HypOxygen – The Oxygenation Enhancement Support Formula

HypOxygen is a potent new product that contains specific nutrients needed to support the production and regulation of red blood cells and hemoglobin, which transport oxygen molecules throughout the body. HypOxygen also provides nutrients with vasodilation effects, which further promotes oxygen delivery to muscle tissue and accelerates the removal of metabolic waste byproducts such as lactic acid and ammonia. High intensity exercise creates an oxygen deficit that causes a buildup of these compounds and results in the rapid onset of fatigue. The synergistic ingredients in HypOxygen have been shown to have positive effects upon VO2 max, which is the maximum amount of oxygen an individual can utilize during exercise.

EPO Stimulators

The sports nutrition industry is rapidly becoming inundated with products touting their ability to stimulate the production of erythropoietin (EPO) and increase red blood cells and hemoglobin. But, what’s the end game for these products? Athletes are looking for legal methods to enhance oxygen uptake and delivery to working muscle tissue and accelerate the removal of metabolic waste byproducts. In a word, they want improved “recovery.” What’s strange is that most of these so-called EPO boosting supplements only contain an insignificant amount of iron, which is the most vital nutrient involved in the production of new oxygen carrying red blood cells. Even injectable EPO being used illegally by athletes requires an adequate supply of iron for red blood cell synthesis. In short, if EPO is present without sufficient iron, there is insufficient fuel for red blood cell production.

Iron Has Been Getting a Bad Rap

For many years now, there has been a tendency for supplement companies to market iron free products. This trend started with an often quoted Finnish study published in 1992 by Salonen, et al. These researchers found that men with high serum ferritin levels (index of iron status) had a two-fold increase in the incidence of heart attacks (1). They hypothesized that free radicals induced by iron caused the increase in the rate of heart disease. However, later research provided an alternate explanation for these observations. It is now believed that there is an inflammatory component to heart disease and that serum ferritin functions as an acute reactant and becomes elevated as a part of the inflammatory process (2). In fact, three major studies have been published since the Finnish report, which have found NO relationship between heart disease and elevated iron status (3, 4, 5). There is little evidence that supplemental iron has played any role in increasing the incidence of heart disease. Nevertheless, iron supplementation has continued to get an undeserved bad rap for almost two decades. There is a danger of iron overload to people with a rare hereditary disease called hemochromatosis (excessive iron accumulation). This condition has been found to exist in between 0.07% and 0.5% of people in various surveys (6). (It is advisable to ask your doctor to check your serum ferritin along with your hemoglobin before iron supplementation).

Exercise at High Altitude and Iron Stores

Nutritional factors, particularly iron stores, play a critical role in an athlete’s ability to respond to high altitude or hypoxic (low oxygen) training. In a series of studies involving more than 100 competitive distance runners, 40% (60% of women and 25% of men) were found to have reduced iron stores based on a low serum ferritin level. The athletes with a low ferritin level prior to high altitude exposure (male and female) were unable to increase the volume of red blood cell mass and did not increase VO2 max or improve performance (7). Iron depletion may not only compromise oxygen carrying capacity, but also reduces VO2 max and performance, even in non-anemic athletes. Thus iron stores should be normalized before undertaking a period of high altitude or simulated altitude training.

High altitude or hypoxic training has been shown to stimulate physiological adaptations, including increases in EPO and red blood cell levels. This enhances the body's oxygen utilization system and increases the efficiency of cellular energy. HypOxygen can be used effectively in conjunction with all hypoxic training methods (tents, chambers, masks, etc.), and offers advantages that can considerably improve athletic training, performance, recovery and overall health.

Enter to Win a Snac Prize Pack>>

Return to Science Behind the Supps>>

Prevalence of Iron Deficiency in Male Athletes

A recent 2009 study was conducted to assess the prevalence of iron deficiency in competitive male athletes. In total, 90 elite athletes practicing a variety of disciplines including judo, rowing, pentathlon and volleyball, aged 16-33 years, were studied. Iron deficiency was found in 43% of the subjects. Despite a lack of anemia among the studied athletes, the incidence of latent iron deficiencies (iron depletion and iron-deficient erythropoiesis) was very high (8).

Iron Status and Female Athletes

Active women with low ferritin levels were studied. After iron supplementation, VO2 max was significantly greater, blood lactate decreased and endurance time to exhaustion increased by 38% (9). In another study, non-anemic female adults were supplemented with iron, vitamin C and folic acid for 15 days. VO2 max and ATP production significantly increased and improved physical work capacity (10).

