Updated: Oct 22
Currently, the evidence is controversial as to whether there is a basis for using hyperbaric oxygen therapy (HBOT) in sport injuries. Professional and college teams have recently started using HBOT to treat sport-related injuries.21 From muscle contusions and ankle sprains to delayed-onset muscle soreness, HBOT is being used to facilitate soft-tissue healing. A review of the internet also revealed that a number of elite athletes are using “bag chamber” to self treat sport-related injuries in the home environment, probably without supplemental oxygen or medical supervision.22 This review will explain the rationale for the use of hyperbaric oxygen therapy and reports on the initial research in the area of hyperbaric oxygen in sports-induced injury.
Sport injuries are frequently associated with bone or soft tissue injuries involving joints, muscle, ligaments, and tendons. The severity of tissue injury varies from relatively minor with rapid recovery to significant tissue injury, prolonged inflammation, and functional impairment. A variety of therapies have been developed to shorten recovery time and preserve mobility. There is inevitably a compromise between early mobilization with the risk of worsening the injury, and delaying the return to training and the sport, with loss of general fitness and sometimes disuse atrophy of muscle groups. These soft tissue injuries inevitably result in a disturbance of the microcirculation, with increased permeability due to the release of inflammatory mediators.1 The development of edema and the invasion of inflammatory cells with a high demand for oxygen can result in local tissue hypoxia, with worsening of the edema allowing a vicious cycle to develop. The resulting ischemia lowers the concentration of adenosine triphosphate (ATP) and increases lactic acid levels in the damaged tissue/muscle. As ATP is necessary for ion and molecular transport across cell membranes and maintenance of cellular viability2,3 increasing oxygen delivery levels with HBOT may prevent tissue/muscle damage or hasten tissue recovery by decreasing the tissue lactic acid level and helping to maintain ATP levels, in much the same way as HBO does with reperfusion/crush injuries and acute traumatic peripheral ischemias. In fact, one could consider the acute soft tissue injury in the athlete as a minor form of ischemia/reperfusion injury, a clinical presentation which when more severe would be readily considered for HBOT.
During hyperbaric oxygen therapy vasoconstriction occurs, which reduces blood flow to local areas by up to 20%.8 This restricted blood flow is compensated for by increased oxygen delivery through the plasma. This mechanism is outlined by Gill and Bell10 who state that vasoconstriction is effective for reducing post-traumatic tissue edema. In applying this physiology to the sporting arena, it seems clear that if a significant muscle injury or ligament tear was treated with HBO within the first 8 to 24 hours, a similar reduction in tissue edema would occur thereby resulting in decreased recovery times. Unfortunately such early interventions have not been studied at this time.
Fibroblast and osteoclast stimulation is another response to HBO that benefits the treatment of fractures and osteomyelitis.8,11 Once again it is reasonable to assume that this adaptation would enhance the process of ligamentisation that occurs after a sport injury. A study by Babul et al12 assessed patients using magnetic resonance imaging pre and post HBO and found no significant differences. However it should be noted that this study examined muscle damage sustained by eccentric exercise, not acute ligament sprains, making direct comparison difficult at best.
HBO is an effective treatment for crush injuries and other acute traumatic peripheral ischemias as it alleviates hypoxia and reduces edema while maintaining high-energy phosphate bonds; however, clinical experience with HBO for sports injuries is somewhat limited.
The small number of studies investigating the effects of HBOT on acute soft tissue injuries makes it relatively easy to examine the scientific design of these studies. HBOT has been used to treat joint, muscle, ligament, and tendon injuries in soccer players in Scotland. When hyperbaric oxygen therapy was used in conjunction with physiotherapy, the time to recovery was reduced by 70%.5 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 applicability of this study in clinical practice but suggest a potential benefit from HBOT in this setting.
The ankle joint, because of its weight-bearing function and the construction of its articulation, is the most commonly injured joint in athletes, representing as many as 73%19,20 of injuries. Hyperbaric oxygen has been used to treat acute ankle inversion injuries. Borromeo et al6 conducted a randomized double-blind study of 32 patients with acute ankle sprains to compare HBO 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 of joint function was greater in the HBO 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 include an average delay of 34 hours from time of injury to diagnosis, administration of only three HBO treatments within seven days, treatment pressure of only 2.0 ATA, and short treatment duration. It would be interesting to reproduce this study with HBO intervention occurring much sooner post-injury. This is supported by Kanhai and Losito7 who concluded that the time between injury and treatment may affect outcomes. Delaney and Montgomery8 also offer that HBO should be initiated within 24 hours of injury.
