Oxygen...the Breath of Life
Hyperbaric Home
About Hyperbaric
Indications for HBOT
HBOT & Rehabilitation
FAQ's - HBOT
Method of Action
HBOT In The News
Download News
HBOT Links
HOC Staff
Progressive Medicine
Contact Us


What is Hyperbaric Oxygenation Therapy?


Exciting new Vancouver location coming soon!

Visit Victoria Hyperbaric Treatment Center

HOC Care Center
Progressive 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

Site Map
    
Read Our
Success Stories

 

Disclaimer
Information within this site is provided for informational and educational purposes only. This information is not meant to substitute for the advice provided by your personal physician or any other medical professional.

You should not use the information contained herein for diagnosing or treating a health problem or disease, or prescribing any medication. If you have or suspect that you have a medical problem, promptly contact your health care provider.

Copyright 2003 HOC Health System. All rights reserved

Hyperbaric Home | About Hyperbaric | Indications for HBOT | HBOT & Rehabilitation | FAQ's - HBOT
Method of Action
| In The News | Download News | HBOT Links | HOC Staff | Progressive Medicine | Contact Us

Webdesign by Mediamage