Joseph Thomas, MD, MBA, Fellow of Metabolic and Nutritional Medicine
In collaboration with Oxygen Health Systems
Abstract
Hyperbaric oxygen therapy has gained traction as an adjunct in sports medicine, particularly in concussion management and musculoskeletal injury. Elevating ambient pressure and inspired oxygen concentration raises plasma-dissolved oxygen and drives diffusion into hypoxic or metabolically compromised tissue. The physiologic rationale is sound. Clinical application in athletic populations, though, remains inconsistent and poorly standardized. This review covers relevant mechanisms and addresses practical considerations including treatment parameters, patient selection, contraindications, and how to fit this into multidisciplinary care.
Introduction
Athletic injuries reliably produce localized hypoxia, microvascular disruption, and impaired oxidative metabolism, even when systemic oxygenation looks entirely normal. In sports-related concussion, a cascade of ionic imbalance, reduced cerebral glucose utilization, mitochondrial dysfunction, and neuroinflammation creates an energy mismatch within neural tissue. Musculoskeletal injuries follow a similar pattern. Edema and compromised perfusion cut oxygen diffusion, delaying tissue repair and sustaining inflammation.¹ Hyperbaric oxygen therapy offers a way to increase tissue oxygen availability that bypasses hemoglobin transport entirely, a meaningful distinction when the delivery system itself is compromised.⁵
Physiological Basis
Elevated ambient pressure raises oxygen dissolved in plasma in proportion to the pressure applied. This widens the diffusion gradient between capillary blood and surrounding tissue, pushing oxygen into areas where edema or vascular compromise would otherwise block normal delivery. At higher partial pressures, dissolved oxygen contributes directly to cellular metabolic demand, supporting aerobic ATP production, easing reliance on anaerobic pathways, and curtailing lactate buildup in injured tissue.⁵
Clinical Application in Concussion
Pathophysiologic Context
Following mild traumatic brain injury, metabolic dysfunction often persists well past the window visible on structural imaging. Impaired oxidative phosphorylation, increased reactive oxygen species, and disrupted neurovascular coupling are consistent findings.² Intermittent hyperoxic exposure activates cellular repair responses through what Hadanny and Efrati described as the hyperoxic-hypoxic paradox: repeated oxygen fluctuations trigger regenerative mechanisms normally associated with hypoxia, including HIF-1α expression and downstream angiogenic signaling, without the tissue damage hypoxia itself would cause.⁴
Clinical Framework
In the acute phase, management stays focused on stabilization, symptom monitoring, and graded activity. Hyperbaric therapy has no established role here.
In the subacute phase, patients carrying persistent cognitive fatigue, headaches, or slowed processing become reasonable candidates for adjunctive treatment.
In persistent post-concussion syndrome, the population most studied, hyperbaric therapy fits best within a broader program that includes cognitive therapy, vestibular rehabilitation, and structured exercise progression. Harch’s 2022 systematic review and dosage analysis found consistent symptomatic and cognitive improvements across four randomized trials at 1.5 ATA, while trials at 2.4 ATA produced negative or mixed results, making clear that pressure selection is not interchangeable.² Shlifer et al.’s 2025 retrospective cohort found that adults with persistent post-concussion syndrome stemming from childhood TBI showed significant improvement in cognitive domains including executive function, processing speed, and attention after 40 sessions at 2 ATA.¹ Weaver et al.’s 2025 double-blind randomized trial found that 40 HBO₂ sessions at 1.5 ATA reduced Neurobehavioral Symptom Inventory scores significantly compared to sham at 13 weeks, with a mean difference of 7.0 points (95% CI 1.7 to 12.3, p=0.01).³
Representative Clinical Parameters
Pressure ranges from 1.3 to 1.5 atmospheres absolute. Sessions run 60 to 90 minutes, three to five times per week. Total course length generally falls between 20 and 40 sessions, adjusted to clinical response. These are starting points. Presentation and tolerance drive individual decisions.
Clinical Application in Musculoskeletal Injury
Mechanistic Considerations
Tissue repair requires adequate oxygen tension to drive angiogenesis, fibroblast proliferation, and collagen synthesis. Sustained hypoxia stalls remodeling and prolongs inflammation. Lindenmann et al.’s 2021 systematic review of molecular mechanisms confirmed that hyperbaric exposure modulates transcription, inflammatory signaling, apoptotic pathways, and vascular response across a broad range of tissue repair indications.⁵ The same review documented effects on stem cell mobilization, neovascularization, and scaffolding proteins, offering multiple mechanistic pathways through which hyperbaric oxygen supports healing beyond simple oxygen delivery.
