ArticlePDF Available

Abstract

In the last decade, competitive sports have taken on a whole new meaning, where intensity has increased together with the incidence of injuries to the athletes. Therefore, there is a strong need to develop better and faster treatments that allow the injured athlete to return to competition faster than with the normal course of rehabilitation, with a low risk of re-injury. Hyperbaric therapies are methods used to treat diseases or injuries using pressures higher than local atmospheric pressure inside a hyperbaric chamber. Within hyperbaric therapies, hyperbaric oxygen therapy (HBO) is the administration of pure oxygen (100%) at pressures greater than atmospheric pressure, i.e. more than 1 atmosphere absolute (ATA), for therapeutic reasons. The application of HBO for the treatment of sports injuries has recently been suggested in the scientific literature as a modality of therapy either as a primary or an adjunct treatment. Although results have proven to be promising in terms of using HBO as a treatment modality in sports-related injuries, these studies have been limited due to the small sample size, lack of blinding and randomization problems. HBO seems to be promising in the recovery of injuries for high-performance athletes; however, there is a need for larger samples, randomized, controlled, double-blinded clinical trials combined with studies using animal models so that its effects and mechanisms can be identified to confirm that it is a safe and effective therapy for the treatment of sports injuries.
Hyperbaric oxygen effects on sports injuries
Pedro Barata, Mariana Cervaens, Rita Resende, O
´scar Camacho and Frankim Marques
Abstract:In the last decade, competitive sports have taken on a whole new meaning, where
intensity has increased together with the incidence of injuries to the athletes. Therefore, there
is a strong need to develop better and faster treatments that allow the injured athlete to return
to competition faster than with the normal course of rehabilitation, with a low risk of re-injury.
Hyperbaric therapies are methods used to treat diseases or injuries using pressures higher
than local atmospheric pressure inside a hyperbaric chamber. Within hyperbaric therapies,
hyperbaric oxygen therapy (HBO) is the administration of pure oxygen (100%) at pressures
greater than atmospheric pressure, i.e. more than 1 atmosphere absolute (ATA), for
therapeutic reasons. The application of HBO for the treatment of sports injuries has recently
been suggested in the scientific literature as a modality of therapy either as a primary or an
adjunct treatment. Although results have proven to be promising in terms of using HBO as
a treatment modality in sports-related injuries, these studies have been limited due to the
small sample size, lack of blinding and randomization problems. HBO seems to be promising
in the recovery of injuries for high-performance athletes; however, there is a need for larger
samples, randomized, controlled, double-blinded clinical trials combined with studies using
animal models so that its effects and mechanisms can be identified to confirm that it is a safe
and effective therapy for the treatment of sports injuries.
Keywords:hyperbaric oxygen therapy, sports injuries
Introduction
In the last decade, competitive sports have taken
on a whole new meaning, where intensity has
increased together with the incidence of injuries
to the athletes. These sport injuries, ranging from
broken bones to disrupted muscles, tendons and
ligaments, may be a result of acute impact forces
in contact sports or the everyday rigors of train-
ing and conditioning [Babul et al. 2003].
Therefore, a need has emerged to discover the
best and fastest treatments that will allow the
injured athlete to return to competition faster
than the normal course of rehabilitation, with a
low risk of re-injury.
Hyperbaric oxygen therapy (HBO) is the thera-
peutic administration of 100% oxygen at pres-
sures higher than 1 absolute atmosphere (ATA).
It is administered by placing the patient in a mul-
tiplace or in a monoplace (one man) chamber
and typically the vessels are pressurized to
1.53.0 ATA for periods between 60 and
120 minutes once or twice a day [Bennett et al.
2005a]. In the monoplace chamber the patient
breathes the oxygen directly from the chamber
but in the multiplace chamber this is done
through a mask. At 2.0 ATA, the blood oxygen
content is increased 2.5% and sufficient oxygen
becomes dissolved in plasma to meet tissue needs
in the absence of haemoglobin-bound oxygen,
increasing tissue oxygen tensions 10-fold
(1000%) [Staples and Clement, 1996]. HBO is
remarkably free of untoward side effects.
Complications such as oxygen toxicity, middle
ear barotrauma and confinement anxiety are
well controlled with appropriate pre-exposure
orientations [Mekjavic et al. 2000].
HBO has been used empirically in the past, but
today information exists for its rational applica-
tion. This review aims to analyse the contribution
of HBO in the rehabilitation of the different
sports injuries.
Hyperbaric oxygen therapy
Hyperbaric therapies are methods used to treat
diseases or injuries using pressures higher than
local atmospheric pressure inside a hyperbaric
chamber. Within hyperbaric therapies, HBO is
http://tab.sagepub.com 111
Therapeutic Advances in Musculoskeletal Disease Review
Ther Adv Musculoskel Dis
(2011) 3(2) 111121
DOI: 10.1177/
1759720X11399172
!The Author(s), 2011.
Reprints and permissions:
http://www.sagepub.co.uk/
journalsPermissions.nav
Correspondence to:
Pedro Barata
Universidade Fernando
Pessoa, Faculdade
Cie
ˆncias da Sau
´de, Rua
Carlos da Maia 296, Porto
4200, Portugal
pedro.barata@gmail.com
Mariana Cervaens
Universidade Fernando
Pessoa, Faculdade
Cie
ˆncias da Sau
´de, Porto,
Portugal
Rita Resende
Hospital Pedro Hispano,
Unidade Medicina
Hiperba
´rica, Porto,
Portugal
O
´scar Camacho
Hospital Pedro Hispano,
Unidade Medicina
Hiperba
´rica, Porto,
Portugal
Frankim Marques
Faculdade Farma
´cia U.P.,
Biochemistry, Porto,
Portugal
the administration of pure oxygen (100%) at
pressures greater than atmospheric pressure, i.e.
more than 1 ATA, for therapeutic reasons
[Albuquerque e Sousa, 2007].
In order to be able to perform HBO, special facil-
ities are required, with the capacity for withstand-
ing pressures higher than 1 ATA, known as
hyperbaric chambers, where patients breathe
100% oxygen [Fernandes, 2009].
In the case of single monoplace chambers (with a
capacity for only one person) the oxygen is
inhaled directly from the chambers’ environment
[Fernandes, 2009]. Although much less expen-
sive to install and support, they have the major
disadvantage of not being possible to access the
patient during treatment. It is possible to monitor
blood pressure, arterial waveform and electrocar-
diogram noninvasively, and to provide intrave-
nous medications and fluids. Mechanical
ventilation is possible if chambers are equipped
appropriately, although it is not possible to suc-
tion patients during treatment. Mechanical ven-
tilation in the monoplace chamber is provided by
a modified pressure-cycled ventilator outside of
the chamber [Sheridan and Shank, 1999].
In multiplace chambers, the internal atmosphere
is room air compressed up to 6 ATA. Attendants
in this environment breathe compressed air,
accruing a nitrogen load in their soft tissues, in
the same way as a scuba diver breathing com-
pressed air. These attendants need to decompress
to avoid the decompression illness by using more
complex decompression procedures when the
treatment tables are more extended (e.g. Navy
tables). The patients, on the other hand, are
breathing oxygen while at pressure. This oxygen
can be administered via face mask, a hood or
endotracheal tube. The advantage of such a
chamber is that the patient can be attended to
during treatment, but the installation and sup-
port costs are very high. These high costs pre-
clude the widespread use of multiplace
chambers [Sheridan and Shank, 1999].
Biochemical, cellular and physiological effects
of HBO
The level of consumption of O
2
by a given tissue,
on the local blood stream, and the relative dis-
tance of the zone considered from the nearest
arteriole and capillary determines the O
2
tension
in this tissue. Indeed, O
2
consumption causes
oxygen partial pressure (pO
2
) to fall rapidly
between arterioles and vennules. This empha-
sizes the fact that in tissues there is a distribution
of oxygen tensions according to a gradient. This
also occurs at the cell level such as in the mito-
chondrion, the terminal place of oxygen con-
sumption, where O
2
concentrations range from
1.5 to 3 M [Mathieu, 2006].
Before reaching the sites of utilization within the
cell such as the perioxome, mitochondria and
endoplasmic reticulum, the oxygen moves down
a pressure gradient from inspired to alveolar gas,
arterial blood, the capillary bed, across the inter-
stitial and intercellular fluid. Under normobaric
conditions, the gradient of pO
2
known as the
‘oxygen cascade’ starts at 21.2 kPa (159 mmHg)
and ends up at 0.53 kPa (3.822.5 mmHg)
depending on the target tissue [Mathieu, 2006].
