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Hyperbaric Oxygen Therapy and Sports Injuries
Breathing Oxygen under increased pressure of more than 1ATA is referred to as hyperbaric oxygen therapy or HBOT. This should be considered an important adjunctive therapy in the management of acute trauma, which is seen in sports injuries.
Trauma is a multi disciplinary medical problem as it could affect many different systems of the body. Trauma, direct or indirect, in turn, can be classified as either minor (contusions, subluxations-ligamental injuries, etc) or major (fractures, spinal injuries, severe contusions, crush injuries - compartment syndrome, burns, etc).
Benefits of HBOT:
•
Reduces swelling and pain
•
Prevents Hypoxia of the traumatized tissues
•
Speeds up the healing of tissues, ligaments and fractured bones
•
Reduces scar tissue formation and damage
•
Helps return players to the game sooner
Ischemia and edema are parts of a vicious circle where Hypoxia is the major component in the changes that affect the injured tissues. Edema (swelling) of the tissues will compound the problem created by hypoxia as it increases the diffusion distance from the capillaries to the cell.
This also affects the micro-circulation or clumping of erythrocytes that in turn impede circulation in already compromised tissue. Although plasma still may go through the capillaries, it may not carry enough oxygen to sustain the life of cells. Here is where the oxygen under pressure proves its benefits (Henry’s Law).
As the partial pressure of inspired oxygen increases, the plasma dissolved in oxygen increases proportionatelly. For each one millimetre of increased pressure of Oxygen, 0.003 millimetres of Oxygen is dissolved in plasma. This amount dissolved in plasma, is sufficient to oxygenate tissues without haemoglobin borne oxygen.
The usual treatment protocols are between 2- 3 ATA and at these pressures there is enough oxygen dissolved in plasma. At 3 ATA there is sufficient amounts of dissolved oxygen in the plasma to sustain life. (Boerema et al.1960)
Traumatized tissue's auto regulatory mechanism increases blood flow to compensate for hypoxia. In a damaged microcirculation this mechanism causes undesirable swelling.
The increases in the oxygen carrying-capacity of the plasma appears to have 2 important effects. Firstly, in-spite of the collapse of the microcirculation (Hargens&Akeson 1981) the plasma carry sufficient amounts of oxygen to avoid problems associated with hypoxia. Hyperbaric oxygen, with the treatment pressure (2 ATA) increases the diffusion distance by a factor of three (Pierce 1969).
Second effect; reduction of edema through vasoconstriction. Oxygen under pressure causes 20% reduction in blood flow (Bird&Telfer 1965, Nylander, Nordstrom and Erickson 1984; Sukoff&Ragatz 1982). Edema is reduced at the same time microcirculation improves and this enhances re-absorption of fluid and a further reduction of swelling. In addition HBOT appears to protect microcirculation by reducing venular leukocyte adherence and inhibiting progressive adjacent arteriolar vasoconstriction.
The important part of treatment and rehabilitation of any injury is physical therapy with the associated application of HBOT, using various protocols according to the type and origin of the injury. In conclusion, data from many studies suggest that treatment should be instituted with in first 24-48 hours. Some studies indicate the first 12 hours is very important and the injury should be treated aggressively from 2.2 ATA to 2.8 ATA between 60-90 min.
(Reprinted with Permission)
Trauma is a multi disciplinary medical problem as it could affect many different systems of the body. Trauma, direct or indirect, in turn, can be classified as either minor (contusions, subluxations-ligamental injuries, etc) or major (fractures, spinal injuries, severe contusions, crush injuries - compartment syndrome, burns, etc).
Benefits of HBOT:
•
Reduces swelling and pain
•
Prevents Hypoxia of the traumatized tissues
•
Speeds up the healing of tissues, ligaments and fractured bones
•
Reduces scar tissue formation and damage
•
Helps return players to the game sooner
Ischemia and edema are parts of a vicious circle where Hypoxia is the major component in the changes that affect the injured tissues. Edema (swelling) of the tissues will compound the problem created by hypoxia as it increases the diffusion distance from the capillaries to the cell.
This also affects the micro-circulation or clumping of erythrocytes that in turn impede circulation in already compromised tissue. Although plasma still may go through the capillaries, it may not carry enough oxygen to sustain the life of cells. Here is where the oxygen under pressure proves its benefits (Henry’s Law).
As the partial pressure of inspired oxygen increases, the plasma dissolved in oxygen increases proportionatelly. For each one millimetre of increased pressure of Oxygen, 0.003 millimetres of Oxygen is dissolved in plasma. This amount dissolved in plasma, is sufficient to oxygenate tissues without haemoglobin borne oxygen.
The usual treatment protocols are between 2- 3 ATA and at these pressures there is enough oxygen dissolved in plasma. At 3 ATA there is sufficient amounts of dissolved oxygen in the plasma to sustain life. (Boerema et al.1960)
Traumatized tissue's auto regulatory mechanism increases blood flow to compensate for hypoxia. In a damaged microcirculation this mechanism causes undesirable swelling.
The increases in the oxygen carrying-capacity of the plasma appears to have 2 important effects. Firstly, in-spite of the collapse of the microcirculation (Hargens&Akeson 1981) the plasma carry sufficient amounts of oxygen to avoid problems associated with hypoxia. Hyperbaric oxygen, with the treatment pressure (2 ATA) increases the diffusion distance by a factor of three (Pierce 1969).
Second effect; reduction of edema through vasoconstriction. Oxygen under pressure causes 20% reduction in blood flow (Bird&Telfer 1965, Nylander, Nordstrom and Erickson 1984; Sukoff&Ragatz 1982). Edema is reduced at the same time microcirculation improves and this enhances re-absorption of fluid and a further reduction of swelling. In addition HBOT appears to protect microcirculation by reducing venular leukocyte adherence and inhibiting progressive adjacent arteriolar vasoconstriction.
