Sports injuries and hyperbaric oxygen therapy: physiological effects and previous findings

Abstract

Problems encountered in the management of sports injuries can lead to a prolonged treatment process and a long period of time away from sports that may cause significant economic loss, as well. To ensure the most effective return to sports, a multidisciplinary approach is often required.

Research has demonstrated that hyperbaric oxygen therapy (HBOT) shows promising results as a treatment modality for sports injuries. A search of the scientific literature was conducted using the keywords "hyperbaric oxygen therapy" and "sports injuries" across PubMed, Cochrane Library, and Web of Science databases. The positive effects of HBOT have been reported in the treatment of various sports injuries, including muscle and soft tissue injuries, as well as bone marrow edema.

This review examines the physiological effects of hyperbaric oxygen therapy, as well as the findings obtained from animal injury models and human clinical studies on its use in sports injuries. The effects of HBOT vary depending on the type of injury, and it is generally more beneficial as an adjunctive treatment rather than as a standalone therapy.

Although numerous studies have been published, a standardized treatment protocol has yet to be established. However, based on current protocols in the literature, it is believed that a 90- to 120-minute treatment session, administered at least five days per week at 2.0-2.5 ATA, will provide the greatest benefit. The total number of sessions should be determined by the physician following the treatment, based on the patient's specific condition and needs.

Introduction

Competing in sports involves significant engagement of various body parts. The pressure to succeed often leads athletes to train without being adequately physically prepared for competitions. Insufficient recovery and improper training can result in decreased performance, fatigue, and an increased risk of injury (1). The approach of the sports physician to injury management plays a critical role in an athlete's ability to resume regular activity. Failure to promptly diagnose and properly manage sports injuries can lead to extended absences from athletic activities. This can also result in substantial financial costs for both amateur and professional sports (2).

Fair and Champa estimate that eliminating contact in college sports could save up to $18.4 billion annually (3). In the English Premier League, injury-related performance declines lead to losses of approximately £900 million GBP each season (4). In the Netherlands, sports injuries cost over €3 billion per year (5).

The management of sports injuries often requires a multidisciplinary approach to ensure that athletes can return to training as quickly as possible. Research indicates that hyperbaric oxygen therapy shows considerable promise in the management of sports injuries (6,7). Many elite athletes from diverse sports, including tennis, swimming, basketball, and golf, have reported using hyperbaric oxygen therapy as part of their recovery (8).

Hyperbaric Oxygen Therapy

Hyperbaric Oxygen Therapy (HBOT) involves the intermittent administration of 100% oxygen at a pressure greater than one atmosphere absolute (ATA) in a closed chamber. For the treatment to be clinically effective, the pressure must be at least 1.4 ATA, though the typical range is between 2.0 and 3.0 ATA. According to the Undersea and Hyperbaric Medical Society (UHMS), for a treatment to be classified as hyperbaric oxygen therapy, the pressure must exceed 2.0 ATA. Treatment duration can be adjusted based on the patient's condition, typically lasting between 90 and 120 minutes. Patients breathe oxygen through a mask, hood, or endotracheal tube, in either a single or multi-patient chamber (9). The indications approved by UHMS and recommended by the European Committee on Hyperbaric Medicine are listed in Tables 1 and 2.

Physiological Effects of HBO₂ on Sports Injuries

The plasma oxygen concentration at sea level is approximately 3 ml/l (10). Under standard perfusion conditions, tissues require about 60 ml/l of oxygen at rest to maintain normal cellular metabolism. Without the contribution of oxygen bound to hemoglobin, dissolved oxygen at a pressure of 3 ATA is nearly sufficient to meet the resting total oxygen requirement of many tissues (11). By increasing PaO2, hyperbaric oxygen therapy (HBOT) promotes the proliferation of endothelial progenitor cells, neoangiogenesis, and neovascularization (12). Additionally, HBOT reduces cellular ischemia and edema and induces vasoconstriction by raising the concentration of extracellular oxygen (13).