Nitric Oxide Products and Iron Supplementation

Strenuously exercised animals have been found to have increased nitric oxide levels and low iron status. Iron levels were decreased in both blood plasma and tissues. This data suggests that increased production of nitric oxide might cause low or suboptimal iron status as an impact of exercise (11). The sports nutrition market is flooded with nitric oxide boosting products and consumers need to be aware that increasing nitric oxide levels can reduce iron stores.

HypOxygen contains iron bisglycinate which is the best form of iron. The absorption rate of iron bisglycinate has been shown to be up to four times higher than other forms of iron supplementation (12). Iron bisglycinate absorption has also been shown to be controlled and regulated by the body’s iron status and to have a lower potential for toxicity compared to the commonly used iron sulfate. Thus, there is little chance of toxicity from the recommended use of this form of iron (13).

Exercised-Induced Destruction of RBCs (Red Blood Cells)

Exercise-induced hemolysis (destruction of red blood cells with release of hemoglobin) has been reported for more than six decades (14). In particular, distance running has been associated with significant hemolysis with RBC turn over being much higher (15). Studies have suggested that mechanical damage to RBCs occurs as they pass through the capillaries of the foot during the foot strike phase (16,17). However, studies on athletes involved in sports without foot impact have also found exercised-induced hemolysis, including swimming, weightlifting and rowing (18, 19, 20). Apart from foot strike, other mechanisms may contribute to hemolysis. Oxidative stress has been implicated in the “aging” of RBCs (21) and there are numerous reports of oxidative damage and antioxidant depletion after exercise (22). It has also been reported that compression of large muscle groups on capillaries may accelerate hemolysis of older RBCs (23). Normally, about 70% of the body’s iron is found in hemoglobin in circulating RBCs. Numerous studies have indicated that distance runners have compromised iron stores (16, 17, 24, 25). The mechanical trauma of foot strike that is associated with iron depletion in runners is consistent with evidence that athletes who participate in other foot impact sports such as basketball and tennis have lower iron stores compared with cyclists and rowers (26).

In addition, exercised-induced hematuria (blood in urine) has been described after several forms of exercise (27, 28, 29). These include contact sports, such as boxing and football, and noncontact sports including running, rowing and swimming (30, 31, 32). In a study of 45 male and female long distance runners, 24% were found to have hematuria after a race (30).

L-Carnitine L-Tartrate and Exercise Recovery Responses

There has been a great deal of research examining the potential of carnitine supplementation to spare muscle glycogen and improve exercise performance (33, 34). The L-carnitine L-tartrate contained in HypOxygen has been found to effectively assist in recovery from high-repetition squat exercise. Researchers found the beneficial effects of carnitine on exercise recovery responses to include improved blood flow and reduced free radical formation, tissue damage and muscle soreness (35). The positive effects of carnitine supplementation on VO2 max have also been demonstrated in studies involving various types of athletes (36, 37). One of the consequences of high-intensity training is hypoxia (low blood oxygen), which increases the concentration of ammonia (38). Ammonia accumulation has been associated with muscle fatigue and L-carnitine L-tartrate has been found to decrease athletes’ ammonia levels in a well-controlled study (39).

There is an overwhelming amount of research data that supports the effectiveness of the ingredients in HypOxygen. This science-based formulation provides a wide range of potential benefits for men and women from everyday fitness enthusiasts to world-class athletes.

This article is supplied and sponsored by SNAC. For more on SNAC, visit www.snac.com.
These statements have not been evaluated by the Food and Drug Administration. Products are not intended to diagnose, treat, cure, or prevent any disease.