The important part of treatment and rehabilitation of any injury is physical therapy with the associated application of HBOT, using various protocols according to the type and origin of the injury. In conclusion, data from many studies suggest that treatment should be instituted with in first 24-48 hours. Some studies indicate the first 12 hours is very important and the injury should be treated aggressively from 2.2 ATA to 2.8 ATA between 60-90 min.
(Reprinted with Permission)
Hyperbaric oxygen as an adjuvant for athletes.
Sports Med. 2005;35(9):739-46.
Hyperbaric oxygen as an adjuvant for athletes. Ishii Y, Deie M, Adachi N, Yasunaga Y, Sharman P, Miyanaga Y, Ochi M.
Source
Department of Orthopaedic Surgery, Hiroshima University, Hiroshima, Japan. [email protected]
Abstract
There has recently been a resurgence in interest in hyperbaric oxygen (HBO) treatment in sports therapy, especially in Japan. Oxygen naturally plays a crucial role in recovery from injury and physiological fatigue. By performing HBO treatment, more oxygen is dissolved in the plasma of the pulmonary vein via the alveolar, increasing the oxygen reaching the peripheral tissues. HBO treatment is therefore expected to improve recovery from injury and fatigue. HBO treatment has been reported to reduce post-injury swelling in animals, and in humans; swelling was also mitigated, but to a lesser extent. Positive results have also been reported regarding tissue remodelling after injury, with injuries involving bones, muscles and ligaments showing improved recovery. Furthermore, HBO treatment has effectively increased recovery from fatigue. This was clearly seen at the Nagano Winter Olympics, where sports players experiencing fatigue were successfully treated, enabling the players to continue performing in the games. Despite its potential, HBO treatment does have its risks. Increasing oxygen levels in tissues poses a risk to DNA through oxidative damage, which can lead to pathological changes in the CNS and the lungs. Regarding the operating of HBO systems, safer administration should be advised. Further research into HBO treatment is required if this therapy is to become more widespread. It should become possible to tailor treatment to an individual's condition in order to use HBO treatment efficiently.
PMID:
16138784
[PubMed - indexed for MEDLINE]
Hyperbaric oxygen as an adjuvant for athletes. Ishii Y, Deie M, Adachi N, Yasunaga Y, Sharman P, Miyanaga Y, Ochi M.
Source
Department of Orthopaedic Surgery, Hiroshima University, Hiroshima, Japan. [email protected]
Abstract
There has recently been a resurgence in interest in hyperbaric oxygen (HBO) treatment in sports therapy, especially in Japan. Oxygen naturally plays a crucial role in recovery from injury and physiological fatigue. By performing HBO treatment, more oxygen is dissolved in the plasma of the pulmonary vein via the alveolar, increasing the oxygen reaching the peripheral tissues. HBO treatment is therefore expected to improve recovery from injury and fatigue. HBO treatment has been reported to reduce post-injury swelling in animals, and in humans; swelling was also mitigated, but to a lesser extent. Positive results have also been reported regarding tissue remodelling after injury, with injuries involving bones, muscles and ligaments showing improved recovery. Furthermore, HBO treatment has effectively increased recovery from fatigue. This was clearly seen at the Nagano Winter Olympics, where sports players experiencing fatigue were successfully treated, enabling the players to continue performing in the games. Despite its potential, HBO treatment does have its risks. Increasing oxygen levels in tissues poses a risk to DNA through oxidative damage, which can lead to pathological changes in the CNS and the lungs. Regarding the operating of HBO systems, safer administration should be advised. Further research into HBO treatment is required if this therapy is to become more widespread. It should become possible to tailor treatment to an individual's condition in order to use HBO treatment efficiently.
PMID:
16138784
[PubMed - indexed for MEDLINE]
The role of hyperbaric oxygen therapy in sports medicine.
Sports Med. 2000 Dec;30(6):395-403.
The role of hyperbaric oxygen therapy in sports medicine. Babul S, Rhodes EC.
Source
British Columbia Injury Research and Prevention Unit, British Columbia Children's Hospital, University of British Columbia, Vancouver, Canada.
Abstract
During the past decade, we have seen a growing number of individuals participating in sport and recreational activities. All indications show an increase in sport participation at every age level. However, the number of sport and recreational injuries as a result of this increase has also risen. Unfortunately, a primary cost related to injury recovery is the time lost from participating in and resuming normal functional activity. This has compelled health care professionals to seek more efficient and effective therapeutic interventions in treating such injuries. Hyperbaric oxygen (HBO) therapy may serve to provide a means of therapy to facilitate a speedier resumption to pre-injury activity levels as well as improve the short and long term prognosis of the injury. Although a growing interest in sports medicine is becoming evident in the literature, the use of HBO as an intervention in this field has received a great deal of cynicism. To date, numerous professional athletic teams, including hockey (NHL), football (NFL), basketball (NBA) and soccer (MLS), utilise and rely on the use of HBO as adjuvant therapy for numerous sports-related injuries acquired from playing competitive sports. However, to date, very little has been published on the application benefits of hyperbaric therapy and sports injuries. The majority of clinical studies examining the efficacy of HBO in treating soft tissue injuries have been limited in their sample size and study design. Further research needs to be conducted suggesting and validating the significant effects of this treatment modality and further grounding its importance in sports medicine.
PMID:
11132122
[PubMed - indexed for MEDLINE]
The role of hyperbaric oxygen therapy in sports medicine. Babul S, Rhodes EC.
Source
British Columbia Injury Research and Prevention Unit, British Columbia Children's Hospital, University of British Columbia, Vancouver, Canada.