HBOT also stimulates the mobilization of hypoxia-inducible factor 1-α, vascular endothelial growth factor (VEGF), stromal-derived factor 1, and bone marrow-derived stem cells (CD34), while reducing neutrophil adhesion through modification of integrin β-2, which helps attenuate ischemia-reperfusion injury (14-17). Furthermore, HBOT enhances cell growth and modulates the inflammatory response by increasing the production of reactive oxygen species (ROS) and reactive nitrogen species. This leads to improved vascularization and better tissue survival following ischemia. ROS play a crucial role in multiple pathways that facilitate neoangiogenesis and vasculogenesis, both of which are mediated by hypoxia-inducible factors (18,19).

Following muscle damage, inflammation is marked by the generation and release of inflammatory cytokines, increased vascular permeability, neutrophil migration, and edema (20). HBOT helps reduce edema through improved homeostatic processes and vasoconstriction. Moreover, by reducing tissue damage and inhibiting leukocyte adhesion to the endothelium, HBOT enhances leukocyte motility and improves microcirculation (21). HBOT accelerates the transition from the inflammatory to the proliferative phase (7). Horie et al. found that HBOT treatment accelerated satellite cell proliferation and myofiber maturation (22). Similarly, Oyaizu et al. reported that HBOT increased the number of proliferating and differentiating satellite cells, as well as regenerating muscle fibers (23).

Complications

Complications of HBO₂ are typically oxygen- or pressure-related and most often include barotrauma or oxygen toxicity affecting the central nervous system or pulmonary systems. Rarely, symptoms such as weakness, dizziness, hypoglycemia, and vision problems (e.g., reversible myopia) may occur. The most common complication is middle ear barotrauma. In a study involving 62,614 HBO₂ sessions with 2,334 patients, middle ear barotrauma occurred in 9.2% of patients and 0.04% of sessions. Other complications, such as hypoglycemia, oxygen toxicity, dizziness, anxiety reactions, shortness of breath, and chest pain, were reported in 0.5%-1.5% of patients (24).

Evaluating patients for potential risks before initiating HBO₂, taking precautions to prevent complications, and closely monitoring patients during treatment are critical for enhancing safety. Most adverse events can be effectively prevented or managed with simple measures. From this perspective, HBO₂ is considered one of the safest medical treatments. It is also important to note that patients undergoing HBO₂ often have multiple comorbidities, which may increase their risk of complications. Conversely, healthy individuals have a significantly lower likelihood of experiencing adverse effects.

WADA's Stance and Potential Risks for Athletes

In 2006, the World Anti-Doping Agency (WADA) banned the use of HBO₂ under the category of oxygen transfer enhancement. However, due to insufficient evidence supporting its potential to enhance performance, WADA reclassified supplemental oxygen as permitted in 2009. In 2016, it was further clarified that supplemental oxygen was allowed only via inhalation (25).

It is important to note that WADA may revise its stance or impose additional restrictions-such as limits on pressure or duration-if future evidence reveals new effects of HBO₂.

Moreover, although rare in healthy individuals, there is always a possibility of complications arising from HBO₂ use. Experiencing any severe complications could delay an athlete's return to the field.

HBO₂ Application in Different Types of Sports Injuries

Muscle Injuries

Muscle injuries encompass a wide range of conditions, including muscle strains, muscular contusions, delayed-onset muscle soreness, and muscle cramps (26). According to a study conducted between 2009 and 2015 on collegiate athletes, muscle strains were the second most common cause of sports suspension lasting more than 21 days (27).

Research on animals by Best et al. demonstrated that HBO₂ therapy promotes both morphological and functional recovery after acute muscular stretch injuries (28). Another animal study found that rats treated with HBO₂ following a muscular contusion exhibited lower levels of creatine kinase-an indicator of muscle injury-and an increase in muscle weight (29).

