Cianci P, Sato RM, Faulkner J. Adjunctive Hyperbaric Oxygen in the Treatment of Thermal Burns. Undersea Hyperb Med. 2026 Second Quarter; 53(2):363-390. A significant and consistently positive body of evidence from animal and human studies of thermal injury sup-ports the use of hyperbaric oxygen as a means of preventing dermal ischemia, reducing edema, modulating the zone of stasis, preventing partial- to full-thickness conversion, preserving cellular metabolism, dampening inflammation, preventing infection, and promoting healing. The overwhelming majority of clinical reports have shown reduced mortality, length of hospital stays, number of surgeries, and cost of care. Hyperbaric oxygen has been demonstrated to be safe in the hands of those thoroughly trained in rendering this therapy in the critical care setting and with appropriate monitoring precautions. Careful patient selection is mandatory.
Camporesi EM, Zanon V, Vezzani G, Bosco G. Avascular Necrosis (Aseptic Osteonecrosis). Undersea Hyperb Med. 2026 Second Quarter; 53(2):391-398. Avascular necrosis (AVN), also referred to as aseptic osteonecrosis (AO), can develop in several osseous districts of the body. Most commonly described is avascular necrosis of the femoral head (AVNFH), a debilitating and progressively disabling condition with partially understood, wide-ranging etiology and pathogenesis. Pathology is chiefly caused by a reduced vascularization of a terminal vascular bed, such as the one perfusing the femoral head, or similar vascular distributions such as femoral condyles, humeral head, the talus, the calcaneus, the navicularis, and other bony structures. Hypoxic conditions mediate the condition and can improve with a course of hyperbaric oxygen (HBO2). The Ficat classification is one of the most widely used staging systems for AVN of the femoral head. It classifies patients with osteonecrosis into four stages based on the appearance on a plain radiograph, at least before the advent of MRI, the ultimate golden standard for the specific case. I- Pain but no radiographic anomalies II- Increased density, cystic changes, or porosity III- Flattening of the femoral head and crescent sign IV- Full collapse of the femoral head with decrease in joint space Many of the treatment options proposed aim to achieve joint preservation. However, when the radiological signs progress to advanced bone collapse in the articular capsule, the single mandatory surgery approach is a femoral head replacement with total hip arthroplasty (THA).
Introduction:We hereby present a case of abdominal pain resulting from a hemolytic reaction after diving. Case Report:The patient had preexisting hemolytic anemia triggered by cold stimuli. We hypothesize that the hemolysis was induced by cold stimuli during winter diving. Discussion:It is recommended that individuals with a preexisting hemolytic anemia refrain from diving.
Introduction:Carbon monoxide (CO) poisoning is a serious public health concern that induces acute hypoxia, leading to organ damage. The effects of CO exposure on renal function remain insufficiently studied. This study aimed to investigate the impact of CO poisoning on kidney function and structure in an experimental rat model and to evaluate the role of hypoxia-inducible factor-2 alpha (HIF-2α) in this process. Methods:A total of 69 female Wistar Albino rats were used in the study. The rats were divided into a control group (n=9) and experimental groups exposed to CO poisoning and sacrificed at one hour (n=12), six hours (n=12), 12 hours (n=12), 24 hours (n=12), and 48 hours (n=12) post-exposure. CO exposure was administered at a concentration of 5000 ppm for 60 minutes. Blood gas analysis was performed, histopathological changes were evaluated using hematoxylin and eosin (H&E) staining, and HIF-2α expression was assessed via immunohistochemistry. Results:Significant histopathological changes were observed in kidney tissue following CO poisoning, including tubular degeneration, epithelial necrosis, and necrotic debris accumulation (p<0.001). Blood gas analysis showed a significantly elevated carboxyhemoglobin (COHb) level at one hour post-exposure (p<0.001), which returned to normal after six hours. Immunohistochemical analysis revealed a significant increase in HIF-2α expression following CO exposure (p<0.001), with a positive correlation between HIF-2α expression and tubular damage. Discussion:CO poisoning induces renal tubular injury and increases HIF-2α expression as a hypoxic response. These findings suggest that HIF-2α could serve as a potential biomarker for assessing renal damage due to CO exposure. Further studies are needed to evaluate the diagnostic and therapeutic implications of these findings in CO poisoning.