Abstract
During the past decade, we have seen a growing number of individuals participating in sport and recreational activities. All indications show an increase in sport participation at every age level. However, the number of sport and recreational injuries as a result of this increase has also risen. Unfortunately, a primary cost related to injury recovery is the time lost from participating in and resuming normal functional activity. This has compelled health care professionals to seek more efficient and effective therapeutic interventions in treating such injuries. Hyperbaric oxygen (HBO) therapy may serve to provide a means of therapy to facilitate a speedier resumption to pre-injury activity levels as well as improve the short and long term prognosis of the injury. Although a growing interest in sports medicine is becoming evident in the literature, the use of HBO as an intervention in this field has received a great deal of cynicism. To date, numerous professional athletic teams, including hockey (NHL), football (NFL), basketball (NBA) and soccer (MLS), utilise and rely on the use of HBO as adjuvant therapy for numerous sports-related injuries acquired from playing competitive sports. However, to date, very little has been published on the application benefits of hyperbaric therapy and sports injuries. The majority of clinical studies examining the efficacy of HBO in treating soft tissue injuries have been limited in their sample size and study design. Further research needs to be conducted suggesting and validating the significant effects of this treatment modality and further grounding its importance in sports medicine.
PMID:
11132122
[PubMed - indexed for MEDLINE]
Hyperbaric Oxygen Effects on Sports Injuries
From Therapeutic Advances in Musculoskeletal Disease
Pedro Barata; Mariana Cervaens; Rita Resende; Óscar Camacho; Frankim Marques
Authors and Disclosures
Posted: 04/08/2011; Ther Adv Musculoskel Dis. 2011;3(2):111-121. © 2011 Sage Publications, Inc.
Abstract and Introduction
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.
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 training 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 therapeutic administration of 100% oxygen at pressures higher than 1 absolute
atmosphere (ATA). It is administered by placing the patient in a multiplace or in a monoplace (one man) chamber and
typically the vessels are pressurized to 1.5–3.0 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 application. 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 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].
Biochemical, Cellular and Physiological Effects of HBO
The level of consumption of O2 by a given tissue, on the local blood stream, and the relative distance of the zone
considered from the nearest arteriole and capillary determines the O2 tension in this tissue. Indeed, O2 consumption
causes oxygen partial pressure (pO2) to fall rapidly between arterioles and vennules. This emphasizes 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
mitochondrion, the terminal place of oxygen consumption, where O2 concentrations range from 1.5 to 3μM [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
interstitial and intercellular fluid. Under normobaric conditions, the gradient of pO2 known as the 'oxygen cascade'
starts at 21.2 kPa (159mmHg) and ends up at 0.5–3 kPa (3.8–22.5mmHg) depending on the target tissue [Mathieu,
2006]. The arterial oxygen tension (PaO2) is approximately 90mmHg and the tissue oxygen tension (PtO2) is
approximately 55mmHg [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 (PaCO2), water vapour pressure and respiratory 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 PO2 of 1423mmHg and, consequently, the alveolar oxygen passes the alveolar–capillary 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 physically, dissolved in plasma.
During normal breathing in the environment we live in, haemoglobin has an oxygen saturation of 97%, representing a
total oxygen content of about 19.5 ml O2/100 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 dissolved 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 intubation the oxygen content
can reach values up to 22.2 vol% [Jain, 2004].
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 (PAO2) is approximately
2180mmHg, the PaO2 is at least 1800mmHg and the tissue concentration (PtO2) is at least 500 mmHg. The oxygen
content of blood is approximately ([1.34×Hbg×SaO2]+[0.0031×PaO2]), where Hbg is serum haemoglobin
concentration and SaO2 is arterial oxygen saturation [Sheridan and Shank, 1999]. At a PaO2 of 1800mmHg, the
dissolved fraction of oxygen in plasma (0.0031×PaO2) is approximately 6 vol%, which means that 6 ml of oxygen will
be physically 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 paO2 in the arteries can reach 2000mmHg. With a
normal lung function and tissue perfusion, a partial pressure of oxygen in the blood (pO2)>1000mmHg 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 pO2 is 95 mmHg; under conditions of a hyperbaric
chamber, the pO2 can reach values greater than 2000mmHg [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 transported by haemoglobin [Albuquerque e
Sousa, 2007].
After removal from the hyperbaric oxygen environment, the PaO2 normalizes in minutes, but the PtO2 may remain
elevated for a variable period. The rate of normalization of PtO2 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 shortterm effects such as vasoconstriction and enhanced oxygen delivery,
reduction of oedema, phagocytosis activation and also an anti-inflammatory 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 provides a significant increase in oxygen availability at the tissue level, as selective
hyperoxic and not hypoxic vasoconstriction, occurring predominantly 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 extremities 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 contribution in the stimulation of reparative and regenerative
processes in some diseases [Mortensen, 2008].
Also many cell and tissue functions are dependent 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
sodium–potassium pump. HBO has the effect of inhibiting leukocyte adhesion to the endothelium, diminishing tissue
damage, which enhances leukocyte motility and improves microcirculation [Mortensen, 2008]. This occurs when the
presence 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,
provokes 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
capillary bed. Two-hour daily treatments with HBO are apparently responsible for stimulating the 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, producing 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 production of collagen matrix and
subsequent angiogenesis, 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 equivalents 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 keratinocyte
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
fibroblasts grown in a serum-free culture environment, 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 dysfunction, restores this defence and also increases the phagocytosis of some bacteria by working
synergistically 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 bactericidal 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 anaemia, 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 bacterial 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-1α, which promotes, for example, the glycolytic system,
vascularization and angiogenesis, has been shown to be important. However, if the oxygen supply could be controlled
without promoting blood flow, the blood vessel permeability could be controlled to reduce swelling and consequently
sharp pain.
In the proliferative phase, in musculoskeletal tissues (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 provided 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 suggested in the scientific literature as a
therapy 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 30–40 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 concordant with those obtained by Fischer and colleagues
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 fractures and ligament injuries,
have proved to benefit 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 Hölmich, 2005].
In sport events in the United States, the incidence 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 [Järvinen 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,
consequently, to their rupture near the myotendinous junction [Järvinen 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 Hölmich, 2005]. DOMS usually occurs
following unaccustomed physical activity and is accompanied by a sensation of discomfort within the skeletal 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, subsides and eventually disappears by 5–7 days postexercise
[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 following 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 12–
48 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 intensity of exercise.
Staples and colleagues in an animal study, used a downhill running model to induce damage, and observed significant
changes in the myeloperoxidase 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 inflammatory process or the
ability to actually modulate the injury to the tissue.