Clinical Use Stratification
In acute injury such as muscle strain or contusion, early hyperbaric therapy may support tissue oxygenation and accelerate recovery. In subacute injury, it becomes useful when recovery plateaus or inflammation runs longer than expected. In chronic presentations like tendinopathy or stalled post-surgical healing, it functions as an adjunct when tissue recovery has otherwise stalled despite ongoing rehabilitation. As Moghadam et al. noted in their 2020 review in Medicine and Science in Sports and Exercise, sporting injuries are typically treated over 3 to 10 sessions at 2.0 to 2.8 ATA, a range distinct from the longer protocols used in neurological applications.⁶
Representative Clinical Parameters
Pressure ranges from 1.3 to 2.0 atmospheres absolute depending on clinical setting. Sessions run 60 to 90 minutes, two to five times per week, over a course of 10 to 30 sessions scaled to severity and response.
Integration into Clinical Practice
Hyperbaric therapy works best as one piece of coordinated care. In concussion, that means active communication with neurology, physical therapy, and cognitive rehabilitation. In musculoskeletal injury, alignment with orthopedics, physical therapy, and performance training is essential. Treatment timing should be deliberate, response monitored consistently, and redundancy in care delivery avoided.
Patient Selection and Clinical Assessment
The patients most likely to benefit are those with persistent symptoms, delayed recovery, or functional limitation that has not responded to standard care. Baseline assessment should cover cognitive evaluation, symptom scoring, functional movement, and sport-specific performance measures where applicable. Regular reassessment drives decisions about continuing, adjusting, or stopping therapy. This is not a set-it-and-forget-it modality.
Contraindications and Safety Considerations
When screened and administered properly, hyperbaric oxygen therapy is generally well tolerated. Untreated pneumothorax is an absolute contraindication. Relative contraindications include COPD with air trapping, uncontrolled seizure disorders, certain ear and sinus pathology, and recent thoracic surgery. Patients should be counseled on barotrauma to the ears or sinuses, transient visual changes, and oxygen toxicity, the last being most relevant at higher pressures or with prolonged exposure. Thorough screening, patient education, and in-session monitoring form the floor of safe delivery.
Discussion
The physiologic rationale for using hyperbaric therapy in sports medicine holds up well. The problems are in the evidence base: inconsistent study design, wide variation in treatment parameters, and small sample sizes make it difficult to define firm protocols. What the literature does support consistently is that dose matters. Harch’s dosage analysis makes clear that 1.5 ATA performs across randomized trials while 2.4 ATA does not, a distinction that has been obscured in studies where lower-pressure air was treated as a true inert placebo rather than recognized as an active dose that itself affects plasma oxygen.² Clinically, this therapy earns its place when standard rehabilitation has plateaued. Patients still symptomatic and still limited weeks into a stalled recovery are where the referral conversation is most worth having.
Conclusion
Hyperbaric oxygen therapy is a physiologically coherent adjunct in both concussion and musculoskeletal injury management. It raises plasma-dissolved oxygen and improves tissue diffusion in ways that conventional care cannot replicate when the vascular and metabolic environment is already compromised. Paired with structured rehabilitation and honest patient selection, it extends the options available in cases that have otherwise run out of runway. The evidence base needs better-powered trials and standardized dosing protocols, but what exists, read carefully, points in a consistent direction.
References
- Shabi Shlifer A, Suzin G, Shorer R, Lang E, Finci S, Elman-Shina K, Doenyas-Barak K, Efrati S. Hyperbaric oxygen therapy improves post-concussion symptoms in adults with childhood traumatic brain injury: a retrospective cohort study. Front Neurol. 2025;16:1641033. doi:10.3389/fneur.2025.1641033.
- Harch PG. Systematic review and dosage analysis: hyperbaric oxygen therapy efficacy in mild traumatic brain injury persistent postconcussion syndrome. Front Neurol. 2022;13:815056. doi:10.3389/fneur.2022.815056.
- Weaver LK, Ziemnik R, Deru K, Russo AA. A double-blind randomized trial of hyperbaric oxygen for persistent symptoms after brain injury. Sci Rep. 2025;15:6885. doi:10.1038/s41598-025-86631-6.
- Hadanny A, Efrati S. The hyperoxic-hypoxic paradox. Biomolecules. 2020;10:958. doi:10.3390/biom10060958.
- Lindenmann J, Smolle C, Kamolz LP, Smolle-Juettner FM, Graier WF. Survey of molecular mechanisms of hyperbaric oxygen in tissue repair. Int J Mol Sci. 2021;22(21):11754. doi:10.3390/ijms222111754.
- Moghadam N, Hieda M, Ramey L, Levine BD, Guilliod R. Hyperbaric oxygen therapy in sports musculoskeletal injuries. Med Sci Sports Exerc. 2020;52(6):1420-1426. doi:10.1249/MSS.0000000000002257.
