"Brief Story of the timeline of events that led me to OXYMED Hyperbaric Oxygen.

Whilst practicing for the 2019 Finke Desert race I had an accident travelling at roughly 80Km/h and broke 4 ribs (2, 3, 4, 5), punctured my left lung and broke my left scapular.

My lung didn't require tubing but had to be monitored in Hospital for 4 days before signing myself out of hospital to fly home to start recovery. I spent the first week resting and spending some time in a sauna. Just over a week into my recovery I started back at the gym with cycling and walking on a treadmill. I continued light training but looked into other ways to speed up my recovery and that's when I came across HBOT.

About 4.5 weeks into my recovery I spent 4 days in Melbourne having 2 sessions a day in HBOT clocking up 14 hours worth.

From there I spent 1 more week in the gym and then flew back to Alice Springs in preparation for our biggest off road race in the country. I rode three days in the lead up to the event then raced over the long weekend. 

Total time from my injury to when I was back on a bike was just over 6 weeks and raced to a 2nd place finish 7 weeks post injury.

The Finke desert race isn't just any race it's the most demanding race we do, it's a 230km race each way from Alice Springs to a remote community called Finke/apatula (camp over night) and race back again on some of the roughest terrain possible. We average speeds of over 108km/h, with a top speed of 180km/h. I completed the course in just on 2 hours each way, stopping twice for refuels on each pass, average heart rates are up around the 170-180bpm for the whole duration of the race.

Brief history for me as an athlete - Started racing dirt bikes at age 3 and raced every year since, I was a junior national and state motocross champion, switched to off road racing when I was 18. I've won 2 Australian Safari's (Australia's Dakar style rally) along with two runner up finishes, Won five Condo 750 rallies, multiple podiums in the Finke desert race, Competed and finished the Dakar rally in South America, Competed in the Baja 1000 in Mexico. I've had many injuries over the years and raced injured in the past but definitely believe the time I spent in HBOT was well worth it and increased my recovery considerably.     


Thanks again OXYMED, for fitting me in and coming in on a Sunday to offer me the treatment. Many people have asked me how I made it back so quick and I tell them HBOT is definitely one of the reasons I made it back so quick.

If you need anything else mate just let me know, I'll be sure to send any of my buddies needing recovery straight to you that's for sure!!

Talk soon,

Regards, JS

What Are the Advantages of Hyperbaric Oxygenation for delayed Fracture Repair?


  • HBOT targets ‘zones of ischemia’ (areas of tissue and bone with retarded blood supply and nutritional status), facilitating new capillary network support and increasing blood supply (neovascularisation) by increasing vascular stem cell mobilization growth factors, reducing painful swelling and inflammation and promoting metabolism and immune system responses overcoming underlying infectious agents.

Using oxygen at high pressure for the treatment of broken bones and delayed repair

The healing of bony fractures is a complex and multifaceted process. However, extensive trauma, bone loss, unstable fixation, premature mobilization, infection, extensive osteonecrosis and ageing are factors that may delay or even stop the healing.


Broken bones (fractures) are very common and sometimes may take a long time to heal or in some cases may fail to heal. The resulting non-union can result in long-term pain and loss of function. The use of hyperbaric oxygen therapy or HBOT has been suggested as a way to enhance healing and treat non-union. HBOT involves the delivery of oxygen at high pressure to patients in a specially designed chamber (like those used for deep sea divers suffering pressure problems after resurfacing). The aim is to increase the supply of oxygen to the fracture site, which theoretically should improve healing.






















PLoS One. 2015 Oct 9;10(10):e0140156. doi: 10.1371/journal.pone.0140156. eCollection 2015.

Hyperbaric Oxygen Promotes Proximal Bone Regeneration and Organized Collagen Composition during Digit Regeneration.

Sammarco MC1, Simkin J1, Cammack AJ1, Fassler D1, Gossmann A2, Marrero L3, Lacey M2, Van Meter K3, Muneoka K4.

