Vol.3, No.7, 432-436 (2
Copyright © 2011 SciRes. Openly accessible at http://www.scirp.org/journal/HEALTH/
011) Health
The effect of mild -pressure hyperb aric therapy (Oas is O2)
on fatigue and oxidative stress
Sungdo Kim1,2 ,Takehiko Yukishita1, Keiko Lee1, Shinichi Yokota1, Ken Nakata1, Daichi Suzuki3,
Hiroyuki Kobay ashi1*
1Department of Hospital Administration, Graduate School of Medicine, Juntendo University School of Medicine, Tokyo, Japan;
Corresponding Author: koba@juntendo.ac.jp
2Mizue Orthopedic Clinic, Tokyo, Japan;
3Department of Sports Science, Graduate School of Health and Sports Science, Juntendo University, Tokyo, Japan.
Received 15 April 2011; revised 20 May 2011; accepted 2 June 2011.
Mild-pressure hyperbaric therapy (mHBT) has
become increasingly popular among elite ath-
letes and most recently among the general pub-
lic yet there is very little scientific underpin-
nings on its therapeutic use. In this study, fif-
teen healthy volunteers (8 men, 7 w omen, mean
age 29.7 ± 8.1 years) were exposed to 1.3 at-
mospheres absolute (ATA) for 40 minutes in a
mild hyperbaric chamber called “Oasis O2” to
determine th e effe ct of am bient air at 1.3 A TA o n
oxidative stress, antioxidant potential, fatigue,
and blood chemistry. Reactive oxygen metabo-
lites (ROMs), an index of oxidative stress, sig-
nificantly reduced by 11% (p = 0.006), while bi-
ological antioxidant potential (BAP), an index of
antioxidant capacity, did not show a significant
change (p = 0.749). WBC count significantly
reduced by 10.4% (p = 0.005) whereas WBC dif-
ferential did not show a marked change. The
mean visual analog scale (VAS) score for fa-
tigue significa ntly decreased fro m 5.0 to 2.1 (p <
0.001). Our findings suggest that mild-pressure
hyperbaric therapy reduces oxidative stress as
indicated by a significant decrease in serum
ROM, and also helps improv e fa tigu e as se en by
a significant decrease in VAS fatigue scores.
Keywords: Mild-Pressure Hyperbaric Chambe;
Oxidative Stress; Free Radicals; Reacti ve Oxygen
Species (RO S)
Mild-pressure hyperbaric therapy (mHBT) has be-
come increasingly popular among elite athletes and most
recently among the general public as a modality to im-
prove 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 such as the “Oasis
O2” used in this study. Many manufacturers distribute
similar chambers for widespread use and they are collec-
tively referred to as “mild-pressure hyperbaric cham-
bers”. These are frequently mistaken for hospital grade
hyperbaric oxygen therapy (HBO) chambers despite the
vastly different specifications between HBO and mHBT.
The “Oasis O2” uses 1.3 atmospheres absolute (ATA)
ambient air whereas HBO is the intermittent administra-
tion of 100% oxygen at therapeutic pressures of 2-3 ATA
with more than 60 minutes of depressurization time.
HBO is claimed to “revitalize” hypoxic tissues, sup-
plement oxygen to under-oxygenated tissues, reduce
edema, promote fibroblast proliferation for tissue regen-
eration, mobilize white blood cells (WBCs), and im-
prove resistance and immunity against infection and
inflammation [1]. HBO 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 ex-
ternal injuries and central nervous system disorders be-
cause of its tissue regenerative capacity [2]. The value of
oxygen therapy has long been known and HBO is a
modern form of this treatment that provides enriched
oxygen under high pressure to promote tissue regenera-
tion. However, the delivery of high-density, pressurized
oxygen has also been found to create problems by gen-
erating free radicals. Oxygen toxicity is a side effect of
HBO that results from breathing high partial pressures of
oxygen accompanied by an uncontrolled increase in re-
active oxygen species (ROS) [3]. 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,
S. Kim et al. / Health 3 (2011) 432-436
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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 [4]. For these reasons, mHBT uses lower
concentration and pressure than HBO to deliver oxygen
to the tissues while checking the development of free
Although mild-pressure hyperbaric chambers have
become widely prevalent, few researches about mHBT
have been made so far. Saito reports mHBT has no sig-
nificant effect for oxidative stress [5]. On the other hand,
mHBT shortens a treatment period of acute lower leg
muscle strain in professional soccer players [6] and de-
creases blood levels of lactate acid and physical fatigue
[7]. Scientific validation of their efficacy and mecha-
nisms of action are still necessary to be explored. There-
fore, our reason for this study was to determine the ef-
fects of mild hyperbaria on oxidative stress, antioxidant
potential, and fatigue.
2.1. Stud y Design and Subjects
Fifteen healthy volunteers (8 men, 7 women, mean
age 29.7 ± 8.1 years) provided oral consent and were
instructed to refrain from intense physical exercise be-
fore participating in the study. All participants were ex-
posed to 1.3 ATA for 40 minutes in “Oasis O2”, a
mild-pressure hyperbaric chamber. Changes in subjec-
tive sensation of fatigue and blood chemistry were eva-
luated before and after hyperbaric exposure to determine
the effects of mHBT on those parameters.