In 1999, the same group conducted a randomized, 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 [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 treatment and sham treatment). The hyperbaric exposures 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 significant 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 allocation of groups was not clarified), which makes
interpretation difficult [Bennett et al. 2005a].
Mekjavic and colleagues did not find any recovery 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 inducing 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 exercise-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 3–4 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 randomized, 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 multiple 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 randomly assigned into two groups [Germain et al. 2003]: the control group that did not
undergo 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 significant 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 colleagues wanted to analyse whether HBO improved functional and
morphologic recovery after a controlled induced muscle stretch in the tibialis anterior muscle–tendon 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 compared 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 formation of lactate and depletion of high-energy phosphates 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 factors, during reperfusion, may cause further damage to local and remote tissues.
However, the mechanisms of ischemia–reperfusion-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 concentration, 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 oxidation in the mitochondria. This maintains the transport of ions and molecules
across the cell membrane and optimizes the possibility of preserving the muscle cell structure.
Gregorevic and colleagues induced muscle degeneration in rats in order to see whether HBO hastens the functional
recovery and myofiber 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 compromised blood supply or with the repair of associated nerve components, as seen in ischemia, but with
the pressure of oxygen inspired with a crucial role in improving the maximum force-producing 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 quantifying the severity of sprains [Staples and Clement, 1996].
Interestingly, Borromeo and colleagues, in a randomized, 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 session and 60 minutes for the other two. The placebo group was exposed
to ambient air, at 1.1 ATA for 90 minutes, both groups for three sessions 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 treatment duration [Bennett et al. 2005a].
Medical Collateral Ligament
Horn and colleagues in an animal study surgically lacerated medial collateral ligament of 48 rats [Horn et al. 1999].
Half were controls without intervention and the other half were exposed to HBO at 2.8 ATA for 1.5 hours 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 deposition as measured by collagen synthesis.
Mashitori and colleagues removed a 2-mm segment 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 increasing 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 neovascularization at the tendon–bone
junction, collagen fibres of the tendon graft and the tendon graft–bony 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 increasing 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 animals
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 procollagen 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 promoting 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 lyophilized 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 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 successfully resolved after
20–30 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
suppresses 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 properties 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 muscle–tendon junctions and ligaments.
With regards to HBO treatment, it is still necessary to determine the optimal conditions for these orthopaedic
indications, such as the atmosphere pressure, the duration of sessions, the frequency 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 ligaments 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 treatments are multifactorial and are rarely published. Therefore, there is a need for larger samples, randomized,
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 treatment
Pedro Barata; Mariana Cervaens; Rita Resende; Óscar Camacho; Frankim Marques
Authors and Disclosures
Posted: 04/08/2011; Ther Adv Musculoskel Dis. 2011;3(2):111-121. © 2011 Sage Publications, Inc.
Abstract and Introduction
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.
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 training 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 therapeutic administration of 100% oxygen at pressures higher than 1 absolute
atmosphere (ATA). It is administered by placing the patient in a multiplace or in a monoplace (one man) chamber and
typically the vessels are pressurized to 1.5–3.0 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 application. 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 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].
Biochemical, Cellular and Physiological Effects of HBO
The level of consumption of O2 by a given tissue, on the local blood stream, and the relative distance of the zone
considered from the nearest arteriole and capillary determines the O2 tension in this tissue. Indeed, O2 consumption
causes oxygen partial pressure (pO2) to fall rapidly between arterioles and vennules. This emphasizes 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
mitochondrion, the terminal place of oxygen consumption, where O2 concentrations range from 1.5 to 3μM [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
interstitial and intercellular fluid. Under normobaric conditions, the gradient of pO2 known as the 'oxygen cascade'
starts at 21.2 kPa (159mmHg) and ends up at 0.5–3 kPa (3.8–22.5mmHg) depending on the target tissue [Mathieu,
2006]. The arterial oxygen tension (PaO2) is approximately 90mmHg and the tissue oxygen tension (PtO2) is
approximately 55mmHg [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 (PaCO2), water vapour pressure and respiratory 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 PO2 of 1423mmHg and, consequently, the alveolar oxygen passes the alveolar–capillary 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 physically, dissolved in plasma.
During normal breathing in the environment we live in, haemoglobin has an oxygen saturation of 97%, representing a
total oxygen content of about 19.5 ml O2/100 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 dissolved 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 intubation the oxygen content
can reach values up to 22.2 vol% [Jain, 2004].
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 (PAO2) is approximately
2180mmHg, the PaO2 is at least 1800mmHg and the tissue concentration (PtO2) is at least 500 mmHg. The oxygen
content of blood is approximately ([1.34×Hbg×SaO2]+[0.0031×PaO2]), where Hbg is serum haemoglobin
concentration and SaO2 is arterial oxygen saturation [Sheridan and Shank, 1999]. At a PaO2 of 1800mmHg, the
dissolved fraction of oxygen in plasma (0.0031×PaO2) is approximately 6 vol%, which means that 6 ml of oxygen will
be physically 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 paO2 in the arteries can reach 2000mmHg. With a
normal lung function and tissue perfusion, a partial pressure of oxygen in the blood (pO2)>1000mmHg 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 pO2 is 95 mmHg; under conditions of a hyperbaric
chamber, the pO2 can reach values greater than 2000mmHg [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 transported by haemoglobin [Albuquerque e
Sousa, 2007].
After removal from the hyperbaric oxygen environment, the PaO2 normalizes in minutes, but the PtO2 may remain
elevated for a variable period. The rate of normalization of PtO2 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 shortterm effects such as vasoconstriction and enhanced oxygen delivery,
reduction of oedema, phagocytosis activation and also an anti-inflammatory 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 provides a significant increase in oxygen availability at the tissue level, as selective
hyperoxic and not hypoxic vasoconstriction, occurring predominantly 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 extremities 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 contribution in the stimulation of reparative and regenerative
processes in some diseases [Mortensen, 2008].