HBO₂ is beneficial not only for treating sports injuries but also for alleviating sports-related fatigue. During the Nagano Winter Olympics, Ishii and colleagues reported using HBO₂ as a recovery method for muscular fatigue. Their findings revealed that athletes who underwent HBO₂ therapy at a pressure as low as 1.3 ATA (approximately 11 feet below sea level) for short sessions of 30-40 minutes (averaging two sessions, with a maximum of six) experienced faster recovery times (30).

Additionally, other studies have shown a significant reduction in blood lactate concentration and notable improvements in maximal oxygen consumption and oxygen consumption at the anaerobic threshold following HBO₂ therapy (31, 32).

As previously reported in the literature, HBO₂ may also be effective in treating delayed-onset muscle soreness (DOMS). DOMS is characterized by soreness in skeletal muscles following intense exercise, typically resolving within 5-7 days (7). However, DOMS can lead to a temporary decline in physical performance and an increased risk of injury (33, 34). HBO₂ has been shown to enhance muscle strength, reduce pain, and accelerate recovery in individuals with DOMS.

Webster et al. investigated the effects of HBO₂ on recovery from exercise-induced muscle damage in a study involving 12 healthy males (35). Muscle damage was induced through calf raises performed to failure. Participants were divided into two groups: one received HBO₂ therapy (2.5 ATA with 100% oxygen for 60 minutes), while the other received a placebo (1.3 ATA with air). Treatments were administered at 3-4 hours, 24 hours, and 48 hours post-exercise. In the placebo group, isometric peak torque declined from baseline on days 1 and 2, whereas no such decline was observed in the HBO₂ group. By day 5, the HBO₂ group reported significantly lower levels of pain and soreness compared to the placebo group.

Staples et al. conducted the largest study on HBO₂ and DOMS, involving 66 untrained males, and demonstrated that HBO₂ significantly accelerated recovery in athletes (36). In this study, DOMS was induced in the non-dominant quadriceps, and pain and muscle torque were measured before, during, and after HBO₂ therapy. Participants were divided into four groups: HBO₂, delayed HBO₂, sham treatment, and control.

The HBO₂ group received 100% oxygen at 2.0 ATA for one hour at 0-, 24-, and 48-hours post-exercise, followed by sham treatments at 72 and 96 hours. The sham treatment group received 21% oxygen at 1.2 ATA for the same duration. The delayed HBO₂ group underwent sham treatments at 0- and 24-hours post-exercise, followed by HBO₂ therapy at 48, 72, and 96 hours. Results showed that the HBO₂ group exhibited significantly improved muscle torque compared to the other groups.

Harrison et al. investigated the use of HBO₂ for treating exercise-induced muscle injuries in 18 untrained, college-aged males (37). Participants were divided into three groups: immediate HBO₂, delayed HBO₂, and control. Muscle injury was induced in the non-dominant arm using preacher curls. The immediate HBO₂ group received oxygen therapy shortly after exercise and for the next four days, while the delayed group initially received sham treatments and began HBO₂ therapy later. Measurements included creatine kinase levels, muscle strength, soreness, and MRI scans. The study found no significant differences between the groups in any measure, suggesting that HBO₂ therapy did not facilitate soft tissue injury recovery. However, the authors cautioned that their findings might not fully apply to soft tissue athletic injuries due to the study's limitations. They suggested that HBO₂ could be more effective for injuries involving more extensive soft tissue damage or where oxygen availability is significantly compromised by the injury's location or severity of edema.

Babul et al. also explored the effects of intermittent HBO₂ on exercise-induced muscle damage in 16 females (38). Participants were divided into HBO₂ and control groups and subjected to 300 maximal eccentric contractions on the non-dominant leg, performed in 30 sets of 10 repetitions with 15-second rests between sets. The HBO₂ group received 100% oxygen at 2 ATA for 60 minutes, while the control group was exposed to 1.2 ATA with air. Four treatment sessions were conducted over four days. Measurements included muscle soreness, eccentric strength, quadriceps circumference, creatine kinase, malondialdehyde, and muscle signal intensity via MRI. No significant differences were observed between the groups. Presti et al. later noted that the small sample size limits the generalizability of these findings (39).