Abbadi and Elrefai 17 also conducted a randomized double-blind study of 36 patients with acute ankle sprains compared HBO treatment at 2.0 and 2.5 ATA with a placebo treatment. All patients were acute ankle sprains (injury within 36 hours) treated in a hospital emergency department. All three groups received seven hyperbaric sessions, as outpatients in five consecutive days, twice a day for two days followed by once a day for the remaining three days. All patients treated at 2.5 ATA were completely free of pain and of swelling by the end of the last day.
Staples and Clement13 reported a clinical study (unpublished observation) which examined the short term recovery of grade II medial collateral ligaments of the knee in a randomized, controlled, double blind study. Patients who presented within 72 hours of injury and had no previous knee problems were included in the study. Prior to acceptance, patients were examined by a MD and had a magnetic resonance imaging test to ensure that no other structures were involved. Once these parameters were met, the patients received either the sham or HBOT over two weeks. Preliminary data analyses suggested positive effects on pain and functional outcomes after 6 weeks.
Bennett and Best et al18 completed a Cochrane review of seven trials examining the effects of delayed onset muscle soreness (DOMS) and found no evidence to support the use of hyperbaric oxygen therapy for DOMS following eccentric exercise in unconditioned volunteers. The pooling of data from these DOMS trials did show significantly and consistently higher pain at 48 and 72 hours in the HBOT group in trials where HBO was started immediately. No studies could be found that examined the effects of HBOT on recovery from training or injury in elite athletes.
Yagishita and Yamami et al23 conducted a recent study in 2007 with twenty patients, who sustained muscle injuries during sport activities and were admitted to the hospital within seven days after injury. All were administered HBO at 2.8 ATA for 1 hour for one to seven treatments. They concluded that HBO was effective at reducing visual analog pain scale values, muscle stiffness, and leg volumes. Although the testing was not randomized or blinded the results are impressive.
When examining the physiology associated with hyperbaric oxygen therapy, the common thread is that these adaptations occur in ischemic environments. To determine if these processes will carry over to sports injuries, any future studies should look closely at measures such as proximity of HBOT to time of injury, post injury edema, angiogenesis, fibroblast proliferation and PMN leukocyte activity for acute soft tissue rupture, and any elevated creatine kinase (CK) activity in the blood pre and post hyperbaric oxygen therapy.
Increasing evidence suggests that adjunctive treatment with hyperbaric oxygen therapy enhances recovery from soft tissue injuries, specifically the type of injury seen most often in sports medicine. The most impressive results appear to be generated by prompt treatment, when hyperbaric oxygen is initiated in the first 8 hours after injury.
Final Recommendations: Soft tissue injuries are a common problem in sports medicine, and hyperbaric oxygen therapy should be used as an adjunctive therapy to enhance recovery in elite athletes. Several different mechanisms are believed to be responsible for the beneficial effects of hyperoxygenation. Hyperbaric oxygen therapy should begin as soon as possible, but no later than 8 to 24 hours post injury, using the acute traumatic peripheral ischemia (ATPI) protocol at 2.5 ATA for 90 minutes. Clearly, the earlier treatment can be initiated, the greater the likelihood of providing benefit. The number of treatments and frequency will vary with the type and severity of the injury. If the Abbadi and Elrefai 17 trial is used as a basis for providing a consistent approach to treatment, then BID treatments would be provided on days 1 and 2 with once daily treatments continuing days 3-5 and a maximum number of treatments between approximately 7 and 15 treatments.4 Serial CPKs when muscle injury is involved and functional assessment for all patients should be followed to (1) determine the treatment course for individual patients and (2) the overall effectiveness of HBOT in acute sports injury.
1. Abbot, N C, Beck, J S, Carnochan, F M, Spencer, V A, and James P B: Estimating skin respiration from transcutaneous PO2/PCO2 at 1 and 2 ATM ABS on normal and inflamed skin. Journal of Hyperbaric Medicine. 1990; 5: 91-102.