The arterial oxygen tension (PaO
2
) is approxi-
mately 90 mmHg and the tissue oxygen tension
(PtO
2
) is approximately 55 mmHg [Sheridan and
Shank, 1999]. These values are markedly
increased by breathing pure oxygen at greater
than atmospheric pressure.
HBO is limited by toxic oxygen effects to a
maximum pressure of 300 kPa (3 bar). Partial
pressure of carbon dioxide in the arterial
blood (PaCO
2
), water vapour pressure and respi-
ratory quotient (RQ) do not vary significantly
between 100 and 300 kPa (1 and 3 bar). Thus,
for example, the inhalation of 100% oxygen at
202.6 kPa (2 ATA) provides an alveolar PO
2
of
1423 mmHg and, consequently, the alveolar
oxygen passes the alveolarcapillary space and
diffuses into the venous pulmonary capillary
bed according to Fick’s laws of diffusion
[Mathieu, 2006].
Hyperoxya and hyperoxygenation
Oxygen is transported by blood in two ways:
chemically, bound to haemoglobin, and physi-
cally, dissolved in plasma. During normal breath-
ing in the environment we live in, haemoglobin
has an oxygen saturation of 97%, representing a
total oxygen content of about 19.5 ml O
2
/100 ml
of blood (or 19.5 vol%), because 1 g of 100%
saturated haemoglobin carries 1.34 ml oxygen.
In these conditions the amount of oxygen dis-
solved in plasma is 0.32 vol%, giving a total of
19.82 vol% oxygen. When we offer 85% oxygen
through a Hudson mask or endotracheal intuba-
tion the oxygen content can reach values up to
22.2 vol% [Jain, 2004].
Therapeutic Advances in Musculoskeletal Disease 3 (2)
112 http://tab.sagepub.com
The main effect of HBO is hyperoxia. During this
therapy, oxygen is dissolved physically in the
blood plasma. At an ambient pressure of 2.8
ATA and breathing 100% oxygen, the alveolar
oxygen tension (PAO
2
) is approximately
2180 mmHg, the PaO
2
is at least 1800 mmHg
and the tissue concentration (PtO
2
) is at least
500 mmHg. The oxygen content of blood is
approximately
([1.34 Hbg SaO
2
]þ[0.0031 PaO
2
]),
where Hbg is serum haemoglobin concentration
and SaO
2
is arterial oxygen saturation [Sheridan
and Shank, 1999]. At a PaO
2
of 1800 mmHg, the
dissolved fraction of oxygen in plasma
(0.0031 PaO
2
) is approximately 6 vol%,
which means that 6 ml of oxygen will be physi-
cally dissolved in 100 ml of plasma, reaching a
total volume of oxygen in the circulating blood
volume equal to 26.9 vol%, equivalent to basic
oxygen metabolic needs, and the paO
2
in the
arteries can reach 2000 mmHg. With a normal
lung function and tissue perfusion, a partial pres-
sure of oxygen in the blood (pO
2
)>1000 mmHg
could be reached [Mayer et al. 2004]. Breathing
pure oxygen at 2 ATA, the oxygen content in
plasma is 10 times higher than when breathing
air at sea level. Under normal conditions the pO
2
is 95 mmHg; under conditions of a hyperbaric
chamber, the pO
2
can reach values greater than
2000 mmHg [Jain, 2004]. Consequently, during
HBO, Hbg is also fully saturated on the venous
side, and the result is an increased oxygen tension
throughout the vascular bed. Since diffusion is
driven by a difference in tension, oxygen will be
forced further out into tissues from the vascular
bed [Mortensen, 2008] and diffuses to areas
inaccessible to molecules of this gas when trans-
ported by haemoglobin [Albuquerque e Sousa,
2007].
After removal from the hyperbaric oxygen envi-
ronment, the PaO
2
normalizes in minutes, but
the PtO
2
may remain elevated for a variable
period. The rate of normalization of PtO
2
has
not been clearly described, but is likely measured
in minutes to a few hours, depending on tissue
perfusion [Sheridan and Shank, 1999].
The physiological effects of HBO include short-
term effects such as vasoconstriction and
enhanced oxygen delivery, reduction of oedema,
phagocytosis activation and also an anti-inflam-
matory effect (enhanced leukocyte function).
Neovascularization (angiogenesis in hypoxic soft
tissues), osteoneogenesis as well as stimulation of
collagen production by fibroblasts are known
long-term effects. This is beneficial for wound
healing and recovery from radiation injury
[Mayer et al. 2004; Sheridan and Shank, 1999].
Physiological and therapeutic effects of HBO
In normal tissues, the primary action of oxygen is
to cause general vasoconstriction (especially in
the kidneys, skeletal muscle, brain and skin),
which elicits a ‘Robin Hood effect’ through a
reduction of blood flow to well-oxygenated
tissue [Mortensen, 2008]. HBO not only pro-
vides a significant increase in oxygen availability
at the tissue level, as selective hyperoxic and not
hypoxic vasoconstriction, occurring predomi-
nantly at the level of healthy tissues, with reduced
blood volume and redistribution oedema for
peripheral tissue hypoxia, which can raise the
anti-ischemic and antihypoxic effects to extremi-
ties due to this physiological mechanism
[Albuquerque e Sousa, 2007]. HBO reduces
oedema, partly because of vasoconstriction,
partly due to improved homeostasis mechanisms.
A high gradient of oxygen is a potent stimuli for
angioneogenesis, which has an important contri-
bution in the stimulation of reparative and regen-
erative processes in some diseases [Mortensen,
2008].
Also many cell and tissue functions are depen-
dent on oxygen. Of special interest are leukocytes
ability to kill bacteria, cell replication, collagen
formation, and mechanisms of homeostasis,
such as active membrane transport, e.g. the
sodiumpotassium pump. HBO has the effect
of inhibiting leukocyte adhesion to the endothe-
lium, diminishing tissue damage, which enhances
leukocyte motility and improves microcirculation
[Mortensen, 2008]. This occurs when the pres-
ence of gaseous bubbles in the venous vessels
blocks the flow and induces hypoxia which
causes endothelial stress followed by the release
of nitric oxide (NO) which reacts with superoxide
anions to form peroxynitrine. This, in turn, pro-
vokes oxidative perivascular stress and leads to
the activation of leukocytes and their adhesion
to the endothelium [Antonelli et al. 2009].
Another important factor is hypoxia. Hypoxia is
the major factor stimulating angiogenesis.
However, deposition of collagen is increased by
hyperoxygenation, and it is the collagen matrix
that provides support for the growth of new cap-
illary bed. Two-hour daily treatments with HBO
are apparently responsible for stimulating the
P Barata, M Cervaens et al.
http://tab.sagepub.com 113
oxygen in the synthesis of collagen, the remaining
22 h of real or relative hypoxia, in which the
patient is not subjected to HBO, provide the
stimuli for angiogenesis. Thus, the alternation
of states of hypoxia and hyperoxia, observed in
patients during treatment with intermittent
HBO, is responsible for maximum stimulation
of fibroblast activity in ischemic tissues, produc-
ing the development of the matrix of collagen,
essential for neovascularization [Jain, 2004].
The presence of oxygen has the advantage of not
only promoting an environment less hospitable to
anaerobes, but also speeds the process of wound
healing, whether from being required for the pro-
duction of collagen matrix and subsequent angio-
genesis, from the presence and beneficial effects
of reactive oxygen species (ROS), or from yet
undetermined means [Kunnavatana et al. 2005].
Dimitrijevich and colleagues studied the effect of
HBO on human skin cells in culture and in
human dermal and skin equivalents
[Dimitrijevich et al. 1999]. In that study,
normal human dermal fibroblasts, keratinocytes,
melanocytes, dermal equivalents and skin equiv-
alents were exposed to HBO at pressures up to 3
ATA for up to 10 consecutive daily treatments
lasting 90 minutes each. An increase in fibroblast
proliferation, collagen production and keratino-
cyte differentiation was observed at 1 and 2.5
ATA of HBO, but no benefit at 3 ATA. Kang
and colleagues reported that HBO treatment up
to 2.0 ATA enhances proliferation and autocrine
growth factor production of normal human fibro-
blasts grown in a serum-free culture environ-
ment, but showed no benefit beyond or below 2
ATA of HBO [Kang et al. 2004]. Therefore, a
delicate balance between having enough and
too much oxygen and/or atmospheric pressure
is needed for fibroblast growth [Kunnavatana
et al. 2005].