Introduction:Swimming-induced pulmonary edema (SIPE) occurs in physically demanding environments. SIPE has been identified among U.S. Naval Special Warfare (NSW) candidates, risking trainees' lives or, less severely, preventing them from completing training. Diagnosis is based on clinical examination and chest X-ray. The MediPines gas exchange monitor AGM-100 is a noninvasive diagnostic tool approved by the FDA and used in hospital settings. This study aimed to assess noninvasive physiological parameters and evaluate the use of the AGM-100 in NSW candidates with SIPE. Methods:In this observational study, eighteen subjects were tested (nine with confirmed SIPE). Data on a noninvasive surrogate for oxygen deficit, based on end-tidal oxygen (EtO₂),carbon dioxide (EtCO₂), and SpO₂ were collected. Chest X-rays (CXR) were graded for interstitial and airspace edema. Results:Subjects with confirmed SIPE displayed an oxygen deficit (28.1 ± 12.9 mm Hg), while eight of nine subjects without SIPE did not (3.1 ± 8.79 mm Hg, p < 0.001). There were no differences in EtCO₂. SpO₂ was lower in individuals with confirmed SIPE (95.1 ± 2.23%) compared to controls/unconfirmed SIPE (98.1 ± 0.31%, p-value < 0.0001). The group with the oxygen deficit had a correspondingly worse edema grade on CXR. Discussion:These limited results showed a possible correlation between O₂ deficit and SIPE, while the AGM-100 performed reliably in this prehospital setting. Future higher-powered studies are needed to substantiate these findings and the AGM-100's utility, possibly extending to other environments, such as combat field hospitals, for rapid diagnosis and severity assessment of pulmonary edema.
Introduction:Cerebral arterial gas embolism (CAGE) is a rare but potentially fatal condition that can occur when air enters the arterial circulation. Case Report:This case report describes a 64-year-old female patient who experienced a sudden onset of left lower extremity weakness and bilateral vision loss following a session of intravenous ozone therapy. Initial diagnostic imaging did not reveal any acute abnormalities. However, her clinical presentation was consistent with CAGE. She was initially administered emergent hyperbaric oxygen (HBO₂) at 2.8 ATA, followed by additional sessions at 2.0 ATA, which led to progressive symptomatic improvement and full resolution of her visual and motor deficits. Discussion:This case highlights the importance of recognizing the potential complications of intravenous ozone therapy, including CAGE. Hyperbaric oxygen treatment should be considered an option for patients with AGE following this procedure.
Introduction:Methemoglobinemia is a rare but potentially serious condition characterized by an increased level of methemoglobin in the blood, which impairs oxygen delivery to tissues. It occurs when hemoglobin's ferrous iron (Fe2+) is oxidized to ferric iron (Fe3+), rendering it unable to bind oxygen effectively. This leads to tissue hypoxia, which can manifest clinically as cyanosis, shortness of breath, fatigue, and, in severe cases, organ dysfunction. Case Report:Nitrofurantoin-induced hemolytic anemia and methemoglobinemia in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency are rare but potentially life-threatening complications. We present the case of a 64-year-old female with G6PD deficiency who developed acute hemolytic anemia and methemoglobinemia following nitrofurantoin therapy for a urinary tract infection. Her initial symptoms included fatigue, jaundice, and dyspnea, progressing rapidly to severe anemia and cyanosis. Laboratory investigations confirmed hemolysis and elevated methemoglobin levels. Although methemoglobinemia is commonly treated with methylene blue, its use in G6PD-deficient patients can exacerbate hemolysis. In this case, we promptly discontinued nitrofurantoin and managed the patient with hyperbaric oxygen treatment, intravenous ascorbic acid, and other supportive measures. Despite aggressive treatment, she required blood transfusion support and prolonged hospitalization. Discussion:This case underscores the importance of recognizing the potential for nitrofurantoin-induced hemolytic anemia and methemoglobinemia in G6PD-deficient individuals, highlighting the need for careful drug selection and vigilant monitoring in this population.