In contrast, Chen et al. studied 41 baseball players already experiencing exercise-induced muscle soreness or grade I muscle strain in their extremities (40). Participants were divided into an HBO₂ group and a placebo group while continuing their training routines. The HBO₂ group was exposed to normal air for 15 minutes while the chamber was pressurized to 2.5 ATA, followed by three 25-minute sessions of 100% oxygen with five-minute air breaks between sessions. The placebo group was pressurized to 1.3 ATA and received 100% oxygen only during depressurization. Treatments were conducted twice a week for five weeks. Blood samples were taken before therapy began, after the fifth and tenth sessions, and two weeks post-treatment to assess creatine phosphokinase, myoglobin, lactate, blood urea nitrogen, and glutamic oxaloacetic transaminase.

Results revealed significant reductions in glutamic oxaloacetic transaminase, myoglobin, creatine phosphokinase, and pain in the HBO₂ group after the fifth and tenth sessions. The HBO₂ group also reported significant improvements in pain intensity and interference compared to the control group. These findings suggest that HBO₂ is effective in reducing markers of muscle injury and alleviating pain, thereby supporting recovery.

Although multiple studies have concluded that HBO₂ has no significant effect on DOMS (6), methodological issues such as small sample sizes, lack of randomization and blinding, and contradictory study designs limit their reliability (41). Further large-scale, randomized controlled trials are needed to obtain more definitive conclusions.

Ligament Injuries

Ishii et al. investigated the effects of HBO₂ on ligament healing in the right hind limbs of 44 male Wistar rats with experimentally induced injuries (42). The rats were divided into four groups post-injury: (a) a control group that breathed room air in a hyperbaric chamber for 60 minutes; (b) HBO₂ at 1.5 ATA for 30 minutes once a day; (c) HBO₂ at 2 ATA for 30 minutes once a day; and (d) HBO₂ at 2 ATA for 60 minutes once a day. Fourteen days after the injury, the researchers compared gross appearance, histology, and pro-alpha (I) mRNA expression across groups. HBO₂ significantly enhanced ligament healing compared to the control group, with the most effective treatment being HBO₂ at 2 ATA for 60 minutes daily, as evidenced by increased extracellular matrix deposition and collagen synthesis.

Horn et al. evaluated HBO₂'s effects on healing lacerated medial collateral ligaments (MCL) in 48 Sprague-Dawley rats (43). The right MCL was surgically lacerated, while the left remained intact as a control. Half of the rats underwent daily HBO₂ at 2.8 ATA for 1.5 hours over five days. Stiffness and force to failure were assessed at 2, 4, 6, and 8 weeks post-surgery. At 4 weeks, the HBO₂ group showed significantly increased force to failure in the injured ligaments compared to the control group, though no additional improvements were observed by 6 weeks.

Mashitori et al. studied 76 Sprague-Dawley rats with a 2-mm segment of the MCL removed (44). Thirty-eight rats received HBO₂ at 2.5 ATA for 2 hours, five days a week, while the remaining rats were exposed to room air. The HBO₂ group exhibited more scar tissue, significantly higher Type I procollagen gene expression at 7 and 14 days, and greater tensile strength and stiffness at 14 days. These findings indicate that HBO₂ enhances scar tissue formation and improves ligament tensile properties.

In a double-blind, randomized, controlled study, Soolsma examined HBO₂'s effect on grade II MCL recovery in humans (45). The protocol included clinical assessments, MRI scans, and two weeks of either HBO₂ (2 ATA, 100% oxygen, one hour daily) or sham treatment (1.2 ATA). Results showed that HBO₂ reduced edema and muscle wasting, improved range of motion, and enhanced maximum knee flexion.

Takeyama et al. investigated the effects of HBO₂ on medial collateral ligament (MCL) and anterior cruciate ligament (ACL) injuries in 64 Sprague-Dawley rats (46). HBO₂-treated groups (2.5 ATA) displayed significantly higher Type I procollagen and TIMPs gene expression compared to controls. While HBO₂ improved structural protein synthesis and inhibited degradation in ACL injuries, it was insufficient for complete healing. The authors suggested that HBO₂ could enhance ACL surgery outcomes when used adjunctively.

