Performance: Protect Your Body

Promoting Bone Health

The years of strenuous physical exertion athletes endure day-in and day-out takes a tremendous toll on the body. While many athletes experience countless injuries throughout the course of their athletic careers, stress fractures can account for up to 20% of these sports related injuries.  Immediately following a stress fracture, the body responds by amplifying the process known as osteoclastic activity, which breaks down the old, damaged bone tissue . Simultaneously, another process, termed osteoblastic activity occurs, and works to replace the old tissue with new material. Together, these processes work to promote bone growth and mend any damage following a fracture. The ideal circumstance for rapid recovery and healing from fractures would insinuate that lower rates of osteoclastic activity and higher rates of osteoblastic activity would promote the greatest results. H2’s incredibly unique antioxidant properties have been shown to create these ideal circumstances, decreasing osteoclast while increasing osteoblast activity and thus protecting the body from the long term repercussions of fractures.  

 


Enhancing Recovery from Ligament, Tendon, Cartilage and Muscle Strain Injuries

Injuries to the ligaments (e.g. ACL, MCL, and PCL inflammation and tears), tendons (e.g. rotator cough tears), cartilage (e.g. labral tears and forms of osteoarthritis), and muscles (e.g. strain in the hamstring, lower back, neck, calf, shoulder, etc.) are very common in athletes, often leading to extended time off during the season. Long days of practice and overuse can lead to damage and the consistent pressure placed on the body can ultimately cause a full-blown tear. When such injuries take place, excessive levels of reactive oxygen species (ROS) and inflammatory cytokines arise, perpetuating the destruction to the site of injury, whether it be a ligament, tendon, cartilage, or muscle. This in turn prolongs the recovery process and can seriously impact the course of an athletes career. However, numerous studies demonstrate the tremendous benefits of antioxidants in mitigating injury to the ligaments, tendons, cartilage, and muscles. In turn, H2’s powerful antioxidant properties can profoundly speed up the body’s healing capacity, protecting athletes from full dealing with the serious consequences of full on injuries in the future. In particular, H2’s capacity to restore and heal muscles reduces the likelihood of damaged joints and future stress fractures, proving yet again to protect the body from sports-related injuries.  
 

H2 helps protect your body by…
References

[1] Stress fractures in athletes

 

“Stress fractures account for 0.7% to 20% of all sports medicine clinic injuries.”

 

Fredericson, M., Jennings, F., Beaulieu, C., & Matheson, G. O. (2006). Stress fractures in athletes. Topics in Magnetic Resonance Imaging, 17(5), 309-325. doi: 10.1097/RMR.0b013e3180421c8c

 

 

[2] Stress fractures in the athlete

 

“Maladaptation to stress causes osteoclastic activity to supersede osteoblastic activity, thereby allowing weakening of the bone. “

 

Sterling, J. C., Edelstein, D. W., Calvo, R. D., & Webb, R. (1992). Stress Fractures in the Athlete. Sports Medicine, 14(5), 336-346. doi: 10.2165/00007256-199214050-00005

 

[3] Osteoblasts and bone formation

 

“Bone is constantly being remodelled in a dynamic process where osteoblasts are responsible for bone formation and osteoclasts for its resorption.”

 

Caetano-Lopes, J., Canhão, H., & Fonseca, J. E. (2007). Osteoblasts and bone formation. Acta Reumatologica Portuguesa, 32(2), 103-110. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/17572649

 

[4] Treatment with hydrogen molecules prevents RANKL-induced osteoclast differentiation associated with inhibition of ROS formation and inactivation of MAPK, AKT and NF-kappa B pathways in murine RAW264.7 cells

 

“The bone protective effects of the hydrogen molecule (H2) have been demonstrated in several osteoporosis models. Hydrogen molecules prevented RANKL-induced osteoclast differentiation associated with inhibition of reactive oxygen species formation and inactivation of NF-κB, mitogen-activated protein kinase and AKT pathways.”