Introduction:Unlike traditional hyperbaric oxygen treatment, which involves the inhalation of 100% oxygen by individuals enclosed in a pressurized treatment chamber at greater than sea level, mild hyperbaric oxygen treatment is performed in a pressurized chamber using shallower treatment depths and lower oxygen concentrations. Methods:This narrative review examines the physiological differences between mild and traditional hyperbaric oxygen treatment, the clinical uses of mild hyperbaric oxygen treatment, and the safety considerations of both treatment modalities. Results:The systemic hyperoxia induced by traditional hyperbaric oxygen treatment promotes wound healing but is associated with adverse events, including oxygen free radical damage. Mild hyperbaric oxygen treatment may benefit peripheral microcirculation, parasympathetic activity, and metabolism but has not been studied extensively as a wound treatment modality. Due to the lower oxygen concentrations used in mild hyperbaric oxygen treatment, the risk of oxidative damage may be lower with this treatment than with traditional hyperbaric oxygenation. However, both mild and traditional hyperbaric oxygenation are associated with potentially life-threatening adverse events, including chamber explosion and/or fire. Careful adherence to safety standards may reduce the occurrence risk of such incidents, but compliance with those standards is not universally mandated and may vary among facilities. Discussion:Traditional and mild hyperbaric oxygen treatment differ in physiology and clinical uses. Both treatments are associated with significant risks, but adherence to safety standards may reduce the incidence of adverse events and optimize patient care.
Introduction:Severe sudden sensorineural hearing loss (SSNHL) is a challenging otological emergency. Hyperbaric oxygen (HBO₂) treatment is an adjunctive treatment for SSNHL, improving oxygen supply and microcirculation and reducing oxidative stress. While HBO₂ is increasingly used for SSNHL, the temporal patterns of hearing recovery during extended treatment protocols remain poorly characterized. This study investigates the frequency-specific recovery patterns and speech recognition improvements during a 30-session HBO₂ protocol with concurrent steroid treatment in patients with severe SSNHL. Methods:This multi-center, retrospective cohort study included patients diagnosed with severe SSNHL at four medical centers from January 2019 to December 2024. Inclusion criteria included patients who initiated HBO₂ with steroids within five days of onset, completed 30 HBO₂ sessions, and underwent pure-tone audiometry and speech recognition assessments at specified intervals. A total of 103 patients receiving combined HBO₂ and steroid treatment were analyzed using SPSS. Results:Low-frequency hearing (125 Hz, 250 Hz, and 500 Hz) exhibited rapid recovery, with significant enhancements noted after ten sessions of HBO₂ (P < 0.05). In contrast, mid-frequency hearing (1000 Hz and 1500 Hz) and high-frequency hearing (2000 Hz) showed notable improvements after 20 and 30 sessions (P < 0.05), with the 30-session treatment resulting in greater enhancements compared to the 20-session treatment (P < 0.05). Speech recognition rates significantly improved after 20 and 30 sessions of HBO₂ compared to pre-treatment levels (P < 0.05), with the 30-session treatment showing statistically significantly higher rates than the ten-session HBO₂ (P < 0.05). Discussion:Hyperbaric oxygen treatment significantly enhances hearing and speech recognition in severe SSNHL, particularly in the mid-frequency range. Long-term HBO₂ treatment may be a viable option for these patients.
Introduction:The 1987 UHMS Workshop on the Validation of Decompression Tables provided standards for the design, testing, and acceptance of decompression tables. Forty years later, research funding has become scarce, and diving companies no longer receive support from universities and Navy research centers. Companies build on their experience and safety culture to improve existing decompression procedures. We list principles and propose guidelines for these internal developments. Principles:Editing decompression tables is a technical activity that aims to provide a practical solution to an immediate operational problem. It relies heavily on current scientific knowledge and experience and on recognized design principles, validation protocols, and acceptance criteria. Validation:Validating decompression procedures fits into the company's Health and Safety management system. Today, decompression tables result from a risk assessment and are presented as a mitigation measure against decompression risks. Management of Change offers a step-by-step approach compatible with the UHMS recommendation for improving existing procedures. Acceptance:Accepting decompression procedures is based on the definition and measurements of relevant endpoints used as acceptance criteria. Endpoints have evolved from DCS incidence to the larger concept of decompression stress. We highlight the importance of dive monitoring in documenting procedure performances and supporting the acceptance decision. Discussion:We conclude that Management of Change can be used by diving companies to develop new or revised decompression procedures, as a complement to the 1987 UHMS recommendations. We recommend that the process be detailed in the company documentation to keep the lessons learned and inform operational personnel.
