it, and remained indistinguishable from each other.

Read conventionally, that is a clean negative, and everyone improved because of attention, routine, expectation and time.

Read the other way, as Xavier Figueroa and James Wright argued in Neurology, mildly pressurised air was never inert. Harch made the same case about the Wolf trial in a 2013 letter to the Journal of Neurotrauma, calling it neither sham nor placebo-controlled but a comparison of two active doses. Morningstar and Strauchman land in similar territory. They accept that sub-1.5 ATA exposures are not necessarily inert, which makes them awkward as shams.

The counterargument is a strong one. If pressure changes that small produced large effects on neurological recovery, you might expect recovery rates to vary with altitude, and nobody has demonstrated that. Spontaneous recovery and regression to the mean remain the simpler explanation for why every arm got better.

The dispute also has a boundary. It comes out of chronic neurological symptoms, where outcomes are questionnaires and the natural history bends toward recovery. It does not reach wound healing, radiation injury or stem cell mobilisation, where the proposed mechanism is oxygen physically arriving in hypoxic tissue and the dose-response has been measured directly. The Haifa electrodes are what that looks like.

What hyperbaric pressure research still has not tested

The questions people most want settled are the ones still open.

Nobody has compared 2.0 ATA with 1.3 ATA on stem cell mobilisation, telomere length, or any longevity endpoint. The nearest thing is Marvin Heyboer's comparison of 2.0 against 2.5, which found more mobilisation higher up. Nobody has run it downward.

The 1.4 to 1.5 band is thin compared with the pressures either side of it, which is part of why that threshold stands better as policy than as biology.

Any provider's offer can be placed on that table with the two numbers from the formula.

Side effects and screening at higher pressure

More oxygen is the point of the exercise. It is also where the risk sits, so the field caps exposure well below what the equipment can reach.

The common problems are mechanical and minor. Ear and sinus barotrauma during compression is the usual one. Compression is slow for that reason, and you are taught to equalise before a first session. A temporary myopic shift can appear across a long course and generally resolves afterwards.

The one that scales directly with inspired oxygen pressure is central nervous system oxygen toxicity. Risk climbs with inspired oxygen pressure, so exposure is capped across the field even in chambers capable of going deeper. At 2.0 ATA it is rare, and air breaks exist to keep it that way.

Screening matters more than the safety record suggests. Before a first session, any supervised facility should be asking about untreated pneumothorax, recent ear surgery, poorly controlled seizure disorders, certain chemotherapy agents including bleomycin, and pregnancy. A provider who books you without asking is not doing you a favour.

Frequently asked questions

What does ATA mean in hyperbaric oxygen therapy?

ATA stands for atmospheres absolute. One ATA is normal pressure at sea level. A chamber at 2.0 ATA holds you at twice that, equivalent to about ten metres underwater, and a soft-shell chamber at 1.3 ATA is equivalent to roughly three metres. The number describes pressure only, and says nothing about what you are breathing.

Is a 1.3 ATA soft-shell chamber the same as hyperbaric oxygen therapy?

Not by the professional definitions. The Undersea and Hyperbaric Medical Society sets its floor at 1.4 ATA with near-100% oxygen, and every indication it approves requires at least 2.0 ATA. The 1.2 to 1.49 ATA range has its own name in the literature, mild hyperbaric oxygen therapy or mHBOT, and Morningstar and Strauchman argue it should be treated as a separate modality. In oxygen terms, 1.3 ATA on room air delivers about 0.27 ATA against 1.86 for a clinical session.

Would adding an oxygen concentrator to a soft-shell chamber close the gap?

It narrows the gap without closing it. A 40% mixture at 1.3 ATA gives roughly 0.52 ATA, about a quarter of a clinical session, and even an implausible 90% reaches only 1.17. The FDA clearance for fabric chambers does not cover supplemental oxygen inside them, and Health Canada warns that combining the two raises fire risk substantially.

Is 1.5 ATA enough to count as real HBOT?

By the letter of the definitions, yes, provided the gas is near-100% oxygen in a hard-shell chamber. No UHMS-approved indication is treated there, though, and most of the supporting research sits in post-concussion symptoms. It is the lower boundary of the evidence rather than the middle of it.

Why not treat at 2.4 ATA or higher?

The approved clinical range runs to 3.0 ATA, and Heyboer's comparison found more stem cell mobilisation at 2.5 than at 2.0. Higher inspired oxygen also raises the risk of central nervous system oxygen toxicity. The research on stem cells, telomeres and healthy physiology was conducted at 2.0 ATA, so treating there keeps the dose aligned with the evidence.

Does higher chamber pressure always mean more oxygen?

Only if the gas stays the same. Inspired oxygen is pressure multiplied by oxygen fraction, so a 2.4 ATA chamber on room air delivers 0.50 ATA, while a 2.0 ATA chamber on 93% oxygen delivers 1.86. Pressure alone is half a number. Both figures are needed to compare providers.