Hold your breath for 60 to 90 seconds and you can increase stem cells, growth hormone and EPO.

That is the kind of claim I keep seeing in breathwork and biohacking content. I understand why it catches people’s attention. Stem cells suggest repair. Growth hormone suggests muscle growth and recovery. EPO suggests more red blood cells and better oxygen-carrying capacity. It sounds like you could get the benefits of altitude training with a few minutes of breathing exercises.

The research is more interesting, and more complicated, than that.

So do breath holds increase EPO, Stem Cells and Growth hormone?

Some demanding breath-hold protocols have produced short-term changes in growth hormone and EPO. But the studies do not show that a 60-second hold repairs tissue, builds muscle or increases your red blood cell mass. In some cases, the study used to support a breath-hold claim did not involve breath holding at all.

To see where the claims get ahead of the evidence, we need to look at what participants actually did, what researchers measured, and whether the result lasted.

Is a breath hold the same as intermittent hypoxia?

A sufficiently demanding breath hold can cause hypoxia: oxygen levels can fall while the person is holding their breath. The size of that response varies with hold duration, starting lung volume, oxygen consumption and recovery between holds.

But “intermittent hypoxia” describes a broad range of exposures. Someone might repeatedly breathe a low-oxygen gas mixture for five minutes at a time. An athlete might live at altitude for many hours each day. An experienced diver might complete repeated maximal underwater apnoeas. These are not equivalent doses simply because each involves less oxygen.

Breath holding also changes carbon dioxide. During a hold, oxygen generally falls and carbon dioxide rises. Someone breathing a low-oxygen gas mixture continues to ventilate, so their carbon dioxide response may be different. Read: The Truth About CO2 Tolerance: Breath-Hold Time, Nasal Breathing and the Bohr Effect

That gives us a useful first question whenever a breath-hold claim cites an intermittent-hypoxia study:

Did the participants actually hold their breath?

After that, ask how low their oxygen level fell, how long they spent there, how often they repeated the exposure and what the researchers measured.

Do breath holds increase stem cells?

One study relevant to the stem-cell claim is a 2011 intermittent-hypoxia experiment by Serebrovskaya and colleagues. Its participants did not hold their breath despite it often being referenced. They breathed air containing 10% oxygen for four five-minute bouts each day over 14 days, with five minutes of normal air between bouts. Their oxygen saturation fell to approximately 84–85%.

During one session, the number of circulating blood-forming stem and progenitor cells increased briefly. That increase had subsided within 30 minutes after the exposure. A week after the full programme, the measured count was 27% below its starting level.

This tells us that a particular low-oxygen intervention changed the number of these cells detectable in blood at particular sampling times. It does not demonstrate that a short breath hold has the same effect. It does not show that tissue was repaired, or that health improved.

A study using repeated five-minute exposures to 10% oxygen cannot be presented as evidence that a 60-second breath hold releases stem cells for repair.

Do breath holds increase growth hormone?

There is a direct breath-hold experiment here. In a 1986 study by Djarova and colleagues, 11 trained men completed separate procedures involving hyperventilation, three maximal voluntary breath holds, and hyperventilation followed by breath holding. The researchers reported a rise in measured human growth hormone after the procedures.

So I would not say the growth hormone response was invented. An acute rise was measured. But we need to be precise about what that means.

The study was small. Blood was sampled before and at five and 30 minutes after each procedure, which does not give us a full picture of how the response developed or how long it lasted. Growth hormone is released in pulses, and there was no quiet-rest comparison day to establish how much of the change exceeded normal variation over the same period.

The protocol cannot isolate the cause either. Maximal breath holding involves effort and discomfort alongside changes in oxygen and carbon dioxide. Hyperventilation changes carbon dioxide substantially. The experiment does not tell us which part of that combined stressor was responsible for the hormone response.

Most of all, a temporary rise in growth hormone concentration is not evidence of muscle growth, improved recovery or a lasting performance benefit. Those outcomes would have to be measured directly over time.

Do breath holds increase EPO?

Here the answer is yes, under some demanding experimental conditions, breath holds have produced a short-term EPO increase.

Erythropoietin, or EPO, helps regulate red blood cell production. That makes it attractive in marketing: if you can raise EPO naturally, the implied next step is more red blood cells and greater oxygen-carrying capacity.