Also many cell and tissue functions are dependent 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
sodium–potassium pump. HBO has the effect of inhibiting leukocyte adhesion to the endothelium, diminishing tissue
damage, which enhances leukocyte motility and improves microcirculation [Mortensen, 2008]. This occurs when the
presence 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,
provokes 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
capillary bed. Two-hour daily treatments with HBO are apparently responsible for stimulating the 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, producing 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 production of collagen matrix and
subsequent angiogenesis, 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 equivalents 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 keratinocyte
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
fibroblasts grown in a serum-free culture environment, 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 dysfunction, restores this defence and also increases the phagocytosis of some bacteria by working
synergistically 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 bactericidal 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 anaemia, 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 bacterial 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-1α, which promotes, for example, the glycolytic system,
vascularization and angiogenesis, has been shown to be important. However, if the oxygen supply could be controlled
without promoting blood flow, the blood vessel permeability could be controlled to reduce swelling and consequently
sharp pain.
In the proliferative phase, in musculoskeletal tissues (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 provided 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 suggested in the scientific literature as a
therapy 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 30–40 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 concordant with those obtained by Fischer and colleagues
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 fractures and ligament injuries,
have proved to benefit 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 Hölmich, 2005].
In sport events in the United States, the incidence 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 [Järvinen 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,
consequently, to their rupture near the myotendinous junction [Järvinen 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 Hölmich, 2005]. DOMS usually occurs
following unaccustomed physical activity and is accompanied by a sensation of discomfort within the skeletal 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, subsides and eventually disappears by 5–7 days postexercise
[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 following 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 12–
48 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 intensity of exercise.
Staples and colleagues in an animal study, used a downhill running model to induce damage, and observed significant
changes in the myeloperoxidase 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 inflammatory process or the
ability to actually modulate the injury to the tissue.
In 1999, the same group conducted a randomized, 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 [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 treatment and sham treatment). The hyperbaric exposures 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 significant 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 allocation of groups was not clarified), which makes
interpretation difficult [Bennett et al. 2005a].
Mekjavic and colleagues did not find any recovery 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 inducing 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 exercise-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 3–4 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 randomized, 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 multiple 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 randomly assigned into two groups [Germain et al. 2003]: the control group that did not
undergo 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 significant 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 colleagues wanted to analyse whether HBO improved functional and
morphologic recovery after a controlled induced muscle stretch in the tibialis anterior muscle–tendon 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 compared 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 formation of lactate and depletion of high-energy phosphates 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 factors, during reperfusion, may cause further damage to local and remote tissues.
However, the mechanisms of ischemia–reperfusion-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 concentration, 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 oxidation in the mitochondria. This maintains the transport of ions and molecules
across the cell membrane and optimizes the possibility of preserving the muscle cell structure.
Gregorevic and colleagues induced muscle degeneration in rats in order to see whether HBO hastens the functional
recovery and myofiber 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 compromised blood supply or with the repair of associated nerve components, as seen in ischemia, but with
the pressure of oxygen inspired with a crucial role in improving the maximum force-producing 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 quantifying the severity of sprains [Staples and Clement, 1996].
Interestingly, Borromeo and colleagues, in a randomized, 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 session and 60 minutes for the other two. The placebo group was exposed
to ambient air, at 1.1 ATA for 90 minutes, both groups for three sessions 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 treatment duration [Bennett et al. 2005a].
Medical Collateral Ligament
Horn and colleagues in an animal study surgically lacerated medial collateral ligament of 48 rats [Horn et al. 1999].
Half were controls without intervention and the other half were exposed to HBO at 2.8 ATA for 1.5 hours 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 deposition as measured by collagen synthesis.
Mashitori and colleagues removed a 2-mm segment 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 increasing 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 neovascularization at the tendon–bone
junction, collagen fibres of the tendon graft and the tendon graft–bony 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 increasing 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 animals
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 procollagen 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 promoting 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 lyophilized 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 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 successfully resolved after
20–30 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
suppresses 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 properties 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 muscle–tendon junctions and ligaments.
With regards to HBO treatment, it is still necessary to determine the optimal conditions for these orthopaedic
indications, such as the atmosphere pressure, the duration of sessions, the frequency 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 ligaments 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 treatments are multifactorial and are rarely published. Therefore, there is a need for larger samples, randomized,
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 treatment
Hyperbaric Oxygen Therapy and its role in Sports Medicine
Hyperbaric Oxygen Therapy and its role in Sports Medicine
In recent years, professional and college teams have started using hyperbaric oxygen therapy (HBO2) to treat sports injuries. From muscle contusions and ankle sprains to delayed-onset muscle soreness, HBO2 has been used to facilitate soft-tissue healing (1-7). To minimize the time between injury and HBO2 treatment, some professional sports teams have on-site centers. Because of the importance of oxygen in the aerobic energy system, many athletes and researchers have also investigated the possible ergogenic effects of HBO2.
Hyperbaric oxygen (HBO2) is used in a sports medicine setting to reduce hypoxia and edema and appears to be particularly effective for treating crush injuries and acute traumatic peripheral ischemias. When used clinically, HBO2 should be considered as an adjunctive therapy as soon as possible after injury diagnosis.
During HBO2 treatment, a patient breathes 95% to 100% oxygen at pressures above 1.0 atmosphere absolute (ATA). Normally, 97% of the oxygen delivered to body tissues is bound to hemoglobin, while only 3% is dissolved in the plasma. At sea level, barometric pressure is 1 ATA, or 760 mm Hg, and the partial pressure of oxygen in arterial blood (PaO2) is approximately 100 mm Hg. At rest, the tissues of the body consume about 5 mL of O2 per 100 mL of blood. During HBO2 treatments, barometric pressures are usually limited to 3 ATA or lower. The oxygen content of inspired air in the chamber is typically 95% to 100%. The combination of increased pressure (3 ATA) and increased oxygen concentration (100%) dissolves enough oxygen in the plasma alone to sustain life in a resting state. Under hyperbaric conditions, oxygen content in the plasma is increased from 0.3 to 6.6 mL per 100 mL of blood with no change in oxygen transport via hemoglobin. HBO2 at 3.0 ATA increases oxygen delivery to the tissues from 20.0 to 26.7 mL of O2 per 100 mL of blood.