Another important feature to take into account is
the potential antimicrobial effect of HBO. HBO,
by reversing tissue hypoxia and cellular dysfunc-
tion, restores this defence and also increases the
phagocytosis of some bacteria by working syner-
gistically with antibiotics, and inhibiting the
growth of a number of anaerobic and aerobic
organisms at wound sites [Mader et al. 1980].
There is evidence that hyperbaric oxygen is bac-
tericidal for Clostridium perfringens, in addition
to promoting a definitive inhibitory effect
on the growth of toxins in most aerobic and
microaerophilic microorganisms. The action of
HBO on anaerobes is based on the production
of free radicals such as superoxide, dismutase,
catalase and peroxidase. More than 20 different
clostridial exotoxins have been identified, and the
most prevalent is alphatoxine (phospholipase C),
which is haemolytic, tissue necrotizing and lethal.
Other toxins, acting in synergy, promote anae-
mia, jaundice, renal failure, cardiotoxicity and
brain dysfunction. Thetatoxine is responsible
for vascular injury and consequent acceleration
of tissue necrosis. HBO blocks the production
of alphatoxine and thetatoxine and inhibits bac-
terial growth [Jain, 2004].
HBO applications in sports medicine
The healing of a sports injury has its natural
recovery, and follows a fairly constant pattern
irrespective of the underlying cause. Three
phases have been identified in this process: the
inflammatory phase, the proliferative phase and
the remodelling phase. Oxygen has an important
role in each of these phases [Ishii et al. 2005].
In the inflammatory phase, the hypoxia-induced
factor-1a, which promotes, for example, the gly-
colytic system, vascularization and angiogenesis,
has been shown to be important. However, if the
oxygen supply could be controlled without pro-
moting blood flow, the blood vessel permeability
could be controlled to reduce swelling and con-
sequently sharp pain.
In the proliferative phase, in musculoskeletal tis-
sues (except cartilage), the oxygen supply to the
injured area is gradually raised and is essential for
the synthesis of extracellular matrix components
such as fibronectin and proteoglycan.
In the remodelling phase, tissue is slowly replaced
over many hours using the oxygen supply pro-
vided by the blood vessel already built into the
organization of the musculoskeletal system, with
the exception of the cartilage. If the damage is
small, the tissue is recoverable with nearly perfect
organization but, if the extent of the damage is
large, a scar (consisting mainly of collagen) may
replace tissue. Consequently, depending on the
injury, this collagen will become deficiently
hard or loose in the case of muscle or ligament
repair, respectively.
The application of HBO for the treatment
of sports injuries has recently been sug-
gested in the scientific literature as a therapy
Therapeutic Advances in Musculoskeletal Disease 3 (2)
114 http://tab.sagepub.com
modality: a primary or an adjunct treatment
[Babul et al. 2003]. Although results have
proven to be promising in terms of using HBO
as a treatment modality in sports-related injuries,
these studies have been limited due to the small
sample sizes, lack of blinding and randomization
problems [Babul and Rhodes, 2000].
Even fewer studies referring to the use of HBO in
high level athletes can be found in the literature.
Ishii and colleagues reported the use of HBO as a
recovery method for muscular fatigue during the
Nagano Winter Olympics [Ishii et al. 2005]. In
this experiment seven Olympic athletes received
HBO treatment for 3040 minutes at 1.3 ATA
with a maximum of six treatments per athlete and
an average of two. It was found that all athletes
benefited from the HBO treatment presenting
faster recovery rates. These results are concor-
dant with those obtained by Fischer and col-
leagues and Haapaniemi and colleagues that
suggested that lactic acid and ammonia were
removed faster with HBO treatment leading to
shorter recovery periods [Haapaniemi et al.
1995; Fischer et al. 1988].
Also in our experience at the Matosinhos
Hyperbaric Unit several situations, namely frac-
tures and ligament injuries, have proved to ben-
efit from faster recovery times when HBO
treatments were applied to the athletes.
Muscle injuries
Muscle injury presents a challenging problem in
traumatology and commonly occurs in sports.
The injury can occur as a consequence of a
direct mechanical deformation (as contusions,
lacerations and strains) or due to indirect
causes (such as ischemia and neurological
damage) [Li et al. 2001]. These indirect injuries
can be either complete or incomplete [Petersen
and Ho¨lmich, 2005].
In sport events in the United States, the inci-
dence of all injuries ranges from 10% to 55%.
The majority of muscle injuries (more than
90%) are caused either by excessive strain or by
contusions of the muscle [Ja¨ rvinen et al. 2000].
A muscle suffers a contusion when it is subjected
to a sudden, heavy compressive force, such as a
direct blow. In strains, however, the muscle is
subjected to an excessive tensile force leading to
the overstraining of the myofibres and, conse-
quently, to their rupture near the myotendinous
junction [Ja¨rvinen et al. 2007].
Muscle injuries represent a continuum from mild
muscle cramp to complete muscle rupture, and
in between is partial strain injury and delayed
onset muscle soreness (DOMS) [Petersen and
Ho¨lmich, 2005]. DOMS usually occurs following
unaccustomed physical activity and is accompa-
nied by a sensation of discomfort within the skel-
etal muscle experienced by the novice or elite
athlete. The intensity of discomfort increases
within the first 24 hours following cessation of
exercise, peaks between 24 and 72 hours, sub-
sides and eventually disappears by 57 days post-
exercise [Cervaens and Barata, 2009].
Oriani and colleagues first suggested that HBO
might accelerate the rate of recovery from injuries
suffered in sports [Oriani et al. 1982]. However,
the first clinical report appeared only in 1993
where results suggested a 55% reduction in lost
days to injury, in professional soccer players in
Scotland suffering from a variety of injuries fol-
lowing the application of HBO. These values
were based on a physiotherapist’s estimation of
the time course for the injury versus the actual
number of days lost with routine therapy and
HBO treatment sessions [James et al. 1993].
Although promising, this study needed a control
group and required a greater homogeneity of
injuries as suggested by Babul and colleagues
[Babul et al. 2000].
DOMS. DOMS describes a phenomenon of
muscle pain, muscle soreness or muscle stiffness
that is generally felt 1248 hours after exercise,
particularly at the beginning of a new exercise
program, after a change in sporting activities, or
after a dramatic increase in the duration or inten-
sity of exercise.
Staples and colleagues in an animal study, used a
downhill running model to induce damage, and
observed significant changes in the myeloperox-
idase levels in rats treated with hyperbaric oxygen
compared with untreated rats [Staples et al.
1995]. It was suggested that hyperbaric oxygen
could have an inhibitory effect on the inflamma-
tory process or the ability to actually modulate
the injury to the tissue.
In 1999, the same group conducted a random-
ized, controlled, double-blind, prospective study
to determine whether intermittent exposures to
hyperbaric oxygen enhanced recovery from
DOMS of the quadriceps by using 66 untrained
men between the ages of 18 and 35 years
P Barata, M Cervaens et al.
http://tab.sagepub.com 115
[Staples et al. 1999]. After the induction of
muscle soreness, the subjects were treated in a
hyperbaric chamber over a 5-day period in two
phases: the first phase with four groups (control,
hyperbaric oxygen treatment, delayed treatment
and sham treatment); and in the second phase
three groups (3 days of treatment, 5 days of treat-
ment and sham treatment). The hyperbaric expo-
sures involved 100% oxygen for 1 hour at 2.0
ATA. The sham treatments involved 21%
oxygen for 1 hour at 1.2 ATA. In phase 1, a sig-
nificant difference in recovery of eccentric torque
was noted in the treatment group compared with
the other groups as well as in phase 2, where
there was also a significant recovery of eccentric
torque for the 5-day treatment group compared
with the sham group, immediately after exercise
and up to 96 hours after exercise. However, there
was no significant difference in pain in either
phase. The results suggested that treatment
with hyperbaric oxygen may enhance recovery
of eccentric torque of the quadriceps muscle
from DOMS. This study had a complex protocol
and the experimental design was not entirely
clear (exclusion of some participants and the allo-
cation of groups was not clarified), which makes
interpretation difficult [Bennett et al. 2005a].
Mekjavic and colleagues did not find any recov-
ery from DOMS after HBO. They studied 24
healthy male subjects who were randomly
assigned to a placebo group or a HBO group
after being induced with DOMS in their right
elbow flexors [Mekjavic et al. 2000]. The HBO
group was exposed to 100% oxygen at 2.5 ATA
and the sham group to 8% oxygen at 2.5 ATA
both for 1 hour per day and during 7 days. Over
the period of 10 days there was no difference
in the rate of recovery of muscle strength between
the two groups or the perceived pain. Although
this was a randomized, double-blind trial, this
was a small study [Bennett et al. 2005a].