Author information

  • 1Department of Cell and Molecular Biology, Tulane University, New Orleans, Louisiana, United States of America.

  • 2Department of Mathematics, Tulane University, New Orleans, Louisiana, United States of America.

  • 3Department of Medicine, Louisiana State University Health Sciences Center, New Orleans, Louisiana, United States of America.

  • 4Department of Veterinary Physiology & Pharmacology, Texas A&M University, College Station, Texas, United States of America.


Oxygen is critical for optimal bone regeneration. While axolotls and salamanders have retained the ability to regenerate whole limbs, mammalian regeneration is restricted to the distal tip of the digit (P3) in mice, primates, and humans. Our previous study revealed the oxygen microenvironment during regeneration is dynamic and temporally influential in building and degrading bone. Given that regeneration is dependent on a dynamic and changing oxygen environment, a better understanding of the effects of oxygen during wounding, scarring, and regeneration, and better ways to artificially generate both hypoxic and oxygen replete microenvironments are essential to promote regeneration beyond wounding or scarring.

To explore the influence of increased oxygen on digit regeneration in vivo daily treatments of hyperbaric oxygen were administered to mice during all phases of the entire regenerative process. Micro-Computed Tomography (μCT) and histological analysis showed that the daily application of hyperbaric oxygen elicited the same enhanced bone degradation response as two individual pulses of oxygen applied during the blastema phase. We expand past these findings to show histologically that the continuous application of hyperbaric oxygen during digit regeneration results in delayed blastema formation at a much more proximal location after amputation, and the deposition of better organized collagen fibers during bone formation. The application of sustained hyperbaric oxygen also delays wound closure and enhances bone degradation after digit amputation.

 * Thus, hyperbaric oxygen shows the potential for positive influential control on the various phases of an epimorphic regenerative response.


J Orthop Res. 2013 Mar;31(3):376-84. doi: 10.1002/jor.22235. Epub 2012 Sep 18.

Hyperbaric oxygen treatment prevents nitric oxide-induced apoptosis in articular cartilage injury via enhancement of the expression of heat shock protein 70

Ueng SW1, Yuan LJ, Lin SS, Niu CC, Chan YS, Wang IC, Yang CY, Chen WJ.

Author information

  • 1Department of Orthopaedic Surgery and Hyperbaric Oxygen Therapy Center, Chang Gung Memorial Hospital, Kweishan, Taoyuan, Taiwan.


Heat shock proteins (HSPs), inflammatory cytokines, nitric oxide (NO), and localized hypoxia-induced apoptosis are thought to be correlated to the degree of cartilage injury. We investigated the effect of hyperbaric oxygen (HBO) on (1) interleukin-1β (IL-1β)-induced NO production and apoptosis of rabbit chondrocytes and (2) healing of articular cartilage defects. For the in vitro study, RT-PCR and Western blotting were performed to detect mRNA and protein expressions of HSP70, inducible NO synthase (iNOS), and caspase 3 in IL-1β-treated chondrocytes. To clarify that the HSP70 was necessary for anti-iNOS and anti-apoptotic activity by HBO, we treated the cells with an HSP70 inhibitor, KNK437. For the in vivo study, cartilage defects were created in rabbits.

The HBO group was exposed to 100% oxygen at 2.5 ATA for 1.5 h a day for 10 weeks. The control group was exposed to normal air. After sacrifice, specimen sections were sent for examination using a scoring system. Immunohistochemical analyses were performed to detect the expressions of iNOS, HSP70, and caspase 3.

Our results suggested that HBO upregulated the mRNA and protein expressions of HSP70 and suppressed those of iNOS and caspase 3 in chondrocytes. KNK437 inhibited the HBO-induced downregulation of iNOS and casapase 3 activities.

 * The histological scores showed that HBO markedly enhanced cartilage repair. Immunohistostaining showed that HBO enhanced HSP70 expression and suppressed iNOS and caspase 3 expressions in chondrocytes.