 

Li, D., Zhang, Q., Dong, X., Li, H., & Ma, X. (2013). Treatment with hydrogen molecules prevents RANKL-induced osteoclast differentiation associated with inhibition of ROS formation and inactivation of MAPK, AKT and NF-kappa B pathways in murine RAW264.7 cells. Journal of Bone and Mineral Metabolism, 32(5), 494-504. doi: 10.1007/s00774-013-0530-1

 

[5] Treatment of hydrogen molecule abates oxidative stress and alleviates bone loss induced by modeled microgravity in rats

 

“Treatment with HW alleviated HLS-induced reduction of bone mineral density, ultimate load, stiffness, and energy in femur and lumbar vertebra. Treatment with HW alleviated HLS-induced augmentation of malondialdehyde content and peroxynitrite content and reduction of total sulfhydryl content in femur and lumbar vertebra. Treatment with molecular hydrogen alleviates microgravity-induced bone loss through abating oxidative stress, restoring osteoblastic differentiation, and suppressing osteoclast differentiation and osteoclastogenesis.”

 

Sun, Y., Shuang, F., Chen, D. M., & Zhou, R. B. (2012). Treatment of hydrogen molecule abates oxidative stress and alleviates bone loss induced by modeled microgravity in rats. Osteoporosis International, 24(3), 969-978. doi: 10.1007/s00198-012-2028-4

 

[6] Hydrogen water consumption prevents osteopenia in ovariectomized rats

 

“In this study, treatment with HW suppressed the increased osteoclast surface in ovariectomized rats. The cytokine IL-6 has been proposed to act as a stimulator of osteoclast formation and activity, in particular following loss of oestrogen. Treatment with HW significantly decreased plasma TNF-α level and femoral TNF-α expression in ovariectomized rats. TNF-α has been shown to decrease osteoblastic bone formation through the suppression of osteoblast proliferation, induction of osteoblast apoptosis and inhibition of osteoblast differentiation.” 

 

Guo, J.-D., Li, L., Shi, Y.-M., Wang, H.-D., & Hou, S.-X. (2013). Hydrogen water consumption prevents osteopenia in ovariectomized rats. British Journal of Pharmacology, 168(6), 1412–1420. doi: 10.1111/bph.12036

 

[7] Treatment with hydrogen molecule alleviates TNFα-induced cell injury in osteoblast

                                     

“Tumor necrosis factor-alpha (TNFα) plays a crucial role in inflammatory diseases such as rheumatoid arthritis and postmenopausal osteoporosis. Recently, it has been demonstrated that hydrogen gas, known as a novel antioxidant, can exert therapeutic anti-inflammatory effect in many diseases. Treatment with H(2) alleviates TNFα-induced cell injury in osteoblast through abating oxidative stress, preserving mitochondrial function, suppressing inflammation, and enhancing NO bioavailability.”

 

Cai, W., Zhang, M., Yu, Y., & Cai, J. (2012). Treatment with hydrogen molecule alleviates TNFα-induced cell injury in osteoblast. Molecular and Cellular Biochemistry, 373(1-2), 1-9. doi: 10.1007/s11010-012-1450-4

 

[8] Oxidative stress, chronic disease, and muscle wasting

                     

“It has been hypothesized that catabolic programs leading to muscle wasting are mediated by oxidative stress.”

 

Moylan, J. S., & Reid, M. B. (2007). Oxidative stress, chronic disease, and muscle wasting. Muscle & Nerve, 35(4), 411-429. doi: 10.1002/mus.20743

 

[9] Rotator cuff degeneration etiology and pathogenesis

 

“Oxidative stress leads to tenocyte apoptosis via the JNK-MMP pathway and likely contributes to further tendon degeneration.”

 

Nho, S. J., Yadav, H., Shindle, M. K., & MacGillivray, J. D. (2008). Rotator cuff degeneration etiology and pathogenesis. The American Journal of Sports Medicine, 36(5), 987-993. doi: 10.1177/0363546508317344

 

 

[10] Involvement of cytochrome c release and caspase-3 activation in the oxidative stress-induced apoptosis in human tendon fibroblasts

 

“The data suggest that oxidative stress-induced apoptosis in human tendon fibroblasts is mediated via pathway(s) that includes release of cytochrome c from mitochondria to the cytosol and activation of caspase-3.”

