Mild-pressure hyperbaric oxygen therapy (mHBOT) has become increasingly popular among elite athletes and most recently among the general public as a modality to improve fatigue, enhance overall health and well-being, heal sports-related injuries, and promote anti-aging. The hyperbaric chambers used for these purposes are soft-sided chambers made of elastic fiber. Many manufacturers distribute similar chambers for widespread use and they are collectively referred to as “mild-pressure hyperbaric chambers”. These are frequently mistaken for hospital grade hyperbaric oxygen therapy (HBOT) chambers despite the vastly different specifications between HBOT and mHBOT. The chambers presented in this study uses 1.3 atmospheres absolute (ATA) ambient air whereas HBOT is the intermittent administration of 100% oxygen at therapeutic pressures of 2-3 ATA with more than 60 minutes of depressurization time.

What do Michael Phelps, Kyle Lorry Josh Taylor and Cristiano Ronaldo have in common? They rely on Mild Hyperbaric Oxygen Therapy (mHBOT) to boost their athletic performance, as do thousands of other world-class athletes, basketball players, football stars, and Olympians.

Facts about HBOT (Hyperbaric Oxygen Therapy)

HBOT is claimed to “revitalize” hypoxic tissues, supplement oxygen to under-oxygenated tissues, reduce edema, promote fibroblast proliferation for tissue regeneration, mobilize white blood cells (WBCs), and improve resistance and immunity against infection and inflammation. HBOT has been traditionally indicated for decompression sickness and acute carbon monoxide poisoning; its clinical applications have since expanded to include the treatment of other conditions such as external injuries and central nervous system disorders because of its tissue regenerative capacity. The value of oxygen therapy has long been known and HBOT is a modern form of this treatment that provides enriched oxygen under high pressure to promote tissue regeneration. However, the delivery of high-density, pressurized oxygen has also been found to create problems by generating free radicals. Oxygen toxicity is a side effect of HBOT that results from breathing high partial pressures of oxygen accompanied by an uncontrolled increase in reactive oxygen species (ROS). Normally the living organism has an “antioxidant system” that controls the development of ROS, but when this system’s scavenging capacity is overcome by the enhanced formation of ROS, the resulting state is called “oxidative stress”. Excessive free radicals can damage lipids, proteins, and DNA which main structural and functional integrity of the organism, as well as accelerate aging and cause a variety of diseases. For these reasons, mHBOT uses lower concentration and pressure than HBOT to deliver oxygen to the tissues while checking the development of free radicals.

Although mild-pressure hyperbaric chambers (mHBOT) have become widely prevalent, few researches about mHBOT have been made so far. Saito reports mHBOT has no significant effect for oxidative stress. On the other hand, mHBOT shortens a treatment period of acute lower leg muscle strain in professional soccer players and decreases blood levels of lactate acid and physical fatigue. Scientific validation of their efficacy and mechanisms of action are still necessary to be explored. Therefore, in this presented study the purpose was to determine the effects of mild hyperbaric oxygen therapy (mHBOT) on oxidative stress, antioxidant potential, and fatigue.

Study Design and Subjects

Fifteen healthy volunteers (8 men, 7 women, mean age between 20-35 years old) provided oral consent and were instructed to refrain from intense physical exercise before participating in the study. All participants were exposed to 1.3 ATA for 40 minutes in a mild-pressure hyperbaric chamber. Changes in subjective sensation of fatigue and blood chemistry were evaluated before and after hyperbaric exposure to determine the effects of mHBOT on those parameters.

Blood chemistry analysis included assessing the derivatives of reactive oxygen metabolites (d-ROMs) as a convenient test to measure the level of oxidative stress in clinical practice, biological antioxidant potential (BAP) as an index of antioxidant capacity, and differential leukocyte count. Blood samples were obtained from participants immediately before and after hyperbaric chamber exposure.

For the d-ROM and BAP tests, the free radical analysis system (FRAS4) (Diacron International, Italy) consisting of a dedicated photometer with an incorporated centrifuge was used. ROM values were reported in Carratelli Unit (CARR.U.) with one CARR.U. equaling 0.08 mg/100 mL of hydrogen peroxide. BAP was expressed as μmol/L.

To evaluate the participants’ subjective sensation of physical fatigue, a visual analog scale (VAS) for fatigue (Japanese Society of Fatigue Science) was administered immediately before and after the exposure. The fatigue VAS consisted of a 100 mm horizontal line and participants were asked to mark the point on the line with an “x” that represented the perception of their fatigue level. The possible score ranged from 0 to 100, with “0” on the far left indicating “no fatigue/full of energy” to “100” on the far right indicating “worst possible fatigue/listlessness”. The score was obtained by measuring the length of line from “0” to the point indicated by the participant that represented their current state. This was divided by 10 to yield a fatigue rating on a 0 to 10 scale.

mild-pressure hyperbaric therapy

Is mild-pressure hyperbaric therapy (mHBOT) the secret weapon of elite athletes?

Our findings revealed that mHBOT was effective in lowering oxidative stress. A significant reduction in serum ROM was noted after the therapy whereas there was no change in BAP or antioxidative capacity.

These findings contrast with those obtained by Kongoji et al. and Yamami et al. which showed elevated ROM and BAP values immediately after exposure to HBOT.

Figure 5. Change in VAS after mild HBOT. Mean VAS fatigue scores dropped significantly before (Pre) and after (Post) mild hyperbaric exposure (Pre: 5.0 ± 1.8; Post: 2.1 ± 1.6; p < 0.001).