But an EPO measurement and an increase in red blood cell mass are two separate outcomes.

What de Bruijn’s breath-hold study actually involved

In de Bruijn and colleagues’ 2008 study, ten healthy volunteers completed 15 maximal dry breath holds, divided into three sets of five. They were not elite freedivers; none had trained in breath-hold diving during the two months before the experiment.

Before every hold, participants hyperventilated for one minute. This was done to extend the hold and produce greater oxygen desaturation. They had two minutes of breathing between holds and ten minutes of rest between sets.

The average hold lasted 3 minutes 26 seconds. Recorded hold durations ranged from 1 minute 34 seconds to 5 minutes 26 seconds. The full protocol took 109 minutes on average, including the breathing and rest periods.

Across the 15 holds, participants spent an average of approximately 12 minutes 25 seconds below 85% oxygen saturation. Their average reported post-hold saturation nadir was 72.7%. Two participants were instructed to resume breathing when their monitored saturation fell below 60%.

That is the experimental exposure behind the headline. It was not one comfortable breath hold while walking down the street. Nor was it a routine I would suggest readers try to reproduce. The researchers monitored the participants, and the hyperventilation used to extend the holds carries a particular danger if combined with water.

EPO rose by 15% at one hour, 12% at two hours and 16% at three hours after the session. It had returned to baseline by five hours. The widely cited 24% figure is the average of each participant’s highest measured increase, with that peak occurring at different sampling times for different people. The researchers also ran a control day without apnoeas and did not see a comparable EPO change.

That supports a real, short-term EPO response to this protocol. The study did not repeat the protocol over weeks or measure whether participants subsequently gained red blood cell mass.

The study did not test whether a single 60- or 90-second breath hold, or five walking holds after an exhale, produces an EPO response.

It certainly cannot establish that those practices improve oxygen-carrying capacity.

What happened in elite divers?

A 2019 study by Elia and colleagues examined repeated maximal static and underwater dynamic apnoeas in elite breath-hold divers and people without breath-hold diving experience.

During the dynamic attempts, the elite divers averaged approximately 94 seconds and 66 metres per hold, compared with 42 seconds and 22 metres in the non-divers. Their reported end-apnoea finger oxygen saturation averaged 62%, compared with 85% in the non-divers. After the dynamic protocol, EPO in the elite divers rose by approximately 60% at 30 minutes and 63% at three hours. The same significant response was not found after the static protocol or in the non-divers.

Those numbers need careful interpretation. Finger pulse oximetry becomes less reliable at very low saturations, and reduced blood flow to the fingers around a breath hold can further complicate measurement. I would treat 62% as evidence of a substantial reported hypoxic exposure, not a precise measure of arterial oxygenation or a threshold to aim for.

Dynamic apnoea also involves muscular work. Swimming underwater on a maximal hold uses oxygen differently from sitting still. We should not take a result from highly trained divers doing maximal underwater attempts and turn it into advice for the general public to do brief breath holds.

The researchers included a control condition and examined measures relevant to changes in blood concentration. Those are strengths. But the outcome was still an acute EPO response. The study did not establish a breath-hold dose that increases red blood cell mass.

How much hypoxia does it take to increase red blood cells?

This is the question the marketing usually leaves unanswered.

Altitude research gives us a sense of the exposure associated with measurable increases in haemoglobin mass, a more relevant measure of oxygen-carrying capacity than a single EPO reading. In one study, trained cyclists spent approximately 14 hours per day for three weeks at a simulated altitude of 3,000 metres. Their haemoglobin mass increased at an average rate of around 1% per week. A meta-analysis estimated an average increase of approximately 1.1% per 100 hours of adequate altitude exposure across the studies it examined. Typical exposures in that research accumulated hundreds of hours.

Those altitude hours cannot be converted directly into an equivalent number of breath-hold minutes. The oxygen stimulus is different and a person breathing normally between holds is not continuously hypoxic. I am using the altitude research to show why an EPO spike after one session does not automatically imply a useful increase in red blood cells.

Even sustained intermittent exposure can produce a hormone response without the hoped-for adaptation. In a controlled study, athletes spent three hours per day, five days per week, for four weeks at simulated altitudes of 4,000–5,500 metres: 60 scheduled hours of hypoxic exposure. EPO doubled after exposure, yet the researchers found no convincing increase in red cell volume or haemoglobin mass.