Harrison and colleagues also studied the effect of
HBO in 21 healthy male volunteers after induc-
ing DOMS in the elbow flexors [Harrison et al.
2001]. The subjects were assigned to three
groups: control, immediate HBO and delayed
HBO. These last two groups were exposed to
2.5 ATA, for 100 min with three periods of 30
min at 100% oxygen intercalated with 5 min with
20.93% oxygen between them. The first group
began the treatments with HBO after 2 hours
and the second group 24 hours postexercise
and both were administered daily for 4 days.
The delayed HBO group were also given a
sham treatment with HBO at day 0 during the
same time as the following days’ treatments but
with 20.93% oxygen at a minimal pressure. The
control group had no specific therapy. There
were no significant differences between groups
in serum creatine kinase (CK) levels, isometric
strength, swelling or pain, which suggested that
HBO was not effective on DOMS. This study
also presented limitations such as a small
sample size and just partial blinding [Bennett
et al. 2005a].
Webster and colleagues wanted to determine
whether HBO accelerated recovery from exer-
cise-induced muscle damage in 12 healthy male
volunteers that underwent strenuous eccentric
exercise of the gastrocnemius muscle [Webster
et al. 2002]. The subjects were randomly
assigned to two groups, where the first was the
sham group who received HBO with atmospheric
air at 1.3 ATA, and the second with 100% oxygen
with 2.5 ATA, both for 60 minutes. The first
treatment was 34 hours after damage followed
by treatments after 24 and 48 hours. There was
little evidence in the recovery measured data,
highlighting a faster recovery in the HBO group
in the isometric torque, pain sensation and
unpleasantness. However, it was a small study
with multiple outcomes and some data were not
used due to difficulties in interpretation [Bennett
et al. 2005a].
Babul and colleagues also conducted a random-
ized, double-blind study in order to find out
whether HBO accelerated the rate of recovery
from DOMS in the quadriceps muscle [Babul
et al. 2003]. This exercise-induced injury was
produced in 16 sedentary female students that
were assigned into two groups: control and
HBO. The first was submitted to 21% oxygen
at 1.2 ATA, and the second to 100% oxygen at
2.0 ATA for 60 minutes at 4, 24, 48 and 72 hours
postinjury. There were no significant differences
between the groups in the measured outcomes.
However, this was also a small study with multi-
ple outcomes, with a complex experimental
design with two distinct phases with somewhat
different therapy arms [Bennett et al. 2005a].
Germain and colleagues had the same objective
as the previous study but this time the sample
had 10 female and 6 male subjects that were ran-
domly assigned into two groups [Germain et al.
2003]: the control group that did not undergo
Therapeutic Advances in Musculoskeletal Disease 3 (2)
116 http://tab.sagepub.com
any treatment and the HBO group that was
exposed to 95% oxygen at 2.5 ATA during 100
minutes for five sessions. There were no signifi-
cant differences between the groups which lead to
the conclusion that HBO did not accelerate the
rate of recovery of DOMS in the quadriceps.
Once again, this was a very small and unblinded
study that presented multiple outcomes [Bennett
et al. 2005a].
Muscle stretch injury. In 1998, Best and col-
leagues wanted to analyse whether HBO
improved functional and morphologic recovery
after a controlled induced muscle stretch in the
tibialis anterior muscletendon unit [Best et al.
1998]. They used a rabbit model of injury and
the treatment group was submitted to a 5-day
treatment with 95% oxygen at 2.5 ATA for 60
minutes. Then, after 7 days, this group was com-
pared with a control group that did not undergo
HBO treatment. The results suggested that HBO
administration may play a role in accelerating
recovery after acute muscle stretch injury.
Ischemia. Another muscle injury that is often a
consequence of trauma is ischemia. Normally it is
accompanied by anaerobic glycolysis, the forma-
tion of lactate and depletion of high-energy phos-
phates within the extracellular fluid of the
affected skeletal muscle tissue. When ischemia
is prolonged it can result in loss of cellular
homeostasis, disruption of ion gradients and
breakdown of membrane phospholipids. The
activation of neutrophils, the production of
oxygen radicals and the release of vasoactive fac-
tors, during reperfusion, may cause further
damage to local and remote tissues. However,
the mechanisms of ischemiareperfusion-
induced muscle injury are not fully understood
[Bosco et al. 2007]. These authors aimed to see
the effects of HBO in the skeletal muscle of rats
after ischemia-induced injury and found that
HBO treatment attenuated significantly the
increase of lactate and glycerol levels caused by
ischemia, without affecting glucose concentra-
tion, and modulating antioxidant enzyme activity
in the postischemic skeletal muscle.
A similar study was performed in 1996
[Haapaniemi et al. 1996] in which the authors
concluded that HBO had positive aspects for at
least 48 hours after severe injury, by raising the
levels of high-energy phosphate compounds,
which indicated a stimulation of aerobic oxida-
tion in the mitochondria. This maintains the
transport of ions and molecules across the cell
membrane and optimizes the possibility of pre-
serving the muscle cell structure.
Gregorevic and colleagues induced muscle
degeneration in rats in order to see whether
HBO hastens the functional recovery and myofi-
ber regeneration of the skeletal muscle
[Gregorevic et al. 2000]. The results of this
study demonstrated that the mechanism of
improved functional capacity is not associated
with the reestablishment of a previously compro-
mised blood supply or with the repair of associ-
ated nerve components, as seen in ischemia, but
with the pressure of oxygen inspired with a cru-
cial role in improving the maximum force-produ-
cing capacity of the regenerating muscle fibres
after this myotoxic injury. In addition, there
were better results following 14 days of HBO
treatment at 3 ATA than at 2 ATA.
Ankle sprains
In 1995 a study conducted at the Temple
University suggested that patients treated with
HBO returned approximately 30% faster than
the control group after ankle sprain. The authors
stated, however, that there was a large variability
in this study design due to the difficulty in quan-
tifying the severity of sprains [Staples and
Clement, 1996].
Interestingly, Borromeo and colleagues, in a ran-
domized, double-blinded study, observed in 32
patients who had acute ankle sprains the effects
of HBO in its rehabilitation [Borromeo et al.
1997]. The HBO group was submitted to 100%
oxygen at 2 ATA for 90 minutes for the first ses-
sion and 60 minutes for the other two. The pla-
cebo group was exposed to ambient air, at 1.1
ATA for 90 minutes, both groups for three ses-
sions over 7 days. The HBO group had an
improvement in joint function. However, there
were no significant differences between groups
in the subjective pain, oedema, passive or active
range of motion or time to recovery. This study
included an average delay of 34 hours from the
time of injury to treatment, and it had short treat-
ment duration [Bennett et al. 2005a].
Medical collateral ligament
Horn and colleagues in an animal study surgi-
cally lacerated medial collateral ligament of 48
rats [Horn et al. 1999]. Half were controls with-
out intervention and the other half were
exposed to HBO at 2.8 ATA for 1.5 hours
P Barata, M Cervaens et al.
http://tab.sagepub.com 117
a day over 5 days. Six rats from each group were
euthanized at 2, 4, 6 and 8 weeks and at 4 weeks
a statistically greater force was required to cause
failure of the previously divided ligaments for
those exposed to HBO than in the control
group. After 4 weeks, an interesting contribution
from HBO could be seen in that it promoted the
return of normal stiffness of the ligament.
Ishii and colleagues induced ligament lacerations
in the right limb of 44 rats and divided them into
four groups [Ishii et al. 2002]: control group,
where animals breathed room air at 1 ATA for
60 min; HBO treatment at 1.5 ATA for 30 min
once a day; HBO treatment at 2 ATA for 30 min
once a day; and 2 ATA for 60 min once a day.
After 14 days postinjury, of the three exposures
the last group was more effective in promoting
healing by enhancing extracellular matrix deposi-
tion as measured by collagen synthesis.
Mashitori and colleagues removed a 2-mm seg-
ment of the medial collateral ligament in 76 rats
[Mashitori et al. 2004]. Half of these rats were
exposed to HBO at 2.5 ATA for 2 hours for 5
days per week and the remaining rats were
exposed to room air. The authors observed that
HBO promotes scar tissue formation by increas-
ing type I procollagen gene expression, at 7 and
14 days after the injury, which contribute for the
improvement of their tensile properties.