Avascular necrosis (AVN), also referred to as aseptic osteonecrosis (AO), can develop in several osseous districts of the body. Most commonly described is avascular necrosis of the femoral head (AVNFH), a debilitating and progressively disabling condition with partially understood, wide-ranging etiology and pathogenesis. Pathology is chiefly caused by a reduced vascularization of a terminal vascular bed, such as the one perfusing the femoral head, or similar vascular distributions such as femoral condyles, humeral head, the talus, the calcaneus, the navicularis, and other bony structures. Hypoxic conditions mediate the condition and can improve with a course of hyperbaric oxygen (HBO₂). The Ficat classification is one of the most widely used staging systems for AVN of the femoral head. It classifies patients with osteonecrosis into four stages based on the appearance on a plain radiograph, at least before the advent of MRI, the ultimate golden standard for the specific case. I- Pain but no radiographic anomalies II- Increased density, cystic changes, or porosity III- Flattening of the femoral head and crescent sign IV- Full collapse of the femoral head with decrease in joint space Many of the treatment options proposed aim to achieve joint preservation. However, when the radiological signs progress to advanced bone collapse in the articular capsule, the single mandatory surgery approach is a femoral head replacement with total hip arthroplasty (THA).
Introduction:Carbon monoxide (CO) poisoning is the most common source of poisoning in the United States. Acute poisoning can cause a wide range of symptoms. CO poisoning can have long-term morbidity as well, the most well-described of which is the development of delayed neurologic sequelae. CO can cause acute and chronic cardiovascular and thrombotic effects as well. Case Report:We describe four cases of severe CO poisoning with distinct cardiac and thrombotic effects. Carboxyhemoglobin levels ranged from 23.1%-42.5%. All four were critically ill and intubated. All four were evaluated with transthoracic echocardiography (TTE), electrocardiogram, and laboratory evaluation. Three of the four patients developed decreased ejection fraction, and two had new wall-motion abnormalities noted on TTE. One underwent cardiac catheterization. Two of the patients developed thrombi. All four cases were quickly and aggressively treated with a course of hyperbaric oxygen. Discussion:Carbon monoxide (CO) can cause significant cardiac and thrombotic effects. All four patients had troponin elevations and changes noted on TTE. Two patients developed thrombi. These changes were resolved in the two patients who were seen in post-hospital follow-up. Physicians should remain vigilant when managing these patients in the Emergency Department.
Introduction:Skeletal muscle compartment syndrome (SMCS) and exertional compartment syndrome (ECS) are two distinct conditions. This case report describes a situation in which both conditions resulted from the same triggering events. The importance of this case lies in the fact that the residual neuropathy associated with the SMCS resolved after a single hyperbaric oxygen (HBO₂) treatment. Case Report:This report was generated from a retrospective analysis of the patient's combined compartment syndromes, SMCS and ECS, residual functional deficit, and resolution of the latter with HBO₂ treatment. Severe leg pain developed after two strenuous back-to-back ballet and gymnastics sessions. Similar leg pains of lesser severity had occurred previously but always resolved after the activity was stopped. During this episode, the pain subsided; however, the next day, the patient began to walk with a steppage gait. The athlete received HBO₂ treatment, which restored her peroneal nerve function. Subsequently, the patient underwent an ECS evaluation, bilateral leg fasciotomies, and returned to athletic activities without symptoms. Discussion:A residual nerve palsy can result from an SMCS. This symptom, combined with the rapid resolution of pain symptoms consistent with an ECS, suggests that both problems resulted from the same cause. The delayed onset of the drop foot was attributed to the self-perpetuating cycle of ischemia and edema associated with the lag phase of the SMCS. The resolution of the peroneal nerve palsy with HBO₂ treatment adds additional validation for the roles of HBO₂ in SMCS.