 ** Accordingly, HBO treatment prevents NO-induced apoptosis in articular cartilage injury via enhancement of the expression of heat shock protein 70.

Hyperbaric oxygen therapy in extremity trauma

J Am Acad Orthop Surg. 2004 Nov-Dec;12(6):376-84.

Greensmith JE. St Elizabeth Hospital, Appleton, WI 54915, USA.


Hyperbaric oxygen therapy potentially can provide enhanced oxygen delivery to peripheral tissues affected by vascular disruption, cytogenic and vasogenic edema, and cellular hypoxia caused by extremity trauma. After appropriate resuscitation, macrovascular repair, and fracture fixation/stabilization, adjunctive hyperbaric oxygen therapy can enhance tissue oxygen content.

In patients with crush injury or early compartment syndrome, hyperbaric oxygen therapy may reduce the penumbra of cells at risk for delayed necrosis and secondary ischemia. Animal experiments and human case series suggest the benefits of such therapy, and recent randomized, prospective studies on trauma patients have confirmed its efficacy in those with extremity trauma. However, more data are necessary to determine additional indications as well as optimal timing and dosing for hyperbaric oxygen therapy.


Vasculogenic stem cell mobilization and wound recruitment in diabetic patients: increased cell number and intracellular regulatory protein content associated with hyperbaric oxygen therapy

Thom SR, Milovanova TN, Yang M, Bhopale VM, Sorokina EM, Uzun G, Malay DS, Troiano MA, Hardy KR, Lambert DS, Logue CJ, Margolis DJ. Institute for Environmental Medicine, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania 19104-6068, USA.


Diabetic patients undergoing hyperbaric oxygen therapies (HBO) for refractory lower extremity neuropathic ulcers exhibit more than a twofold elevation (p=0.004) in circulating stem cells after treatments and the post-HBO(2)T CD34(+) cell population contains two- to threefold higher levels of hypoxia inducible factors-1, -2, and -3, as well as thioredoxin-1 (p<0.003), than cells present in blood before HBO(2)T.

Skin margins obtained from 2-day-old abdominal wounds exhibit higher expression of CD133, CD34, hypoxia inducible factor-1, and Trx-1 vs. margins from refractory lower extremity wounds and expression of these proteins in all wounds is increased due to HBO(2)T (p<0.003).

HBO is known to mobilize bone marrow stem cells by stimulating nitric oxide synthase. We found that nitric oxide synthase activity is acutely increased in patients' platelets following HBO(2)T and remains elevated for at least 20 hours.

 * We conclude that HBO stimulates vasculogenic stem cell mobilization from bone marrow of diabetics and more cells are recruited to skin wounds.


Connect Tissue Res. 2010 Dec;51(6):497-509. doi: 10.3109/03008201003746679. Epub 2010 May 24.

Hyperbaric oxygen-stimulated proliferation and growth of osteoblasts may be mediated through the FGF-2/MEK/ERK 1/2/NF-κB and PKC/JNK pathways

Hsieh CP, Chiou YL, Lin CY.


Orthopaedic Surgery Department and Hyperbaric Center, Changhua Christian Hospital, Changhua, Taiwan, ROC.


We investigated whether the hyperbaric oxygen (O₂) could promote the proliferation of growth-arrested osteoblasts in vitro and the mechanisms involved in this process. Osteoblasts were exposed to different combinations of saturation and pressure of O₂ and evaluated at 3 and 7 days.

Control cells were cultured under ambient O₂ and normal pressure [1 atmosphere (ATA)]; high-pressure group cells were treated with high pressure (2.5 ATA) twice daily; high-O₂ group cells were treated with a high concentration O₂ (50% O₂) twice daily; and high pressure plus high-O₂ group cells were treated with high pressure (2.5 ATA) and a high concentration O₂ (50% O₂) twice daily.