In a randomized, controlled and double-blind
study, Soolsma examined the effect of HBO at
the recovery of a grade II medial ligament of
the knee presented in patients within 72 hours
of injury. After one group was exposed to HBO
at 2 ATA for 1 hour and the control group at 1.2
ATA, room air, for 1 hour, both groups for 10
sessions, the data suggested that, at 6 weeks,
HBO had positive effects on pain and functional
outcomes, such as decreased volume of oedema,
a better range of motion and maximum flexion
improvement, compared with the sham group
[Soolsma, 1996].
Anterior cruciate ligament
Yeh and colleagues used an animal model to
investigate the effects of HBO on neovasculariza-
tion at the tendonbone junction, collagen fibres
of the tendon graft and the tendon graftbony
interface which is incorporated into the osseous
tunnel [Yeh et al. 2007]. The authors used 40
rabbits that were divided into two groups: the
control group that was maintained in cages at
normal air and the HBO group that was exposed
to 100% oxygen at 2.5 ATA for 2 hours, for 5
days. The authors found that the HBO group had
significantly increased the amount of trabecular
bone around the tendon graft, increasing its
incorporation to the bone and therefore increas-
ing the tensile loading strength of the tendon
graft. They assumed that HBO contributes to
the angiogenesis of blood vessels, improving the
blood supply which leads to the observed
outcomes.
Takeyama and colleagues studied the effects of
HBO on gene expressions of procollagen and
tissue inhibitor of metalloproteinase (TIMPS)
in injured anterior cruciate ligaments
[Takeyama et al. 2007]. After surgical injury ani-
mals were divided into a control group and a
group that was submitted to HBO, 2.5 ATA for
2 hours, for 5 days. It was found that even though
none of the lacerated anterior cruciate ligaments
(ACLs) united macroscopically, there was an
increase of the gene expression of type I procolla-
gen and of TIMPS 1 and 2 for the group treated
with HBO. These results indicate that HBO
enhances structural protein synthesis and inhibits
degradative processes. Consequently using HBO
as an adjunctive therapy after primary repair of
the injured ACL is likely to increase success, a
situation that is confirmed by the British
Medical Journal Evidence Center [Minhas,
2010].
Fractures
Classical treatment with osteosynthesis and bone
grafting is not always successful and the attempt
to heal nonunion and complicated fractures,
where the likelihood of infection is increased, is
a challenge.
A Cochrane review [Bennett et al. 2005b] stated
that there is not sufficient evidence to support
hyperbaric oxygenation for the treatment of pro-
moting fracture healing or nonunion fracture as
no randomized evidence was found. During the
last 10 years this issue has not been the subject of
many studies.
Okubo and colleagues studied a rat model in
which recombinant human bone morphogenetic
protein-2 was implanted in the form of lyophi-
lized discs, the influence of HBO [Okubo et al.
2001]. The group treated with HBO, exposed to
2 ATA for 60 min daily, had significantly
increased new bone formation compared with
Therapeutic Advances in Musculoskeletal Disease 3 (2)
118 http://tab.sagepub.com
the control group and the cartilage was present at
the outer edge of the implanted material after 7
days.
Komurcu and colleagues reviewed retrospectively
14 cases of infected tibial nonunion that were
treated successfully [Komurcu et al. 2002].
Management included aggressive debridement
and correction of defects by corticotomy and
internal bone transport. The infection occurred
in two patients after the operation which was suc-
cessfully resolved after 2030 sessions of HBO.
Muhonen and colleagues aimed to study, in a
rabbit mandibular distraction osteogenesis
model, the osteogenic and angiogenic response
to irradiation and HBO [Muhonen et al. 2004].
One group was exposed to 18 sessions of HBO
until the operation that was performed 1 month
after irradiation. The second group did not
receive HBO and the controls underwent surgery
receiving neither irradiation nor HBO. The
authors concluded that previous irradiation sup-
presses osteoblastic activity and HBO changes
the pattern of bone-forming activity towards
that of nonirradiated bone.
Wang and colleagues, in a rabbit model, were
able to demonstrate that distraction segments of
animals treated with HBO had increased bone
mineral density and superior mechanical proper-
ties comparing to the controls and yields better
results when applied during the early stage of the
tibial healing process [Wang et al. 2005].
Conclusion
In the various studies, the location of the injury
seemed to have an influence on the effectiveness
of treatment. After being exposed to HBO, for
example, injuries at the muscle belly seem to
have less benefit than areas of reduced perfusion
such as muscletendon junctions and ligaments.
With regards to HBO treatment, it is still neces-
sary to determine the optimal conditions for
these orthopaedic indications, such as the atmo-
sphere pressure, the duration of sessions, the fre-
quency of sessions and the duration of treatment.
Differences in the magnitude of the injury and in
the time between injury and treatment may also
affect outcomes.
Injuries studies involving bones, muscles and lig-
aments with HBO treatment seem promising.
However, they are comparatively scarce and the
quality of evidence for the efficacy of HBO is low.
Orthopaedic indications for HBO will become
better defined with perfection of the techniques
for direct measurement of tissue oxygen tensions
and intramuscular compartment pressures.
Despite evidence of interesting results when
treating high-performance athletes, these treat-
ments are multifactorial and are rarely published.
Therefore, there is a need for larger samples, ran-
domized, controlled, double-blind clinical trials
of human (mainly athletes) and animal models
in order to identify its effects and mechanisms
to determine whether it is a safe and effective
therapy for sports injuries treatments.
Funding
This research received no specific grant from any
funding agency in the public, commercial, or not-
for-profit sectors.
Conflict of interest statement
None declared.
References
Albuquerque e Sousa, J.G. (2007) Oxigenoterapia
hiperba
´rica (OTHB). Perspectiva histo
´rica, efeitos
fisiolo
´gicos e aplicac¸o
˜es clı
´nicas. Rev Soc Poruguesa
Med Interna 14: 219227.
Antonelli, C., Franchi, F., Della Marta, M.E., Carinci,
A., Sbrana, G., Tanasi, P. et al. (2009) Guiding prin-
ciples in choosing a therapeutic table for DCI hyper-
baric therapy. Minerva Anestesiologica 75: 151161.
Babul, S. and Rhodes, E. (2000) The Role of
Hyperbaric Oxygen Therapy in Sports Medicine.
Sports Med 30: 395403.
Babul, S., Rhodes, E., Taunton, J. and Lepawsky, M.
(2003) Effects of intermittent exposure to hyperbaric
oxygen for the treatment of an acute soft tissue injur y.
Clin J Sports Med 13: 138147.
Bennett, M., Best, T., Babul-Wellar, S. and Taunton, J.
(2005a) Hyperbaric oxygen therapy for delayed onset
muscle soreness and closed soft tissue injury. Cochrane
Database Syst Rev 19: 139.
Bennett, M.H., Stanford, R.E. and Turner, R. (2005b)
Hyperbaric oxygen therapy for promoting fracture
healing and treating fracture non-union. Cochrane
Database Syst Rev 1: CD004712DOI: 004710.001002/
14651858.CD14004712.pub14651852.
Best, T., Loitz-Ramage, B., Corr, D. and Vanderby,
R.J. (1998) Hyperbaric oxygen in the treatment of
acute muscle stretch injuries: results in an animal
model. Am J Sports Med 26: 367372.
Borromeo, C.N., Ryan, J.L., Marchetto, P.A.,
Peterson, R. and Bove, A.A. (1997) Hyperbaric
P Barata, M Cervaens et al.
http://tab.sagepub.com 119
oxygen therapy for acute ankle sprains. Am J Sports
Med 25: 619625.
Bosco, G., Yang, Z.-j., Nandi, J., Wang, J., Chen, C.
and Camporesi, E.M. (2007) Effects of hyperbaric
oxygen on glucose, lactate, glycerol and anti-oxidant
enzymes in the skeletal muscle of rats during ischaemia
and reperfusion. Clin Exp Pharmacol Physiol 34: 7076.
Cervaens, M. and Barata, P. (2009) Sensac¸a
˜o
Retardada de Dor Muscular. Universidade Fernando
Pessoa: Rev Fac Cie
ˆncias Sau
´de 6: 186196.
Dimitrijevich, S.D., Paranjape, S., Wilson, J.R., Gracy,
R.W. and Mills, J.G. (1999) Effect of hyperbaric oxygen
on human skin cells in culture and in human dermal
and skin equivalents. Wound Repair Regen 7: 5364.
Fernandes, T.D. (2009) Medicina Hiperba
´rica. Acta
Medica Portuguesa 22: 324334.
Fischer, B., Lehrl, S., Jain, K. and Braun, E. (1988)
Handbook of Oxygen Therapy, Springer Verlag:
Berlin, pp. 251260.