2. Nylander, G, Nordstrom, H, Lewis, D, et al: Metabolic effects of hyperbaric oxygen in post ischemic muscle. Plastic and Reconstructive Surgery. 1987; 79 (1): 91-97.
3. Stewart, R J, Yamaguchi, K T, Mason, S W, et al: Tissue ATP levels in burn injured skin treated with hyperbaric oxygen, abstracted. Undersea and Biomedicine Research 1998; 16 (suppl): 53.
4. Zamboni, W A, Roth, A C, Russell R C, et al: The effects of acute hyperbaric oxygen therapy on axial pattern skin flap survival when administered during and after total ischemia. Journal of Reconstructive Microsurgery. 1989; 5 (4): 343-347.
5. James, P B, Scott, B, Allen, M W: Hyperbaric oxygen therapy in sports injuries. Physiotherapy. 1993; 79 (8): 571-572.
6. Borromeo, C N, Ryan, J L, Marchetto, P A, et al: Hyperbaric oxygen therapy for acute ankle sprains. American Journal of Sports Medicine. 1997; 25 (5): 619-625.
7. Kanhai, A, and Losito, J M: Hyperbaric oxygen therapy for lower-extremity soft-tissue sport injuries. Journal of the American Podiatric Association. 2003; 93 (4): 298-306.
8. Delaney, J S, and Montgomery, D L: How can hyperbaric oxygen contribute to treatment? The Physician and Sportsmedicine. 2001; 29 (3): 77-84.
9. Ishii, Y, Deie, M, Adachi, N, Yasunaga, Y, Sharman, P, et al: Hyperbaric oxygen as an adjuvant for athletes. Sports Medicine. 2005; 35 (9): 739-746.
10. Gill, A L, and Bell, C N A: Hyperbaric oxygen; its uses, mechanisms of action and outcomes. QJM. 2004; 97 (7): 385-395.
11. Wang, J, Li, F, Calhoun, J H, and Mader, JT: The role and effectiveness of adjunctive hyperbaric oxygen therapy in the management of musculoskeletal disorders. Journal of Postgraduate Medicine. 2002; 48: 226-231.
12. Babul, S, Rhodes, E C, Taunton, J E, and Lepawsky, M: Effects of intermittent exposure to hyperbaric oxygen for the treatment of an acute soft tissue injury. Clinical Journal of Sports Medicine. 2003; 13 (3): 138-147.
13. Staples, J, and Clement, D: Hyperbaric oxygen chambers and the treatment of sports injuries. Sport Medicine 1996; 22 (4): 219-227.
14. Gottrup, F, Firmin, R, Hunt, T K, et al: The dynamic properties of tissue oxygen in healing flaps. Surgery 1984; 95 (5): 527-536.
15. LaVan, F B, Hunt, T K, (eds): Oxygen and wound healing. Clinical Plastic Surgery. 1990; 17 (3): 463-472.
17. Abbadi, S M, and Elrefai, J M: The role of hyperbaric oxygen in managing ankle sprain. Clinical Journal of Sports Medicine. 2002; 12 (3): 139-150.
18. Bennett, M, Best, T M, Babul, S, Taunton, J, Lepawsky, M: Hyperbaric oxygen therapy for delayed onset muscle soreness and closed soft tissue injury. (Cochrane Review) In: The Cochrane Library, Issue 1, 2006. Oxford: Update Software.
19. Hockenbury, R T, and Sammarco, G J: Evaluation and treatment of ankle sprain. The Physician & Sport Medicine 2002; 29 (2): 105-108.
20. Yeung, M S, Chan, K M, So, C H, Yuan W Y: An epidemiological survey on ankle sprain. British Journal of Sports Medicine. 1994; 28 (2): 112-116.
23. Yagishita, K, Yamami, N, Togawa, S, Nakayama, T, Mano, Y: The effect of hyperbaric oxygen therapy on patients with muscle injury, abstracted. UHMS, Inc. Annual Scientific Meeting held June 14-16, 2007. Ritz-Carlton Kapalua Maui, Hawaii.