 

Yuan, J., Murrell, G. A., Trickett, A., & Wang, M. (2003). Involvement of cytochrome c release and caspase-3 activation in the oxidative stress-induced apoptosis in human tendon fibroblasts. Biochimica et Biophysica Acta, 1641(1), 35-41. doi: 10.1016/s0167-4889(03)00047-8

 

 

[11] Potential involvement of oxidative stress in cartilage senescence and development of osteoarthritis: Oxidative stress induces chondrocyte telomere instability and downregulation of chondrocyte function

 

“Our findings clearly show that the presence of oxidative stress induces telomere genomic instability, replicative senescence and dysfunction of chondrocytes in OA cartilage, suggesting that oxidative stress, leading to chondrocyte senescence and cartilage ageing, might be responsible for the development of OA. New efforts to prevent the development and progression of OA may include strategies and interventions aimed at reducing oxidative damage in articular cartilage.”

 

Yudoh, K., Nguyen, V. T., Nakamura, H., Hongo-Masuko, K., Kato, T., & Nishioka, K. (2005). Potential involvement of oxidative stress in cartilage senescence and development of osteoarthritis: Oxidative stress induces chondrocyte telomere instability and downregulation of chondrocyte function. Arthritis research and therapy, 7(2), 380-391. doi: 10.1186/ar1499

 

 

[12] The role of reactive oxygen species in homeostasis and degradation of cartilage

 

“Some intracellular signaling pathways are redox sensitive and ROS are involved in the regulation of the production of some biochemical factors involved in cartilage degradation and joint inflammation. Further, ROS may cause damage to all matrix components, either by a direct attack or indirectly by reducing matrix components synthesis, by inducing apoptosis or by activating latent metalloproteinases. This review of the literature supports the concept that ROS are not only deleterious agents involved in cartilage degradation, but that they also act as integral factors of intracellular signaling mechanisms.”

 

Henrotin, Y., Bruckner, P., & Pujol, J. (2003). The role of reactive oxygen species in homeostasis and degradation of cartilage. Osteoarthritis and Cartilage, 11(10), 747-755. doi: 10.1016/s1063-4584(03)00150-x

 

[13] Development of vitamin C irrigation saline to promote graft healing in anterior cruciate ligament reconstruction

 

“In conclusion, this study supports the use of vitamin C irrigation saline for clinical application in ACL reconstruction in order to promote graft healing.”

 

Fu, S., Cheng, W., Cheuk, Y., Mok, T., Rolf, C., Yung, S., & Chan, K. (2013). Development of vitamin C irrigation saline to promote graft healing in anterior cruciate ligament reconstruction. Journal of Orthopaedic Translation, 1(1), 67-77. doi: 10.1016/j.jot.2013.06.001

 

 

[14] Antioxidant enzyme peroxiredoxin 5 is upregulated in degenerative human tendon

 

“The differential expression of PRDX5 in normal and degenerate tendon shows that a thioredoxin peroxidase with antioxidant properties is upregulated under pathophysiological conditions and suggests that oxidative stress may be involved in the pathogenesis of tendon degeneration.”

                                                               

Wang, M., Wei, A., Yuan, J., Clippe, A., Bernard, A., Knoops, B., & Murrell, G. A. (2001). Antioxidant enzyme peroxiredoxin 5 is upregulated in degenerative human tendon. Biochemical and Biophysical Research Communications, 284(3), 667-673. doi: 10.1006/bbrc.2001.4991

 

[15] Overexpression of antioxidant enzyme peroxiredoxin 5 protects human tendon cells against apoptosis and loss of cellular function during oxidative stress

 

“Overexpression of PRDX5 in human tendon cells via transfection inhibited H(2)O(2)-induced tendon cell apoptosis by 46% (P<0.05), and prevented the decrease in tendon cell collagen synthesis which occurs under H(2)O(2) challenge, although the decrease in collagen synthesis was small. Results from our study indicate that the antioxidant enzyme PRDX5 plays a protective role in human tendon cells against oxidative stress by reducing apoptosis and maintaining collagen synthesis.”