Germain, G., Delaney, J., Moore, G., Lee, P., Lacroix,
V. and Montgomery, D. (2003) Effect of hyperbaric
oxygen therapy on exercise-induced muscle soreness.
Undersea Hyperbaric Med 30: 135145.
Gregorevic, P., Lynch, G.S. and Williams, D.A. (2000)
Hyperbaric oxygen improves contractile function of
regenerating rat skeletal muscle after myotoxic injury.
J Appl Physiol 89: 14771482.
Haapaniemi, T., Nylander, G., Sirsjo¨, A. and Larsson,
J. (1996) Hyperbaric oxygen reduces ischemia-induced
skeletal muscle injury. Am Soc Plastic Surg
97: 602607.
Haapaniemi, T., Sirsjo, A., Nylander, G. and Larsson,
J. (1995) Hyperbaric oxygen treatment attenuates
glutathione depletion and improves metabolic restitu-
tion in post-ischemic skeletal muscle. Free Radic Res
23: 91101.
Harrison, B., Robinson, D., Davison, B., Foley, B.,
Seda, E. and Byrnes, W. (2001) Treatment of exercise-
induced muscle injury via hyperbaric oxygen therapy.
Med Sci Sports Exercise 33: 3642.
Horn, P.C., Webster, D.A., Amin, H.M., Mascia,
M.F., Werner, F.W. and Fortino, M.D. (1999) The
effect of hyperbaric oxygen on medial collateral liga-
ment healing in a rat model. Clin Orthopaed Rel Res
360: 238242.
Ishii, Y., Deie, M., Adachi, N., Yasunaga, Y., Sharman,
P., Miyanaga, Y. et al. (2005) Hyperbaric oxygen as an
adjuvant for athletes. Sports Med 35: 739746.
Ishii, Y., Ushida, T., Tateishi, T., Shimojo, H. and
Miyanaga, Y. (2002) Effects of different exposures of
hyperbaric oxygen on ligament healing in rats.
J Orthopaed Res 20: 353356.
Jain, K.K. (2004) Textbook of Hyperbaric Medicine.
Military Medicine.
James, P.B., Scott, B. and Allen, M.W. (1993)
Hyperbaric oxygen therapy in sports injuries.
Physiotherapy 79: 571572.
Ja¨rvinen, T., Ja¨rvinen, T., Ka¨a¨ria¨ inen, M., A
¨a¨ rimaa, V.,
Vaittinen, S., Kalimo, H. et al. (2007) Muscle injuries:
optimising recovery. Best Practice Res Clin Rheumatol
21: 317331.
Ja¨rvinen, T., Ka¨a¨ria¨inen, M., Ja¨ rvinen, M. and
Kalimo, H. (2000) Muscle strain injuries. Curr Opin
Rheumatol 12: 155161.
Kang, T.S., Gorti, G.K., Quan, S.Y., Ho, M. and
Koch, R.J. (2004) Effect of hyperbaric oxygen on the
growth factor profile of fibroblasts. Arch Facial Plastic
Surg 6: 3135.
Komurcu, M., Atesalp, A.S., Basbozkurt, M. and
Kurklu, M. (2002) The treatment of infected tibial
nonunion with aggressive debridement and internal
bone transport. Military Med 167: 978981.
Kunnavatana, S.S., Quan, S.Y. and Koch, R.J. (2005)
Combined effect of hyberbaric oxygen and
N-acetylcysteine on fibroblast proliferation. Arch
Otolaryngol Head Neck Surg 131: 809814.
Li, Y., Cummins, J. and Huard, J. (2001) Muscle
injury and repair. Curr Opin Orthopaed 12: 409415.
Mader, J.T., Brown, G.L., Guckian, J.C., Wells, C.H.
and Reinarz, J.A. (1980) A mechanism for the ame-
lioration by hyperbaric oxygen of experimental staph-
ylococcal osteomyelitis in rabbits. J Infectious Dis
142: 915922.
Mashitori, H., Sakai, H., Koibuchi, N., Ohtake, H.,
Tashiro, T., Tamai, K. et al. (2004) Effect of hyper-
baric oxygen on the ligament healing process in rats.
Clin Orthopaed Rel Res 423: 268274.
Mathieu, D. (2006) Handbook on Hyperbaric Medicine.
Kluwer: Dordrecht.
Mayer, R., Hamilton-Farrell, M.R., Kleij, A.J.v.d.,
Schmutz, J., Granstro¨ m, G., Sicko, Z. et al. (2004)
Hyperbaric oxygen and radiotherapy. Strahlenther
Onkol 181: 113123.
Mekjavic, I.B., Exner, J.A., Tesch, P.A. and Eiken, O.
(2000) Hyperbaric oxygen therapy does not affect
recovery from delayed onset muscle soreness. Med Sci
Sports Exercise 32: 558563.
Minhas, R. (2010) Best Practice, BMJ Evidence
Center. Available at: http://group.bmj.com/products/
evidence-centre/best-practice.
Mortensen, C. (2008) Hyperbaric oxygen therapy.
Curr Anaesth Crit Care 19: 333337.
Muhonen, A., Haaparanta, M., Gro¨ nroos, T.,
Bergman, J., Knuuti, J., Hinkka, S. et al. (2004)
Osteoblastic activity and neoangiogenesis in distracted
bone of irradiated rabbit mandible with or without
hyperbaric oxygen treatment. Int J Oral Maxillofacial
Surg 33: 173178.
Therapeutic Advances in Musculoskeletal Disease 3 (2)
120 http://tab.sagepub.com
Okubo, Y., Bessho, K., Fujimura, K., Kusumoto, K.,
Ogawa, Y. and Iizuka, T. (2001) Effect of hyperbaric
oxygenation on bone induced by recombinant human
bone morphogenetic protein-2. Br J Oral Maxillofacial
Surg 39: 9195.
Oriani, G., Barnini, C. and Marroni, G. (1982)
Hyperbaric oxygen therapy in the treatment of
various orthopedic disorders. Minerva Medica
73: 29832988.
Petersen, J. and Ho¨ lmich, P. (2005) Evidence based
prevention of hamstring injuries in sports. Br J Sports
Med 39: 319323.
Sheridan, R.L. and Shank, E.S. (1999) Hyperbaric
oxygen treatment: a brief overview of a controversial
topic. J Trauma 47: 426435.
Soolsma, S.J. (1996) The effect of intermittent hyperbaric
oxygen on short term recovery from grade II medial col-
lateral ligament injuries. Thesis, University of British
Columbia, Vancouver.
Staples, J. and Clement, D. (1996) Hyperbaric oxygen
chambers and the treatment of sports injuries. Sports
Med 22: 219227.
Staples, J., Clement, D., McKenzie, D., Booker, T.,
Sbeel, A. and Belcastro, A. (1995) The effects of
intermittent hyperbaric oxygen on biochemical muscle
metabolites of eccentrically-exercised rats. (abstract).
Can J Appl Physiol 20(Suppl): 49.
Staples, J., Clement, D., Taunton, J. and McKenzie, D.
(1999) Effects of hyperbaric oxygen on a human model
of injury. Am J Sports Med 27: 600605.
Takeyama, N., Sakai, H., Ohtake, H., Mashitori, H.,
Tamai, K. and Saotome, K. (2007) Effects of hyper-
baric oxygen on gene expressions of procollagen,
matrix metalloproteinase and tissue inhibi-
tor of metalloproteinase in injured
medial collateral ligament and anterior cruciate
ligament. Knee Surg Sports Traumatol Arthrosc
15: 443452.
Wang, I.-C., Ueng, S.W.-N., Yuan, L.-J., Tu, Y.-K.,
Lin, S.-S., Wang, C.-R. et al. (2005) Early adminis-
tration of hyperbaric oxygen therapy in distraction
osteogenesis: a quantitative study in New Zealand
rabbits. J Trauma Injury Infect Cr it Care
58: 12301235.
Webster, A., Syrotuik, D., Bell, G., Jones, R. and
Hanstock, C. (2002) Effects of hyperbaric
oxygen on recovery from exercise-induced
muscle damage in humans. Clin J Sports Med
12: 139150.
Visit SAGE journals online
http://tab.sagepub.com
P Barata, M Cervaens et al.
http://tab.sagepub.com 121
... While soft chambers made of fabric, instead of steel or polymer, do exist and are increasing in popularity, they are not capable of reaching above 1.4 ATA, and will not be the main focus of this overview [12,13]. Due to the higher cost of multiplace chambers, monoplace chambers are the most common [14]. The concept of using compressed air at higher pressures than sea level has an extensive history and is closely tied to diving medicine. ...