Yeh et al. studied HBO₂'s effects on ACL reconstruction in rabbits (47). Forty rabbits were divided into an HBO₂ group (2.5 ATA, 100% oxygen, 2 hours daily) and a control group. Postoperative analyses revealed that the HBO₂ group exhibited increased Sharpey's fibers, enhanced neovascularization, and better tendon-bone integration. Biomechanical testing showed higher pullout strength, while electron microscopy revealed more compact collagen fibers in the HBO₂ group.

HBO₂ generally promotes ligament and tendon healing by enhancing scar tissue formation, collagen synthesis, and tensile strength. Its effectiveness is dose-dependent, with higher-pressure and longer-duration treatments yielding better results. However, some studies suggest benefits may plateau over time, highlighting the need for further research into optimal treatment protocols.

Bone Marrow Edema

Bone marrow edema is a common sports injury, particularly following acute trauma (48). If untreated, it can lead to complications such as osteonecrosis (49-51). Treatment options include pharmaceuticals like non-steroidal anti-inflammatory drugs (NSAIDs) and bisphosphonates, weight-bearing restrictions, and core decompression. However, these interventions may be less effective in cases of poor circulation (49,51,52).

HBO₂ therapy offers additional benefits, including circulation improvement and anti-edema effects. It also promotes bone regeneration by enhancing osteosynthesis, neoangiogenesis, and vasculogenesis (18). Studies show that HBO₂ stimulates the expression of osteogenic markers and increases mineral deposition in mesenchymal stem cells (53).

Clinical studies support the beneficial effects of HBO₂ on osteonecrosis and bone marrow edema. Numerous reports document reduced pain scores, improved range of motion, enhanced quality of life, and radiographic improvements in patients with avascular necrosis of the femoral head following HBO₂ therapy (54-60).

Moghamis et al. identified HBO₂ as a promising, non-invasive alternative to core decompression for treating non-traumatic pre-collapse avascular necrosis of the femoral head (61). Additionally, Ververidis et al. reviewed eight studies (2004-2018) and found that HBO₂ effectively resolved edema, relieved pain, and improved range of motion in patients unresponsive to conservative treatments. Although the time required for remission (15-90 sessions) was noted as a drawback, HBO₂ was highlighted as a potential alternative for these cases (51).

Conclusion

This systematic review examines the potential benefits of HBO₂ for various sports injuries. The literature is extensive, but standardization is challenging due to the diversity of injury types, the use of different animal models in experiments, the limited number of human studies, and the lack of randomization and blinding. Narrowing the scope of future reviews to specific injury types could improve the practical value of such studies.

HBO₂ appears more effective as an adjunctive treatment than a standalone therapy, with its impact varying by injury type. While no standardized treatment protocol has been established, evidence from existing studies suggests that a protocol involving 90 to 120 minutes of HBO₂ at 2.0-2.5 ATA for at least five days a week could be optimal. The total number of sessions should be tailored to the patient's condition.

Future research should focus on standardizing treatment protocols, evaluating long-term effects, and conducting randomized, controlled, double-blind clinical trials with larger human sample sizes, particularly among athletes. This would enable more precise conclusions about the efficacy of HBO₂ in sports injury management.

Despite some limitations, the literature provides encouraging evidence of HBO₂'s therapeutic potential for sports injuries. Continued research will help solidify its role as a valuable treatment modality.

Cite this article as: Canarslan Demir K, Avci, AU. Sports injuries and hyperbaric oxygen therapy: physiological effects and previous findings. Turk J Sports Med. 2025 Feb 18th; https://doi.org/10.47447/tjsm.0856

Both authors contributed to all stages of the manuscript writing process. All authors contributed to the final version of the manuscript and discussed the results and contributed to the final manuscript.

The authors declared no conflicts of interest with respect to authorship and/or publication of the article.

The authors received no financial support for the research and/or publication of this article.

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