The direct breath-hold training studies also complicate the story.

A 2022 controlled study tested six weeks of five maximal static breath holds daily. It found no acute EPO increase during its test protocol and no increase in haemoglobin mass or measured exercise performance after training.

A separate six-week study of repeated maximal dynamic apnoeas found an increase in reticulocytes, which are immature red blood cells. It did not find a significant increase in mature red blood cell or haemoglobin concentration. That is an interesting sign of activity within the red cell production process, but it is not proof of improved oxygen-carrying capacity.

So what breath-hold schedule would reliably increase red blood cell mass? At present, we do not have a validated answer. The available studies do not establish a minimum number of weeks, a number of daily holds or a saturation target that delivers that result.

An acute response is not the outcome you were promised

This is the central issue across all three claims:

• A controlled low-oxygen gas study finds a brief change in circulating progenitor cells. It becomes a claim that breath holds release stem cells for repair.
• A small study finds a short-term growth hormone rise after demanding respiratory manoeuvres. It becomes a claim about muscle growth and recovery.
• A protocol of 15 maximal breath holds produces a temporary EPO increase. It becomes a claim that a minute of breath holding will boost red blood cells.

At each step, an observed response is turned into an unmeasured benefit.

This does not mean breath-hold training has no purpose. It means we should describe its effects at the level the evidence supports. If the promise is better oxygen-carrying capacity, measure haemoglobin mass. If the promise is better athletic performance, measure performance. If the promise is repair, show that repair occurred. A change in a blood marker cannot stand in for all of those outcomes.

Oxygen Advantage presents breath holds as a way to simulate altitude training and improve red blood cell production over time. See their explanation. The key question is whether the brief hypoxic exposure in these protocols is enough to produce a sustained, meaningful increase in red cell mass. An acute EPO measurement alone cannot answer that.

Why this matters to practitioners

I regularly see people put a study abstract on a screen, quote the most exciting percentage and sell a protocol as though that percentage validates the entire method. Some may know they are stretching the evidence. Others may simply never have checked what the participants actually did.

Either way, the person buying the promise pays for the gap between the claim and the result. They spend time, money and effort on an outcome the protocol has not been shown to deliver.

At the School of Breath Science, I want practitioners to be able to hold two thoughts at once: yes, a physiological response may be real; no, it does not automatically prove a meaningful benefit. That means reading past the abstract, checking the dose and comparison group, and choosing methods that fit the person and the outcome they are actually trying to achieve.

That takes more time than a quick biohacking headline. It also makes you better at helping people.

If you want training that challenges you to assess the research, understand the physiology and apply it responsibly, use our training selector survey. It will help you find a starting point based on your professional background, goals, finances and timing.

Explore the School of Breath Science training selector survey

Watch or listen to the podcast episode

Watch on YouTube | Listen on Spotify

References

1. Serebrovskaya TV, et al. Intermittent hypoxia mobilizes hematopoietic progenitors and augments cellular and humoral elements of innate immunity in adult men. High Altitude Medicine & Biology. 2011. Read the study.
2. Djarova T, et al. Human growth hormone, cortisol, and acid-base balance changes after hyperventilation and breath-holding. International Journal of Sports Medicine. 1986. Read the study.
3. de Bruijn R, Richardson M, Schagatay E. Increased erythropoietin concentration after repeated apneas in humans. European Journal of Applied Physiology. 2008. Read the study.
4. Elia A, et al. Erythropoietic responses to a series of repeated maximal dynamic and static apnoeas in elite and non-breath-hold divers. European Journal of Applied Physiology. 2019. Read the study.
5. Gore CJ, et al. Increased serum erythropoietin but not red cell production after 4 wk of intermittent hypobaric hypoxia. Journal of Applied Physiology. 2006. Read the study.
6. Elia A, et al. Six weeks of dynamic apnoeic training stimulates erythropoiesis but does not increase splenic volume. European Journal of Applied Physiology. 2021. Read the study.
7. Bouten J, et al. Six weeks of static apnea training does not affect Hbmass and exercise performance. Journal of Applied Physiology. 2022. Read the study.