Despite conflicting results, our data are highly meaningful because of the paucity of reports on mHBOT. The differences in the results may be attributed to the relatively faster exhaustion of antioxidant enzymes and substances due to their increased activity after HBOT to counteract oxidative damage. In general, as the level of oxidative stress rises, antioxidative enzymes and substances are mobilized by the body as a defense mechanism to clear ROS and to restore the balance between oxidative stress and antioxidant activity. We surmised that in our study mHBOT-induced ROS were effectively eliminated in a relatively short period because our participants were young, were free from underlying diseases, and had strong antioxidative capacity.

In addition, it is empirically known that 100% oxygen administered at pressures greater than 3 ATA induces oxygen toxicity, while pure oxygen at pressures greater than 1.75 ATA demonstrably causes a higher incidence of oxygen toxicity than 1.5 ATA. Accordingly, we used compressed air at a very low pressure of 1.3 ATA in this study to eliminate the need for providing additional oxygen and minimize oxygen poisoning – a worrisome side effect of HBOT.

Moreover, we found that mHBOT had a beneficial effect on fatigue. VAS fatigue scores significantly improved after the therapy in nearly all the participants who felt the physical improvement. These findings are in line with Ishihara’s data that showed reduced blood lactate level and improved muscle stiffness and fatigue in college volleyball players after exposure to 35% oxygen at 1.25 ATA. It is possible that a placebo effect from mHBOT may have influenced a subjective symptom like fatigue; however, the effect of mild hyperbaric oxygen therapy in alleviating fatigue was confirmed by all the participants who reported feeling “refreshed”, “warmer”, or “lighter” afterwards. For this study, data were obtained from participants who abstained from intense physical activity before undergoing mHBT. To further probe the efficacy of mHBT on fatigue, future studies would benefit from manipulating fatigue induction and evaluating the effects in participants undergoing similar physical load.

Although WBC count significantly decreased after mHBT, WBC differential did not show a remarkable change. These findings are congruent with Osbourne et al.’s data which showed a decrease in WBC count by 32% and 13% in rats exposed to hyperbaric pressures at 4 ATA with 100% oxygen for 90 minutes and at 4 ATA with 21% oxygen for 90 minutes, respectively. Additionally, the investigators hypothesized that stress from HBOT induced greater adrenal cortisol secretion, which in turn caused a decrease in WBCs. In this study WBCs decreased in almost all the participants after mHBOT; however, WBC differential did not change in response to the therapy. A reevaluation of the latter 4-6 hours after the exposure is warranted as differential leukocyte activity is known to change over time.

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Marcus Rashford used OxyNova 7 to speed up his recovery period following surgery for a long-standing shoulder injury.

Is mild-pressure hyperbaric therapy (mHBOT) safer and more effective for elite athletes than high-pressure HBOT?

Much controversy currently exists over the efficacy of mHBOT. In May 2006, a panel entitled “Round table discussion on mild HBOT” was held at the Third Annual Meeting of Japanese Association for Clinical Hyperbaric Oxygen and Diving (JACHOD). At this meeting, a vigorous debate over the efficacy of mHBOT ensued between JACHOD, an opponent of mHBOT, and Japan International Hyperbaric Association Inc. (JIHA), a proponent of mHBOT. Although the main purpose of HBOT is to raise the levels of oxygen in body fluids, most oxygen carried in the blood is bound to hemoglobin, rendering absolute hemoglobin concentration as the limiting factor for oxygen uptake. However, the mechanism of HBOT rests on Henry’s Law that states a gas is dissolved by a liquid in direct proportion to its partial pressure, i.e., HBOT utilizes increased atmospheric pressure to enhance oxygen dissolution in the plasma and resultant higher concentration of liquefied oxygen to reverse hypoxia. Further, mHBOT was developed and based on the theory that liquefied oxygen is more refined than conjugated oxygen and therefore has a greater capacity to transport oxygen to peripheral tissues. However, several studies have found that mild hyperbaria at 1.3 ATA yields 0.57 mL/dL of liquefied oxygen, which is significantly less than 2.0 mL/dL of liquefied oxygen from compressed air at 1.0 ATA, leading to some investigators to refute the ability of mHBOT (pressurized ambient air at 1.3 ATA) to deliver the benefits of oxygen therapy.

Meanwhile, Ishii et al. studied the effects of various hyperbaric pressures and discovered that lactate clearance rate after maximal exercise at 1.3 ATA and 100% oxygen was significantly greater than the rate at normal atmosphere and room air; hence, the authors reported that atmospheric pressure need not be raised to 2.0 ATA because 1.3 ATA, which imposes comparatively less stress than 2.0 ATA on the biological system, was sufficiently effective. Moreover, Ikeda et al. found that compressed air at 1.3 ATA using a soft hyperbaric chamber for the treatment of acute lower leg muscle strain in professional soccer players significantly reduced the time to return to sport after injury, as observed from the difference in recovery time between the non-treatment group versus the treatment group (2.9 ± 1.4 weeks vs. 1.9 ± 0.5 weeks). It appears that further research is necessary to clarify the dearth of studies on the controversial effects of 1.3 ATA.


“Our findings suggest that mHBOT is helpful in reducing oxidative stress and improving fatigue while posing minimal risks, yet its effect on antioxidant capacity is less clear. Research will be needed to examine the therapeutic significance of 1.3 ATA in health promotion and disease prevention.”

The effect of mild-pressure hyperbaric therapy on fatigue and oxidative stress.

Source: Vol.3, No.7, 432-436 (2011)

Authors: Sungdo Kim1,2 ,Takehiko Yukishita1, Keiko Lee1, Shinichi Yokota1, Ken Nakata1, Daichi Suzuki3, Hiroyuki Kobayashi1*

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