Blood chemistry analysis included assessing the de-
rivatives 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 leu-
kocyte count. Blood samples were obtained from par-
ticipants immediately before and after hyperbaric cham-
ber exposure.
For the d-ROM and BAP tests, the free radical analy-
sis system (FRAS4) (Diacron International, Italy) con-
sisting 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 ex-
pressed as μmol/L.
To evaluate the participants’ subjective sensation of
physical fatigue, a visual analog scale (VAS) for fatigue
(Japanese Society of Fatigue Science) [8] was adminis-
tered 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 fa-
tigue level. The possible score ranged from 0 to 100,
with “0” on the far left indicating “no fatigue/full of en-
ergy” to “100” on the far right indicating “worst possible
fatigue/listlessness”. The score was obtained by measur-
ing 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
2.2. Statistical Anlysis
Student’s t-test was used to compare the means of se-
rum ROM, serum BAP and differential leukocyte count
obtained from participants immediately before and after
mHBT. The significance level for all cases was set at 5%.
The SPSS Ver.11.5 software was used for analysis.
The mean serum ROM before exposure to mild hy-
perbaria was 269.4 ± 49.7 CARR.U., which significantly
reduced by 11% to 239.7 ± 30.4 CARR.U. after the ex-
posure (p = 0.006) (Figure 1). In contrast, mean serum
BAP values before and after hyperbaric exposure were
2288.3 ± 350.4 μmol/L and 2265.4 ± 284.7 μmol/L, re-
spectively. There was no significance between the two
BAP values (p = 0.749) (Figure 2).
The mean WBC count before hyperbaric exposure
was 6233.3 ± 1173.3/uL, which significantly decreased
by 10% to 5580.0 ± 984.3/uL after the exposure (p =
0.005) (Figure 3). There was no significant difference in
WBC differential before and after the exposure (Figure
The mean VAS fatigue score was 5.0 ± 1.8 before ex-
posure to hyperbaric chambers, which significantly re-
duced to 2.1 ± 1.6 after the exposure (p < 0.001) (Figure
Figure 1. Change in serum ROM after mild HBT. A sig-
nificant decrease of 11% in mean serum ROM was ob-
served before (Pre) and after (Post) hyperbaric exposure
(Pre: 269.4 ± 48.7 CARR.U.; Post: 239.7 ± 30.4 CARR.U; p
= 0.006).
S. Kim et al. / Health 3 (2011) 432-436
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Figure 2. Change in serum BAP after mild HBT. Mean
serum BAP decreased from 2288.3 ± 350.4 μmol/L before
hyperbaric exposure to 2265.4 ± 284.7 μ after exposure, but
the difference was not significant (p = 0.749).
Figure 3. Change in WBC after mild HBT. A significant
decrease of 10.4% in mean WBC count was observed be-
fore (Pre) and after (Post) hyperbaric exposure (Pre: 6233.3
± 1173.3/uL; Post: 5580.0 ± 984.3/uL; p = 0.005).
Figure 4. Change in WBC Differentiation after mild HBT.
No significant changes were observed in the differential
WBC count before and after hyperbaric exposure.
Our findings revealed that mHBT was effective in lo-
wering 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 Kon-
goji et al. and Yamami et al. which showed elevated
ROM and BAP values immediately after exposure to HBO
Figure 5. Change in VAS after mild HBT. Mean VAS fa-
tigue scores dropped significantly before (Pre) and after
(Post) hyperbaric exposure (Pre: 5.0 ± 1.8; Post: 2.1 ± 1.6; p
< 0.001).
[9,10]. Despite conflicting results, our data are highly
meaningful because of the paucity of reports on mHBT.
The differences in the results may be attributed to the
relatively faster exhaustion of antioxidant enzymes and
substances due to their increased activity after HBO to
counteract oxidative damage. In general, as the level of
oxidative stress rises, antioxidative enzymes and sub-
stances are mobilized by the body as a defense mecha-
nism to clear ROS and to restore the balance between
oxidative stress and antioxidant activity [4]. We sur-
mised that in our study mHBT-induced ROS were effec-
tively eliminated in a relatively short period because our
participants were young, were free from underlying dis-
eases, 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 [11]. 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 HBO.
Moreover, we found that mHBT had a beneficial ef-
fect on fatigue. VAS fatigue scores significantly im-
proved 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 lac-
tate level and improved muscle stiffness and fatigue in
college volleyball players after exposure to 35% oxygen
at 1.25 ATA [12]. It is possible that a placebo effect from
mHBT may have influenced a subjective symptom like
fatigue; however, the effect of mild hyperbaria in allevi-
ating fatigue was confirmed by all the participants who
reported feeling “refreshed”, “warmer”, or “lighter” af-
terwards. For this study, data were obtained from par-
ticipants who abstained from intense physical activity
before undergoing mHBT. To further probe the efficacy
S. Kim et al. / Health 3 (2011) 432-436
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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. Addi-
tionally, the investigators hypothesized that stress from
HBO induced greater adrenal cortisol secretion, which in
turn caused a decrease in WBCs [13]. In this study
WBCs decreased in almost all the participants after
mHBT; however, WBC differential did not change in
response to the therapy. A re-evaluation of the latter 4-6
hours after the exposure is warranted as differential leu-
kocyte activity is known to change over time.