... Exposure to HBOT increases oxygen content available in tissues, and this accelerates the process of healing [19]. When patients are exposed to 2 atmospheres absolute (ATA) and 100% oxygen, the oxygen content in plasma can be up to "10 times higher than breathing regular air at sea level" [14]. The effects of this increased oxygen content include vasoconstriction which acts to reduce oedema and improve neutrophil phagocytic function to mitigate infection, phagocytosis activation, neovascularization, neoangiogenesis, collagen production and inhibition of anaerobic organisms [1,11,14]. ...
... When patients are exposed to 2 atmospheres absolute (ATA) and 100% oxygen, the oxygen content in plasma can be up to "10 times higher than breathing regular air at sea level" [14]. The effects of this increased oxygen content include vasoconstriction which acts to reduce oedema and improve neutrophil phagocytic function to mitigate infection, phagocytosis activation, neovascularization, neoangiogenesis, collagen production and inhibition of anaerobic organisms [1,11,14]. ...
Article
Full-text available
Hyperbaric Oxygen Therapy (HBOT) has been a recognised treatment for a multitude of injuries for decades and presents significant opportunities for the improvement of wound healing, blood vessel restoration, reduction in recovery time after surgery, treatment of neurological and neurodegenerative disorders, improvement of memory and cognition, sports injury rehabilitation, cartilage regeneration, and overall quality of life. This paper aims to investigate HBOT and its indications for use, both as an adjuvant with other established treatments and independently, in order to provide an overview of treatment avenues with immense possibilities and versatility.
... These results suggest that hyperoxygenation induces cellular and genomic responses by increased availability of molecular oxygen. In fact, HO 2 treatment at 2.0 ATA in animals has been reported to increase the O 2 tension in the brain tissues by 7-10 fold compared with the O 2 tension under ambient room air [52][53][54]. Hyperoxygenation therapy in brain injury produced neuroprotective effects in association with preservation of mitochondrial function [54,55]. Because high oxygen levels could oxidize the sulfur-con-taining amino acids cysteine and methionine in cellular proteins [56], increased availability of O 2 in brain cells likely facilitates the functionality of cellular and nuclear factors to increase expression of neurotrophic expression [30] or mitochondrial genes (Fig. 5). ...
Article
Hyperoxygenation therapy remediates neuronal injury and improves cognitive function in various animal models. In the present study, the optimal conditions for hyperoxygenation treatment of stress-induced maladaptive changes were investigated. Mice exposed to chronic restraint stress (CRST) produce persistent adaptive changes in genomic responses and exhibit depressive-like behaviors. Hyperoxygenation treatment with 100% O2 (HO2) at 2.0 atmospheres absolute (ATA) for 1 h daily for 14 days in CRST mice produces an antidepressive effect similar to that of the antidepressant imipramine. In contrast, HO2 treatment at 2.0 ATA for 1 h daily for shorter duration (3, 5, or 7 days), HO2 treatment at 1.5 ATA for 1 h daily for 14 days, or hyperbaric air treatment at 2.0 ATA (42% O2) for 1 h daily for 14 days is ineffective or less effective, indicating that repeated sufficient hyperoxygenation conditions are required to reverse stress-induced maladaptive changes. HO2 treatment at 2.0 ATA for 14 days restores stress-induced reductions in levels of mitochondrial copy number, stress-induced attenuation of synaptophysin-stained density of axon terminals and MAP-2-staining dendritic processes of pyramidal neurons in the hippocampus, and stress-induced reduced hippocampal neurogenesis. These results suggest that HO2 treatment at 2.0 ATA for 14 days is effective to ameliorate stress-induced neuronal and behavioral deficits.
... HBOT is a process involving pure oxygen (100%) at pressures higher than local atmospheric pressure to treat injury or disease [12] . The mechanisms of action include causing reactive vasoconstriction [13] , improving and intensifying osteoclasts and osteoblasts, increasing the synthesis of collagen, encouraging angio- genesis in hypoxic tissues [14] , increasing oxygen pressure removing toxic gases [ 15 , 16 ], and producing antibacterial effects [17] . A related study revealed HBOT could be used in traumatic crush injuries. ...
Article
Background: Mangled Extremity Severity Score (MESS) was first described more than 30 years ago by attempting to predict the need for empiric amputation. In severe traumatic crush and blast injuries, achieving satisfactory limb salvage may be difficult. Notably, a MESS of 7 or higher is consistently predictive of amputation. Additionally, Hyperbaric Oxygen Therapy (HBOT) has been described for many purposes, and related studies have reported HBOT showed benefits in wound healing properties. Objective: The study aimed to evaluate the results of a prospective series of a new modality of adjuvant HBOT for severe mangled extremities. Method: A total of 18 patients were evaluated for clinical and radiographic review. Current standard treatments followed by adjuvant HBOT were administered, and the mean follow-up period was 22 months. Time to wound closure, the number of surgeries and adjuvant HBOT treatment were analyzed for patient clinical evaluation. Complications and limb amputation rates were also recorded. Result: Most clinical findings on follow-up were good to excellent after adjunctive HBOT. Minimal soft tissue infection was recorded, and limb salvage was successful in most cases. Only 1 patient (5.56 %) needed limb amputation because of a dying limb with chronic refractory osteomyelitis. Conclusion: HBOT is an excellent adjunctive option in severely mangled extremities. Nevertheless, the main treatments are eliminating infection and managing surgery, and are promising in the recovery of severe extremity injuries. Although the MESS was evaluated at 7 or higher, limb salvage procedures followed by HBOT should be considered.
... One promising alternative use has been the potential to treat mild traumatic brain injuries (mTBIs) or traumatic brain injuries (TBIs). This possibility has received attention from multiple communities where concussive incidents are pervasive problems, especially for the military and athletes in contact sports (2)(3)(4)(5)(6). Multiple reviews have strongly suggested that HBO should be widely used to treat mTBI/TBI (7)(8)(9)(10). ...
Article
Full-text available
Hyperbaric oxygen therapy has been proposed as a method to treat traumatic brain injuries. The combination of pressure and increased oxygen concentration produces a higher content of dissolved oxygen in the bloodstream, which could generate a therapeutic benefit for brain injuries. This dissolved oxygen penetrates deeper into damaged brain tissue than otherwise possible and promotes healing. The result includes improved cognitive functioning and an alleviation of symptoms. However, randomized controlled trials have failed to produce consistent conclusions across multiple studies. There are numerous explanations that might account for the mixed evidence, although one possibility is that prior evidence focuses primarily on statistical significance. The current analyses explored existing evidence by calculating an effect size from each active treatment group and each control group among previous studies. An effect size measure offers several advantages when comparing across studies as it can be used to directly contrast evidence from different scales, and it provides a proximal measure of clinical significance. When exploring the therapeutic benefit through effect sizes, there was a robust and consistent benefit to individuals who underwent hyperbaric oxygen therapy. Placebo effects from the control condition could account for approximately one-third of the observed benefits, but there appeared to be a clinically significant benefit to using hyperbaric oxygen therapy as a treatment intervention for traumatic brain injuries. This evidence highlights the need for design improvements when exploring interventions for traumatic brain injury as well as the importance of focusing on clinical significance in addition to statistical significance.
Chapter
Lateral hip pain and peritrochanteric disorders are a common cause of hip pain in athletes. The term greater trochanteric pain syndrome (GTPS) has been used over the years to describe a spectrum of conditions that cause lateral-sided hip pain, including tendinopathies and strains of the hip abductor complex, trochanteric bursitis, external snapping hip syndrome, and proximal iliotibial band syndrome. Diagnosis of these conditions may be challenging due to variability and sometimes overlap in their clinical presentations. Recent advancements in our understanding of pathomechanics, biomechanics, and anatomic relationships between bony structures and soft tissues in the hemipelvis have resulted in better treatments and more accurate diagnostic tools. In this chapter, we will review common peritrochanteric disorders and the current treatments and diagnostic modalities.
Chapter
Muscle injuries are the most common injuries in professional athletes forced to high-intensity sprinting efforts. Due to a high recurrence rate and possible consequences for elite athletes, it is one of the most challenging tasks for a sports medicine team to prepare a professional athlete to return to performance. This results in an ongoing search for new treatments to improve and accelerate muscle healing. In this chapter, we describe the principle of muscle healing and discuss the contemporary biological therapies with the available scientific evidence on their efficacy and safety.