Proposed Healing Mechanisms Increased oxygen delivery to the tissues is believed to facilitate healing through a number of mechanisms.
Vasoconstriction.
High tissue oxygen concentrations cause blood vessels to constrict, which can lead to a 20% decrease in regional blood flow (10). In normoxic environments, tissue hypoxia may develop; however, this is not the case with HBO2. The decrease in regional blood flow is more than compensated for by the increased plasma oxygen that reaches the tissue. The net effect is decreased tissue inflammation without hypoxia--a mechanism by which hyperbaric oxygen therapy is believed to improve crush injuries, thermal burns, and compartment syndrome (11,12).
Neovascularization and epithelialization.
High tissue oxygen concentrations accelerate the development of new blood vessels (12). This can be induced in both acute and chronic injuries. Regenerating epithelial cells also function more effectively in a high-oxygen environment (13). These effects have proven effective in treating tissue ulcers and skin grafts (14).
Stimulation of fibroblasts and osteoclasts.
In a hypoxic milieu, fibroblasts are unable to synthesize collagen, and osteoclasts are unable to lay down new bone (7,14,15). Collagen deposition, wound strength, and the rate of wound healing are affected by the amount of available oxygen. Ischemic areas of wounds benefit most from the increased delivery of oxygen (16). HBO2 increases tissue levels of oxygen, allowing for fibroblasts and osteoclasts to function appropriately (13,17). This mechanism may play a role in the treatment of osteomyelitis and slowly healing fractures.
Immune response.
When tissue oxygen tensions fall below 30 mm Hg, host responses to infection and ischemia are compromised (18). Studies have shown that the local tissue resistance to infection is directly related to the level of oxygen found in the tissue (19,20). High oxygen concentrations may prevent the production of certain bacterial toxins and may kill certain anaerobic organisms such as Clostridium perfringens. More important, however, oxygen aids polymorphonuclear leukocytes (PMN). Oxygen is believed to aid the migration and phagocytic function of the PMN (21). Oxygen is converted within the PMN into toxic substrates (superoxides, peroxides, and hydroxyl radicals) that are lethal to bacteria (16,22). These effects on the immune system allow HBO2 to aid the healing of soft-tissue infections and osteomyelitis (21). HBO2 has also been found to inhibit PMN adherence on postcapillary venules (23). Although this may seem paradoxic, this effect is beneficial because it helps limit reperfusion injury after crush injury and compartment syndrome.
Maintaining high-energy phosphate bonds.
When circulation to a wound is compromised, resultant ischemia lowers the concentration of adenosine triphosphate (ATP) and increases lactic acid levels. ATP is necessary for ion and molecular transport across cell membranes and maintainance of cellular viability (24,25). Increased oxygen delivery to the tissue with HBO2 may prevent tissue damage by decreasing the tissue lactic acid level and helping maintain the ATP level. This may help prevent tissue damage in ischemic wounds and reperfusion injuries. HBO2 is an effective treatment for crush injuries and other acute traumatic peripheral ischemias because it alleviates hypoxia and reduces edema; however, clinical experience with HBO2 for sports injuries is limited. Also, the criteria for using HBO2 in acute traumatic peripheral ischemias are not clearly established. HBO2 should be considered as an adjunctive therapy as soon as possible after injury diagnosis. Treatment pressures for acute traumatic peripheral ischemia range from 2.0 to 2.5 ATA, with a minimum of 90 minutes for each treatment (26). HBO2 has been used to treat joint, muscle, ligament, and tendon injuries in soccer players in Scotland. When HBO2 was used in conjunction with physiotherapy, the time to recovery was reduced by 70% (27). The results compared a physiotherapist's estimation of the time course for the injury and the actual number of training days missed. The absence of a control group and objective measures to assess the injury weaken the encouraging findings in this study. HBO2 has been used to treat acute ankle injuries. Borromeo et al (1) conducted a randomized double-blind study of 32 patients who had acute ankle sprains to compare HBO2 treatment at 2.0 ATA with a placebo treatment. Each group received three treatments: one for 90 minutes and two for 60 minutes. The improvement in joint function was greater in the HBO2 group compared with the placebo group. There were no statistically significant differences between the groups when assessed for subjective pain, edema, passive or active range of motion, or time to recovery. Study limitations included an average delay of 34 hours from the time of injury to diagnosis, administration of only three treatments within 7 days, treatment pressure of only 2.0 ATA, and short treatment duration.