Much controversy currently exists over the efficacy of
mHBT. In May 2006, a panel entitled “Round table dis-
cussion on mild HBT” was held at the Third Annual
Meeting of Japanese Association for Clinical Hyperbaric
Oxygen and Diving (JACHOD). At this meeting, a vig-
orous debate over the efficacy of mHBT ensued between
JACHOD, an opponent of mHBT, and Japan Interna-
tional Hyperbaric Association Inc. (JIHA), a proponent
of mHBT. Although the main purpose of HBO 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 oxy-
gen uptake. However, the mechanism of HBO rests on
Henry's Law that states a gas is dissolved by a liquid in
direct proportion to its partial pressure, i.e., HBO utilizes
increased atmospheric pressure to enhance oxygen dis-
solution in the plasma and resultant higher concentration
of liquefied oxygen to reverse hypoxia. Further, mHBT
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 mHBT (pressurized ambient air at 1.3 ATA) to deliver
the benefits of oxygen therapy [14-16].
Meanwhile, Ishii et al. studied the effects of various
hyperbaric pressures and discovered that lactate clear-
ance 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 [7]. Moreover, Ikeda et al. found that com-
pressed air at 1.3 ATA using Oasis O2 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 treat-
ment group (2.9 ± 1.4 weeks vs. 1.9 ± 0.5 weeks) [6]. 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 mHBT is helpful in reducing
oxidative stress and improving fatigue while posing mi-
nimal risks, yet its effect on antioxidant capacity is less
clear. Research will be needed to examine the therapeu-
tic significance of 1.3 ATA in health promotion and dis-
ease prevention.
[1] Cho, S. (2008) Oxigen toxicity and hyperbaric oxygen
therapy. Laser Interferometer Space Antenna, 15, 344-
[2] Tamura, H. (2005) Indication of hyperbaric oxygen ther-
apy. Clinical Engineerin g, 16, 126-133.
[3] Narkowicz, C.K. (1993) Hyperbaric oxygen therapy
increases free radical level in the blood of humans. Free
Radical Research Communications, 19, 71-80.
[4] Speit, G., et al. (2000) Induction of heme oxygenase-1
and adaptive protection against the induction of DNA
damage after hyperbaric oxygen treatment. Carcinogene-
sis, 21, 1795-1799. doi:10.1093/carcin/21.10.1795
[5] Saito, K. (2009) Effects of exposure time to hyperbaric
air chamber (HBA) on oxidative stress, peripheral blood
counta and blood filtration time in male students. Journal
of Japanese Association for Hyperbaric Oxygen and Di-
ving, 6, 27-30.
[6] Ikeda, H. (2005) Hyperbaric oxygen therapy for acute
muscle strain. Orthopaedic Surgery and Traumatology,
48, 955-958.
[7] Ishii, Y. (1995) The effect of hyperbaric oxygen therapy
on the lactate concentration after maximal exercise. The
Japanese Journal of Hyperbaric Medicine, 30, 109-114.
[8] Japanese Society of Fatigue Science (2008) Visual ana-
logue scale for fatigue.
[9] Kongoji, J., et al. (2007) Reactive oxygen metabolites
and biological antioxidant potential in humans after a
single exposure to hyperbaric oxygen therapy. The Japa-
nese Journal of Hyperbaric and Undersea Medicine, 42,
[10] Yamami, N., et al. (2007) A discussion on oxidative and
antioxidative markers under a hyperbaric oxygen envi-
ronment. The Japanese Journal of Hyperbaric and Un-
dersea Medicine, 42, 85-91.
[11] Nishii, Y. (2006) Expectation for the maintenance and
S. Kim et al. / Health 3 (2011) 432-436
Copyright © 2011 SciRes. http://www.scirp.org/journalT / Openly accessible at /HEALH
improvement of health by health care chamber with
pressured air without supplying oxygen. Journal of Jap-
anese Association for Clinical Hyperbaric Oxygen and
Diving, 3, 68-74.
[12] Ishihara, A. (2005) Effects of hyperbaric exposure with
high concentration of oxygen on recovery of muscle
stiffness. Descente Sports Science, 26, 16-22.
[13] Osborne, C.K., et al. (1970) Effects of hyperoxia on
white blood cells: 1. In Vivo changes in the total white
blood cell counts of normal rats. Aerospace Medicine, 41,
[14] Sakakibara, K. (2005) A question about hyperbaric air
chamber system. The Japanese Journal of Medical In-
strumentation, 75, 485-490.
[15] Yagi, H. (2006) On mild HBO - should be changed the
terms mild HBO to mild HBA. Journal of Japanese As-
sociation for Clinical Hyperbaric Oxygen and Diving, 3,
[16] Oiwa, H. (2005) Is mild HBO allowed to enter in HBOT?
Journal of Japanese Association for Clinical Hyperbaric
Oxygen and Diving, 2, 87-94.