 

Yuan, J., Murrell, G. A., Trickett, A., Landmeters, M., Knoops, B., & Wang, M. X. (2004). Overexpression of antioxidant enzyme peroxiredoxin 5 protects human tendon cells against apoptosis and loss of cellular function during oxidative stress. Biochimica et Biophysica acta, 1693(1), 37-45. doi: 10.1016/j.bbamcr.2004.04.006

 

[16] Vulnerability to ROS-induced cell death in ageing articular cartilage: The role of antioxidant enzyme activity

 

“Substantial loss of chondrocytes occurs in rat articular cartilage which may result from increased vulnerability to elevated intracellular ROS levels, consequent upon a decline in antioxidant defense.”

 

Jallali, N., Ridha, H., Thrasivoulou, C., Underwood, C., Butler, P., & Cowen, T. (2005). Vulnerability to ROS-induced cell death in ageing articular cartilage: The role of antioxidant enzyme activity. Osteoarthritis and Cartilage, 13(7), 614-622. doi: 10.1016/j.joca.2005.02.011

 

[17] The relationship between oxidative stress and the functional capacity of skeletal muscle

 

“The ROS increase due to changes in antioxidant enzyme activity may also be at the root of the observed modifications in membrane fluidity and may affect the functional capacity of muscle by determining fatigue and weakness.”

 

Kondo, H. (1998). Oxidative stress in skeletal muscle atrophy induced by immobilization. Oxidative Stress in Skeletal Muscle, 197-213. doi: 10.1007/978-3-0348-8958-2_12

 

[18] Recent progress toward hydrogen medicine: Potential of molecular hydrogen for preventative and therapeutic applications

“H2 shows not only effects against oxidative stress, but also various anti-inflammatory and anti-allergic effects. H2 prevented the decline of the mitochondrial membrane potential. This suggested that H2 protected mitochondria from OH. Along with this protective effect, H2 also prevented a decrease in the cellular level of ATP synthesized in mitochondria. The fact that H2 protected mitochondria and nuclear DNA provided evidence that H2 penetrated most membranes and diffused into organelles.”

 

Ohta, S. (2011). Recent progress toward hydrogen medicine: Potential of molecular hydrogen for preventative and therapeutic applications. Current Pharmaceutical Design, 17(22), 2241-2252. doi: 10.2174/138161211797052664

 

 

[19] Molecular hydrogen in sports medicine: New therapeutic perspectives

“In the past 2 decades, molecular hydrogen emerged as a novel therapeutic agent, with antioxidant, anti-inflammatory and anti-apoptotic effects demonstrated in plethora of animal disease models and human studies. In particular, hydrogen therapy may be an effective and specific innovative treatment for exercise-induced oxidative stress and sports injury, with potential for the improvement of exercise performance.”

 

Ostojic, S. (2014). Molecular hydrogen in sports medicine: New therapeutic perspectives. International Journal of Sports Medicine, 36(4), 273-279. doi: 10.1055/s-0034-1395509

 

[20] The effects of hydrogen-rich formulation for treatment of sports-related soft tissue injuries

 

“Since hydrogen therapy in humans seems to be beneficial for treating inflammation, ischemia-reperfusion injury and oxidative stress, it seems plausible to evaluate the effects of exogenously administered hydrogen as an element of instant management of sport-related soft tissue injuries (e.g. muscle strain, ligament sprain, tendonitis, contusion). The investigators expect that the administration of hydrogen will significantly improve inflammation outcomes (e.g. decrease in serum C-reactive protein) as compared to the placebo, with topical hydrogen administration will additionally improve post-injury recovery outcomes (e.g. pain intensity, degree of swelling). These results could support the hypothesis that hydrogen-rich intervention may be included as an element of immediate treatment for sport-related soft tissue injuries.”

 

Ostojic, S, M. (2013, September). The effects of hydrogen-rich formulation for treatment of sports-related soft tissue injuries. Retrieved from https://clinicaltrials.gov/ct2/show/study/NCT01759498

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