Introduction:Non-alcoholic fatty liver disease (NAFLD) is characterized by the accumulation of liver fat (steatosis), which can progress to non-alcoholic steatohepatitis (NASH), cirrhosis, and cancer. NASH is estimated to affect up to 32% of the world's population. Different treatments, such as hyperbaric oxygen (HBO₂), are being investigated, but the molecular mechanisms associated with this treatment are unknown. The effect of HBO₂ on NAFLD associated with Cd36 expression was evaluated. Methods:Rats were divided into the following groups: rats that developed steatosis and consumed sucrose but did not receive HBO₂, rats with steatosis that consumed sucrose and received HBO₂, rats that developed steatosis and received HBO₂ but did not receive sucrose, and a control group. The HBO₂ groups underwent the procedure for 20 days (2.4 ATA pressure 60 min). An IYOCA hyperbaric chamber model for rats was used. The expression of HIF-1α, PPAR-γ, and Cd36 mRNA from hepatic tissue was measured with the StepOn™ real-time polymerase chain reaction (PCR) system. Results:The expression levels of hepatic HIF-1α, PPAR-γ, and Cd36 genes increased in NAFLD rats that consumed sucrose but did not receive HBO₂ compared to the control group (p <0.05). The rats that received HBO₂ with and without sucrose ingestion showed decreased expression levels of these genes compared to those with NAFLD that consumed sucrose. Discussion:HBO₂ decreased expression levels of HIF-1α and PPRA-γ, which independently or coordinately regulate Cd36 expression. Cd36 expression was significantly decreased in association with the reversal of NAFLD in rats.
Introduction:Warfarin is a widely used oral anticoagulant for the treatment of thromboembolic disorders. Warfarin-induced skin necrosis (WISN), a serious but rare complication, typically affects the breasts, hips, and abdomen. Penile necrosis, however, has been reported only in exceptionally rare cases. Case Report:In this report, we present the successful outcome of early hyperbaric oxygen treatment (HBO₂) in a patient who developed glans penis necrosis during warfarin treatment and was subsequently diagnosed with protein C deficiency. The patient underwent nine HBO₂ sessions initiated early in the disease course and achieved full recovery without tissue loss. Discussion:To our knowledge, this is the first reported case in which HBO₂ was used as part of a combination treatment for penile necrosis in a patient with protein C deficiency. Hyperbaric oxygen treatment may represent an effective therapeutic option in rare cases of warfarin-associated penile necrosis.
Introduction:Acute Kidney Injury (AKI) is a critical condition with high morbidity and mortality, often caused by ischemia-reperfusion (I/R) injury. Hyperbaric oxygen treatment (HBO₂) enhances tissue oxygenation and has shown potential in hypoxic conditions. This study evaluated the efficacy of HBO₂ in mitigating renal I/R injury in a rat model. Methods:Sprague-Dawley rats were divided into three groups: Control (sham surgery, n = 9), I/R (n = 9), and I/R +HBO (n = 9). I/R was induced by 30-minute bilateral renal pedicle occlusion followed by reperfusion. The I/R +HBO group received two sessions of HBO₂ (90 min at 1.6 ATA) at two and 22 hours post-reperfusion. Renal function was assessed via serum creatinine and blood urea nitrogen (BUN) levels. Histopathological and molecular analyses examined tissue damage, inflammation, and necroptosis markers (p-RIP3/pMLKL). Results:The I/R group showed significantly elevated BUN and creatinine levels compared to the Control (p < 0.05). HBO₂ significantly reduced these levels compared to the I/R group. Histopathology revealed severe tubular damage and neutrophil infiltration in I/R rats, while HBO₂ improved renal structure and decreased necroptosis activation. Discussion:HBO₂ effectively reduced renal I/R injury by mitigating inflammation, oxidative stress, and necroptosis. These findings suggest HBO₂ as a potential therapeutic strategy for AKI, warranting further clinical investigation.
Introduction:Wildlife exposure is a risk that trained divers are fully aware of. Examples of hazardous wildlife that divers may encounter include, but are not limited to, sharks, coral, sponges, eels, and jellyfish. Encountering wildlife can lead to a diver panicking or being forced to surface rapidly or in an uncontrolled manner due to panic or avoidance of the hazard. This may increase the risk of decompression illness (DCI), mainly pulmonary overinflation syndrome (POIS). Injuries caused by hazardous aquatic wildlife can also be distracting, leading dive supervisors and/or medical personnel to overlook unrelated injuries, such as DCI. If this occurs, the affected diver may suffer a grave outcome that could otherwise have been prevented. Case Report:A 23-year-old Army Engineer diver developed sharp chest pain shortly after a 70-foot SCUBA dive complicated by suspected Portuguese man-of-war envenomation. He had painful tentacle contact on both hands/arms and neck, treated immediately with oxygen, vinegar, and seawater irrigation. In the ED, he was stable with normal oxygenation, ECG, labs, venous blood gas, and troponin. His chest pain resolved within 90 minutes, and skin findings improved with topical steroids and antihistamine therapy. He was diagnosed with jellyfish envenomation and atypical chest pain rather than a diving-related injury. At one-month follow-up, he was asymptomatic with normal chest radiographs and was cleared to return to diving. Discussion:It is of the utmost importance to be aware of all possible injuries or maladies that could have occurred to a diver, and for medical personnel to avoid becoming hyper-focused on a single injury, such as wildlife exposure or trauma.