Chapter
Acute and chronic hamstring injuries are common in athletics. Acute injuries account for 17.1% of all injuries. Chronic injuries (proximal hamstring tendinopathy) are seen less frequently, however, but true incidences are unknown. Acute injuries occur at the (from most frequent to less frequent) musculotendinous junction (MTJ), the intramuscular tendon and the free tendons (partial- or full-thickness injury). Proximal hamstring tendinopathy occurs in the proximal hamstring free tendons. Diagnosis of these injuries is mostly clinical but can be supported by imaging such as magnetic resonance imaging or ultrasound. Treatment for partial-thickness MTJ acute hamstring injuries is informed by 14 RCTs. For proximal hamstring tendinopathy and partial- or full-thickness free tendon injuries, there is little evidence to guide treatment. Cornerstone of treatment is physiotherapy-based interventions with progressive (eccentric) loading and activity modification, combined with expectation management. Surgery is usually reserved for full-thickness free tendon injuries. Other treatments such as platelet-rich plasma injections, corticosteroid injections and non-steroidal anti-inflammatory medication have little supportive evidence and should be avoided.
Chapter
Stress fractures of the foot and ankle in athletes represent a challenging problem for the orthopedic surgeon, as they are associated with high rates of reoccurrence and long-lasting absence from daily sport activities. In elite sports, stress fractures most commonly occur in the lower extremity.
Chapter
Full-text available
Ankle sprains and instability are among the most common musculoskeletal disorders in track and field athletes. They are associated with pain, loss of function, inability to sport, and loss of performance. Adequate diagnosis and treatment of ankle sprains will minimize the risk of long-term consequences including chronic instability and cartilage degeneration. The current chapter serves as a comprehensive overview of the most important aspects of diagnosis and treatment of lateral ankle sprains and instability with a special consideration for this type of injury in track and field athletes.
Article
With a possibility for the use of chemical weapons in battlefield or in terrorist activities, effective therapies against the devastating ocular injuries, from their exposure, are needed. Oxygen plays a vital role in ocular tissue preservation and wound repair. We tested the efficacy of supersaturated oxygen emulsion (SSOE) in reducing ex vivo corneal and keratocyte injury from chloropicrin (CP). CP, currently used as a pesticide, is a chemical threat agent like the vesicating mustard agents and causes severe corneal injury. Since our previous study in human corneal epithelial cells showed the treatment potential of SSOE (55%), we further tested its efficacy in an ex vivo CP-induced rabbit corneal injury model. Corneas were exposed to CP (700 nmol) for 2 h, washed and cultured with or without SSOE for 24 h or 96 h. At 96 h post CP exposure, SSOE treatment presented a healing tendency of the corneal epithelial layer, and abrogated the CP-induced epithelial apoptotic cell death. SSOE treatment also reduced the CP induced DNA damage (H2A.X phosphorylation) and inflammatory markers (e.g. MMP9, IL-21, MIP-1β, TNFα). Further examination of the treatment efficacy of SSOE alone or in combination with other therapies in in vivo cornea injury models for CP and vesicants, is warranted.
Article
Objective: To determine whether hyperbaric oxygen (HBO) therapy could accelerate recovery from exercise-induced muscle damage in humans. Design: Pretest-posttest design with random assignment to either a treatment (HBO) or placebo control (sham) group. Setting: University of Alberta and Misericordia Hospital, Edmonton. Participants: 12 healthy male students (24.2 +/- 3.2 years) who were unaccustomed to strenuous eccentric exercise of the calf muscles. Interventions: All subjects performed a strenuous eccentric exercise protocol designed to elicit muscle damage within the right gastrocnemius muscle. Subjects subsequently received either HBO (100% oxygen at 253 kPa [2.5 ATA] for 60 min; n = 6) or sham (atmospheric air at 132 kPa [1.3 ATA] for 60 min; n = 6) treatment conditions. The first treatment was administered 3-4 hours after damage, with a second and third at 24 and 48 hours after the first, respectively. Main Outcome Measures: Dependent variables included peak torque at 0.52 radians/s, peak isometric torque, and muscular endurance using isokinetic dynamometry; muscle cross-sectional area using magnetic resonance imaging; inorganic phosphate levels and T-2 relaxation time. using P-31 and H-1 magnetic resonance spectroscopy; pain sensation and unpleasantness using the Descriptor Differential Scale. These variables were assessed at baseline and until day 5 postdamage. Results: There was little evidence of a difference in recovery rate between the HBO and sham groups. Faster recovery was observed in the HBO group only for isometric peak torque and pain sensation and unpleasantness. Conclusions: HBO cannot be recommended as an effective method of treatment of this form of muscle injury.
Book
It is now ten years since the first Handbook on Hyperbaric Medicine was published. During this time there have been many major advances: our understanding of the actions of hyperbaric oxygenation, and the pathophysiological processes it engages, have been elucidated by several studies; clinical practice is becoming more scientific with the application of evidence-based medicine (EBM) principles and the appearance of a number of randomised clinical trials; various consensus-derived organisational and operational recommendations and guidelines have become normative and are now widely accepted. For the European part, these positive developments are largely due to the continuous action of the European Committee for Hyperbaric Medicine (ECHM) - the springboard of many of these initiatives. One of the most successful initiatives was the start of a specific European research action sponsored by the EU Co-operation in Science and Technology (COST) programme. The specific COST Action for hyperbaric medicine, COST B14, as been completed and, in combination with the results of a number of experimental and clinical studies performed over the last 6 years, has provided the impetus for the publication of this new Handbook. The final product is a reference document for researchers and clinicians alike, to be used both in the research laboratory and in everyday hyperbaric clinical practice. It also provides support material for teachers and will assist students in obtaining ECHM level II and III qualifications in hyperbaric medicine. This Handbook will be of excellent use for the international scientific community.
Article
HARRISON, B. C., D. ROBINSON, B. J. DAVISON, B. FOLEY, E. SEDA, and W. C. BYRNES. Treatment of exercise-induced muscle injury via hyperbaric oxygen therapy. Med. Sci. Sports Exerc., Vol. 33, No. 1, 2001, pp. 36–42. Purpose: This study examined the role of hyperbaric oxygen therapy (HBO) in the treatment of exercise-induced muscle injury. Methods: 21 college-aged male volunteers were assigned to three groups: control, immediate HBO (iHBO), and delayed HBO (dHBO). All subjects performed 6 sets (10 repetitions per set) of eccentric repetitions with a load equivalent to 120% of their concentric maximum. HBO treatments consisted of 100-min exposure to 2.5 ATA and 100% oxygen with intermittent breathing of ambient air (30 min at 100% O2, 5 min at 20.93% O2). HBO treatments began either 2 (iHBO) or 24 h (dHBO) postexercise and were administered daily through day 4 postexercise. Forearm flexor cross-sectional area (CSA) and T2 relaxation time via magnetic resonance imaging (MRI) were assessed at baseline, 2, 7, and 15 d postinjury. Isometric strength and rating of perceived soreness of the forearm flexors were assessed at baseline, 1, 2, 3, 4, 7, and 15 d postinjury. Serum creatine kinase (CK) was assessed on day 0 and on days 1, 2, 7, and 15 postinjury. Results: Mean baseline CSA values were: 2016.3, 1888.5, and 1972.2 mm2 for control, iHBO, and dHBO, respectively. All groups showed significant increases in CSA in response to injury (21% at 2 d, 18% at 7 d) (P < 0.0001), but there were no significant differences between groups (P = 0.438). Mean baseline T2 relaxation times were: 26.18, 26.28, and 27.43 msec for control, iHBO, and dHBO, respectively. Significant increases in T2 relaxation time were observed for all groups (64% at 2 d, 66% at 7 d, and 28% at 15 d) (P < 0.0001), but there were no significant differences between groups (P = 0.692). Isometric strength (P < 0.0001), serum CK levels (P = 0.0007), and rating of perceived soreness (P < 0.0001) also indicated significant muscle injury for all groups, but there were no differences between groups (P = 0.459, P = 0.943, and P = 0.448, respectively). Conclusion: These results suggest that hyperbaric oxygen therapy was not effective in the treatment of exercise-induced muscle injury as indicated by the markers evaluated.
Article
Hyperbaric oxygen therapy is a treatment with a number of different indications. It is managed by different specialities, but most of the hyperbaric facilities are driven by departments of anaesthesiology, and some of the patients are critically ill. This paper deals briefly with modes of administration, mechanisms of action, indications and risks. Two indications, carbon monoxide poisoning and necrotising soft tissue infections, are of special interest for the anaesthesiologist, and are therefore dealt with in little more detail.