References
Borromeo CN, Ryan JL, Marchetto PA, et al: Hyperbaric oxygen therapy for acute ankle sprains. Am J Sports Med 1997;25(5):619-625 James PB: New horizons in hyperbaric oxygenation. Adv Exp Med Biol 1997;428:129-133 Kaijser L: Physical exercise under hyperbaric oxygen pressure. Life Sci 1969;8(pt 1):929-934 Nylander G, Lewis D, Nordstrom H, et al: Reduction of postischemic edema with hyperbaric oxygen. Plast Reconstr Surg 1985;76(4):596-603 Nylander G, Nordstrom H, Franzen L, et al: Effects of hyperbaric oxygen treatment in post-ischemic muscle: a quantitative morphological study. Scand J Plast Reconstr Surg 1988;22(1):31-39 Sirsjo A, Lehr HA, Nolte D, et al: Hyperbaric oxygen treatment enhances the recovery of blood flow and functional capillary density in postischemic striated muscle. Circ Shock 1993;40(1):9-13 Staples JR, Clement DB, Taunton JE, et al: Effects of hyperbaric oxygen on a human model of injury. Am J Sports Med 1999;27(5):600-605 Undersea and Hyperbaric Medical Society: in Hampson NB (ed): Hyperbaric Oxygen Therapy: Committee Report 1999. Kensington, MD, 1999, pp 1-82 Arntzenius AKW: De Pneumatische Therapie. Scheltema & Holkemas, Boekhandel, Amsterdam, 1887 Marino PL: Oxygen transport, in Marino PL (ed): The ICU Book, ed 1. Philadelphia, Lea & Febiger, 1991, pp 14-24 Clark JM, Lambertsen CJ: Alveolar-arterial O2 differences in man at 0.2, 1.0, 2.0, and 3.5 Ata inspired PO2. J Appl Physiol 1971;30(5):753-763 Boerema I, Meyne NG, Brummelkamp WK, et al: Life without blood: a study of the influence of high atmospheric pressure and hypothermia on dilution of the blood. J Cardiovasc Surg 1960;1:161-164 Bird AD, Telfer AM: Effect of hyperbaric oxygen on limb circulation. Lancet 1965;13(1):355-356 Bouachour G, Cronier P, Gouello JP, et al: Hyperbaric oxygen therapy in the management of crush injuries: a randomized double-blind placebo-controlled clinical trial. J Trauma 1996;41(2):333-339 Knighton DR, Halliday B, Hunt TK: Oxygen as an antibiotic: the effect of inspired oxygen on infection. Arch Surg 1984;119(2):199-204 LaVan FB, Hunt TK: Oxygen and wound healing. Clin Plast Surg 1990;17(3):463-472 Davis JC, Hunt TK (eds): Problem Wounds: The Role of Oxygen. New York City, Elsevier, 1988, pp 5-30 Weiss EL: Connective tissue in wound healing, in McCulloch JM, Kloth LC, Feedar JA (eds): Wound Healing: Alternatives in Management, ed 2. Philadelphia, FA Davis Co, 1994, pp 16-31 Hammarlund C: The physiologic effects of hyperbaric oxygenation, in Whelan HT, Kindwall EP (eds): Hyperbaric Medicine Practice, ed 2. Flagstaff, Arizona, Best Pub Co, 1995, pp 37-68 Jonsson K, Jensen JA, Goodson WH III, et al: Tissue oxygenation, anemia, and perfusion in relation to wound healing in surgical patients. Ann Surg 1991;214(5):605-613 Hunt TK, Zederfeldt B, Goldstick TK: Oxygen and healing. Am J Surg 1969;118(4):521-525 Chang N, Mathes SJ: Comparison of
the effect of bacterial inoculation in musculocutaneous and random-pattern flaps. Plast Reconstr Surg 1982;70(1):1-10 Gottrup F, Firmin R, Hunt TK, et al: The dynamic properties of tissue oxygen in healing flaps. Surgery 1984;95(5):527-536 Knighton DR, Halliday B, Hunt TK: Oxygen as an antibiotic: a comparison of the effects of inspired oxygen concentration and antibiotic administration on in vivo bacterial clearance. Arch Surg 1986;121(2):191-195 Badwey JA, Karnovsky ML: Active oxygen species and the functions of phagocytic leukocytes. Annu Rev Biochem 1980;49:695-726 Zamboni WA, Roth AC, Russell RC, et al: The effect of acute hyperbaric oxygen therapy on axial pattern skin flap survival when administered during and after total ischemia. J Reconstr Microsurg 1989;5(4):343-347 Nylander G, Nordstrom H, Lewis D, et al: Metabolic effects of hyperbaric oxygen in postischemic muscle. Plast Reconstr Surg 1987;79(1):91-97 Stewart RJ, Yamaguchi KT, Mason SW, et al: Tissue ATP levels in burn injured skin treated with hyperbaric oxygen, abstracted. Undersea Biomed Res 1989;16(suppl):53 Staples J, Clement D: Hyperbaric oxygen chambers and the treatment of sports injuries. Sports Med 1996;22(4):219-227 James PB, Scott B, Allen MW: Hyperbaric oxygen therapy in sports injuries. Physiotherapy 1993;79(8):571-572 Potera C: Healing under pressure. Phys Sportsmed 1995;23(11):46-47 Cabric M, Medved R, Denoble P, et al: Effect of hyperbaric oxygenation on maximal aerobic performance in a normobaric environment. J Sports Med Phys Fitness 1991;31(3):362-366 Webster AL, Syrotuik DG, Bell GJ, et al: Exercise after acute hyperbaric oxygenation: is there an ergogenic effect? Undersea Hyperb Med 1998;25(3):153-159 McGavock JM, Lecomte JL, Delaney JS, et al: Effects of hyperbaric oxygen on aerobic performance in a normobaric environment. Undersea Hyperb Med 1999;26(4):219-224 Kelly DL Jr, Lassiter KR, Vongsvivut A, et al: Effects of hyperbaric oxygenation and tissue oxygen studies in experimental paraplegia. J Neurosurg 1972;36(4):425-429 Fernau JL, Hirsch BE, Derkay C, et al: Hyperbaric oxygen therapy: effect on middle ear and eustachian tube function. Laryngoscope 1992;102(1):48-52 Kindwall E: Contraindications and side effects to hyperbaric oxygen treatment, in Whelan HT, Kindwall EP (eds): Hyperbaric Medicine Practice, ed 2. Flagstaff, AZ, Best Pub Co, 1995 pp 83-97 Stone JA, Loar H, Rudge FW: An eleven year review of hyperbaric oxygenation in a military clinical setting, abstracted. Undersea Biomed Res 1991;18(suppl):80 Lyne AJ: Ocular effects of hyperbaric oxygen. Trans Ophthalmol Soc UK 1978;98(1):66-68 Palmquist BM, Philipson B, Barr PO: Nuclear cataract and myopia during hyperbaric oxygen therapy. Br J Ophthalmol 1984;68(2):113-117 Patz A: The effect of oxygen on immature retinal vessels. Invest Ophthalmol 1965;4(6):988-989
In recent years, professional and college teams have started using hyperbaric oxygen therapy (HBO2) to treat sports injuries. From muscle contusions and ankle sprains to delayed-onset muscle soreness, HBO2 has been used to facilitate soft-tissue healing (1-7). To minimize the time between injury and HBO2 treatment, some professional sports teams have on-site centers. Because of the importance of oxygen in the aerobic energy system, many athletes and researchers have also investigated the possible ergogenic effects of HBO2.