Like all medical treatments, hyperbaric oxygen (HBO₂) has known potential side effects. HBO₂ is provided in different clinical settings by providers and staff with differing levels of expertise. It is important to understand the potential side effects of HBO₂ in order to allow for consideration of risk and benefit in discussion with the patient who is considering HBO₂. In this chapter, we will describe and quantify these side effects. Hyperbaric oxygen therapy is the treatment of patients with 100% oxygen at higher than atmospheric pressure provided in either a monoplace chamber (single person) typically compressed with oxygen or a multiplace chamber (multiple persons) compressed with air while oxygen is delivered by a hood or mask. The benefits of treatment are the result of both primary and secondary effects. Primary effects are from increased pressure and hyperoxia, while various secondary effects are the result of controlled oxidative stress mediated by reactive oxygen and nitrogen species [1-3]. These very same primary and secondary beneficial effects can lead to side effects associated with HBO₂ including different forms of barotrauma and oxygen toxicity.
Introduction:Tension pneumothorax is a life-threatening complication during hyperbaric oxygen treatment (HBO₂). The presence of a pleural catheter is assumed to mitigate this risk, but its efficiency under hyperbaric conditions remains unclear. Case Report:We describe a 37-year-old female undergoing HBO₂ with a pigtail pleural catheter in situ for secondary pneumothorax. The patient developed respiratory and cardiovascular symptoms during decompression. To investigate gas flow dynamics, we conducted an experimental analysis measuring flow resistance in pigtail catheters under chamber pressures up to a chamber gauge pressure of 172.37 kPa. Flow rates were analyzed across a range of differential pressures and catheter fenestration numbers. Gas flow increased non-linearly with pressure but plateaued at higher differentials, indicating drainage limitations. Catheters with fewer fenestrations exhibited significantly reduced flow rates. Under simulated HBO₂ conditions, pressure differentials exceeding 2.4 kPa resulted in delayed gas evacuation, mirroring the clinical event. Discussion:This case and experimental study highlight the potential risk of inadequate pneumothorax drainage with pigtail catheters during HBO₂. We recommend decompression rates ≤1 psi/min to mitigate this risk. Further studies are needed to evaluate alternative catheter designs for hyperbaric environments.
Introduction:Hyperbaric oxygen treatment (HBO₂) uses increased atmospheric pressure and fractional oxygen to enhance tissue oxygen delivery. HBO₂ has gained attention as a tool for athletic recovery and performance, but past reviews in the literature are limited or inconclusive. This systematic review and meta-analysis aim to provide an update and assess the effect of HBO₂ on athletic recovery. Methods:Literature searches were performed across PubMed, Cochrane Central, Google Scholar, and Embase (January 1, 2015-September 15, 2024), following PRISMA guidelines. Studies included healthy athletes undergoing HBO₂ to assess athletic performance, metabolic recovery, and physiological responses. Quality assessment was performed using Cochrane's risk of bias tools (ROB2 and ROBINS-1). A meta-analysis with subgroup analyses by age, body mass index, and body fat mass percentage was conducted, along with a meta-regression examining HBO₂ protocol characteristics and outcomes. Results:Eleven met the eligibility criteria; six studies were included in the meta-analysis. The meta-analysis showed that HBO₂ significantly reduced post-recovery blood lactate levels (effect size: -1.71; 95% CI: -3.10 to -0.32). Subgroup analysis revealed that younger athletes and those with lower fat mass receiving HBO₂ exhibited significant reductions in post-recovery lactate levels. Meta-regression was inconclusive but suggested treatment effect heterogeneity based on HBO₂ protocol characteristics. HBO₂ showed limited application in short-term power output and force production. Discussion:Hyperbaric oxygen treatment is an efficient method for improving athletic performance, particularly by reducing post-exercise lactate levels, thereby supporting faster metabolic recovery. Future studies should focus on standardized protocols, diverse populations, and long-term outcomes to better understand HBO₂'s potential in orthopedics and sports medicine.