Hyperbaric O₂ significantly promoted osteoblast proliferation and cell cycle progression after 3 days of treatment. Hyperbaric O₂ treatment stimulated significantly increased mRNA expression of fibroblast growth factor (FGF)-2 as well as protein expression levels of Akt, p70(S6K), phosphorylated ERK, nuclear factor (NF)-κB, protein kinase C (PKC)α, and phosphorylated c-Jun N-terminal kinase (JNK). Our findings indicate that high pressure and high O₂ saturation stimulates growth-arrested osteoblasts to proliferate. These findings suggest that the proliferative effects of hyperbaric O₂ on osteoblasts may contribute to the recruitment of osteoblasts at the fracture site. The FGF-2/MEK/ERK 1/2/Akt/p70(S6K)/NF-κB and PKC/JNK pathways may be involved in mediating this process.


Hyperbaric oxygen induces placental growth factor expression in bone marrow-derived mesenchymal stem cells

Shyu KG, Hung HF, Wang BW, Chang H. Life Sci. 2008 Jul 4;83(1-2):65-73. Epub 2008 May 23.


Division of Cardiology, Shin Kong Wu Ho-Su Memorial Hospital, and Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.


The bone marrow is home to mesenchymal stem cells (MSCs) that are able to differentiate into many different cell types. The effect of hyperbaric oxygen (HBO) on MSCs is poorly understood. Placental growth factor (PlGF) is an attractive therapeutic agent for stimulating revascularization of ischemic tissue. HBO has been shown to improve diabetic wound healing by increase circulating stem cells. We hypothesized that HBO induces PlGF expression in bone marrow-derived MSCs. The MSCs were obtained from adult human bone marrow and expanded in vitro. The purity and characteristics of MSCs were identified by flow cytometry and immunophenotyping. HBO at 2.5 ATA (atmosphere absolute) significantly increased PlGF protein and mRNA expression. The induction of PlGF protein by HBO was significantly blocked by the addition of N-acetylcysteine, while wortmannin, PD98059, SP600125 and SB203580 had no effect on PlGF protein expression. However, the specific inhibitor of nitric oxide synthase, L-NAME did not alter the PlGF protein expression induced by HBO. HBO significantly increased the reactive oxygen species production and pretreatment with N-acetylcysteine significantly blocked the induction of reactive oxygen species by HBO.

 * HBO significantly increased the migration and tube formation of MSCs and pretreatment with N-acetylcysteine and PlGF siRNA significantly blocked the induction of migration and tube formation by HBO.

 ** In conclusion, HBO induced the expression of PlGF in human bone marrow-derived MSCs at least through the oxidative stress-related pathways, which may play an important role in HBO-induced vasculogenesis.


Hyperbaric oxygen results in increased vascular endothelial growth factor (VEGF) protein expression

Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2008 Apr;105(4):417-22. Epub 2008 Feb 21.

Schulich School of Medicine and Dentistry, University of Western Ontario, London, Canada.


Hyperbaric oxygen therapy (HBO) promotes osseous healing, however the mechanism by which this occurs has not been elucidated.

 * HBO may promote angiogenesis, which is vital for bone healing.

 ** Vascular endothelial growth factor (VEGF) is one of the key factors that stimulates angiogenesis.

The objective of this study was to investigate whether HBO altered VEGF expression during bone healing.

Archived samples from calvarial defects of rabbits exposed to HBO (2.4 ATA, 90 minutes a day, 5 days a week for 4 weeks) and normobaric oxygen controls (NBO) were analyzed by immunohistochemistry.

VEGF expression in 6-week HBO samples was elevated compared to NBO (P = .012). Staining of the 12-week HBO samples was reduced compared to 6-week HBO (P = .008) and was similar to 6- and 12-week NBO control samples.

 * HBO therapy resulted in increased VEGF expression in the defects even 2 weeks after the termination of treatment (6 weeks postsurgery).