Hyperbaric oxygen (HBO2) is used in a sports medicine setting to reduce hypoxia and edema and appears to be particularly effective for treating crush injuries and acute traumatic peripheral ischemias. When used clinically, HBO2 should be considered as an adjunctive therapy as soon as possible after injury diagnosis.
During HBO2 treatment, a patient breathes 95% to 100% oxygen at pressures above 1.0 atmosphere absolute (ATA). Normally, 97% of the oxygen delivered to body tissues is bound to hemoglobin, while only 3% is dissolved in the plasma. At sea level, barometric pressure is 1 ATA, or 760 mm Hg, and the partial pressure of oxygen in arterial blood (PaO2) is approximately 100 mm Hg. At rest, the tissues of the body consume about 5 mL of O2 per 100 mL of blood. During HBO2 treatments, barometric pressures are usually limited to 3 ATA or lower. The oxygen content of inspired air in the chamber is typically 95% to 100%. The combination of increased pressure (3 ATA) and increased oxygen concentration (100%) dissolves enough oxygen in the plasma alone to sustain life in a resting state. Under hyperbaric conditions, oxygen content in the plasma is increased from 0.3 to 6.6 mL per 100 mL of blood with no change in oxygen transport via hemoglobin. HBO2 at 3.0 ATA increases oxygen delivery to the tissues from 20.0 to 26.7 mL of O2 per 100 mL of blood.
Proposed Healing Mechanisms Increased oxygen delivery to the tissues is believed to facilitate healing through a number of mechanisms.
Vasoconstriction.
High tissue oxygen concentrations cause blood vessels to constrict, which can lead to a 20% decrease in regional blood flow (10). In normoxic environments, tissue hypoxia may develop; however, this is not the case with HBO2. The decrease in regional blood flow is more than compensated for by the increased plasma oxygen that reaches the tissue. The net effect is decreased tissue inflammation without hypoxia--a mechanism by which hyperbaric oxygen therapy is believed to improve crush injuries, thermal burns, and compartment syndrome (11,12).
Neovascularization and epithelialization.
High tissue oxygen concentrations accelerate the development of new blood vessels (12). This can be induced in both acute and chronic injuries. Regenerating epithelial cells also function more effectively in a high-oxygen environment (13). These effects have proven effective in treating tissue ulcers and skin grafts (14).
Stimulation of fibroblasts and osteoclasts.
In a hypoxic milieu, fibroblasts are unable to synthesize collagen, and osteoclasts are unable to lay down new bone (7,14,15). Collagen deposition, wound strength, and the rate of wound healing are affected by the amount of available oxygen. Ischemic areas of wounds benefit most from the increased delivery of oxygen (16). HBO2 increases tissue levels of oxygen, allowing for fibroblasts and osteoclasts to function appropriately (13,17). This mechanism may play a role in the treatment of osteomyelitis and slowly healing fractures.
Immune response.
When tissue oxygen tensions fall below 30 mm Hg, host responses to infection and ischemia are compromised (18). Studies have shown that the local tissue resistance to infection is directly related to the level of oxygen found in the tissue (19,20). High oxygen concentrations may prevent the production of certain bacterial toxins and may kill certain anaerobic organisms such as Clostridium perfringens. More important, however, oxygen aids polymorphonuclear leukocytes (PMN). Oxygen is believed to aid the migration and phagocytic function of the PMN (21). Oxygen is converted within the PMN into toxic substrates (superoxides, peroxides, and hydroxyl radicals) that are lethal to bacteria (16,22). These effects on the immune system allow HBO2 to aid the healing of soft-tissue infections and osteomyelitis (21). HBO2 has also been found to inhibit PMN adherence on postcapillary venules (23). Although this may seem paradoxic, this effect is beneficial because it helps limit reperfusion injury after crush injury and compartment syndrome.
Maintaining high-energy phosphate bonds.
When circulation to a wound is compromised, resultant ischemia lowers the concentration of adenosine triphosphate (ATP) and increases lactic acid levels. ATP is necessary for ion and molecular transport across cell membranes and maintainance of cellular viability (24,25). Increased oxygen delivery to the tissue with HBO2 may prevent tissue damage by decreasing the tissue lactic acid level and helping maintain the ATP level. This may help prevent tissue damage in ischemic wounds and reperfusion injuries. HBO2 is an effective treatment for crush injuries and other acute traumatic peripheral ischemias because it alleviates hypoxia and reduces edema; however, clinical experience with HBO2 for sports injuries is limited. Also, the criteria for using HBO2 in acute traumatic peripheral ischemias are not clearly established. HBO2 should be considered as an adjunctive therapy as soon as possible after injury diagnosis. Treatment pressures for acute traumatic peripheral ischemia range from 2.0 to 2.5 ATA, with a minimum of 90 minutes for each treatment (26). HBO2 has been used to treat joint, muscle, ligament, and tendon injuries in soccer players in Scotland. When HBO2 was used in conjunction with physiotherapy, the time to recovery was reduced by 70% (27). The results compared a physiotherapist's estimation of the time course for the injury and the actual number of training days missed. The absence of a control group and objective measures to assess the injury weaken the encouraging findings in this study. HBO2 has been used to treat acute ankle injuries. Borromeo et al (1) conducted a randomized double-blind study of 32 patients who had acute ankle sprains to compare HBO2 treatment at 2.0 ATA with a placebo treatment. Each group received three treatments: one for 90 minutes and two for 60 minutes. The improvement in joint function was greater in the HBO2 group compared with the placebo group. There were no statistically significant differences between the groups when assessed for subjective pain, edema, passive or active range of motion, or time to recovery. Study limitations included an average delay of 34 hours from the time of injury to diagnosis, administration of only three treatments within 7 days, treatment pressure of only 2.0 ATA, and short treatment duration.
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