Enter to Win a Snac Prize Pack>>

Return to Science Behind the Supps>>


1. Salonen JU, et al. High stored iron levels associated with excess risk of myocardial infarction in Western Finnish men. Circulation (1992) 86:803-811.
2.  Alexander RW. Inflammation and coronary heart disease. N Engl J Med    
 (1994) 331:468-69.
3. Sempos CT, et al. Body iron stores and the risk of coronary heart disease. N Eng J Med (1994) 330:1119-1124.
4. Stampfer MJ, et al. A prospective study of plasma ferritin and the risk of 
myocardial infarction is US physicians. Circulation (1993) 87:11.
5. Giles WH, et al. Body iron stores and the risk of coronary heart disease. N 
Engl J Med (1994) 331:1159-60.
6.  Lynch SR. Iron overload: Prevalence and impact on health. Nutrition   
Reviews (1995) (53) 9:255-60.
7. BD Levine and J Stray-Funderson. Exercise at High Altitude. Chapter 21, page 125. Sports Medicine Secrets by Morris D Mellion, et al.
8. Jadwiga Malczewska-Lenczowska, et al. Prevalence of iron deficiency in male elite athletes. Biomedical Human Kinetics (2009) Vol.1 (1): 36-41.
9. Lamanca JJ, Haymes EM. Effects of iron repletion on VO2 max, endurance and blood lactate in women. Med sci sports exerc. 1993 Dec;25(12):1386-92.
10. Basu S, etal. Effects of supplementation of iron with vitamin C and folic acid on aerobic capacity of adult females. Biomedicine. 1997;17(1):35-40.
11. Zhong Mingqian, et al. Increased nitric oxide is one of the causes of changes in iron metabolism in strenuously exercised rats. Am J Physiol Regul Integr Comp Physiol. Mar 20001, vol. 28, issue 3 R739-743.
12. Adeliac Bovell-Benjamin, et al.  Iron absorption from ferrous bisglycinate and ferric trisglycinate in whole maize is regulated by iron status. June 2000, Amer Journ of Clin Nutr, Vol. 71, No. 6, 1563-1569.
13. Jeppsen RD, et al. Safety evaluation of ferrous bisglycinate chelate. Food Chem Toxicol. July 1999. 37(7):723-31.
14. Gilligan Dr, et al. Physiological intra-vascular hemolysis of exercise hemoglobinemia and hemoglobinuria following cross-country run. 
J Clin Lab Inest (1943) 22:859-869.
15. Weight LM, et al. Haemolytic Effects of Exercise. Clin Sci (Lond) (1991) 81:147-152.
16. Colt E, et al. Low Ferritin Levels in Runners. J Sports Med Phys Fitness (1984) 24:13-17.
17. Dufaux B, et al. Serum ferritin, transferrin, haptoglobin and iron is middle and long distance runners, elite towers, and professional racing cyslists. Int J Sports Med (1981) 2:43-46.
18. Bula B, et al. Myogeenic Causes of Hemolysis. Phys Ed Sport (1966)2:33-68.
19. Schobersberger W, et al. Consequences of 6 weeks of strength training on red cell O2 transport and iron status. Eur J Appl Physio (1990) 60:163-168.
20. Eichner ER, et al. Gastrointestinal bleeding in athletes. Phy Sports Med (1989) 17:128-140
21. Clark MR, et al. Senescence of Red Blood Cells: Progress and Problems. Physiol Rev (1988) 68:503-554.
22. Smith JA. Exercise, Training and Red Blood Cell Turnover. Sports Med (1995) 19:9-31.
23. Miller BJ, er al. Foot Impact and Intravascular Hemolysis During Distance Running. Int J Sports Med (1988) 9:56-60.
24. Hunding A, et al. Runer’s Anemia and Iron Deficiency. Acta Med Scand (1981) 209:315-318.
25. Resina AL, et al. Comparison of RBD Indices and Serum Iron Parameters in Trained Runners and Control Subjects. Haematologica (1988) 73:449-454.
26. Telford RD,et al. Sex, Sport and Body-Size Dependency of Hematology in Highly Trained Athletes. Med Sci Sports Exerc (1991) 23:788-794.
27. Jones GR, et al. Sports related hematuria: A Review. Clin J Sport Med 
(1997 Apr) (2):119-25.
28. Gambrell et al. Exercised-induced hematuria. Am Fam Physician 
(1996 Feb) 53(3):905-14.
29. Abarbanel J, et al. Sports hematuria. J Urol (1990 May) 143(5):887-90.
30. Kallmeyer JC, et al. Urinary changes in ultra long distance marathon runners. Nephron (1993) 64(1):119-21.
31. Blacklock NJ. Bladder trauma in the long distance runner. Br J Urol (1977 Apr) 49(2):129-32.
32. Fassett RG, et al. Urinary red cell morphology during running. Br Med J (Clin Res Ed) (1982 Nov 20) 285 (6353):1455-7.
33. Brass EP, et al.  The role of carnitine and carnitine supplementation during   exercise in man and in individuals with special needs.  J Am Coll Nutr (1998) 17:207-215.
34. Heinonen OJ. Carnitine and physical exercise. Sports Med (1996) 22:109-132.
35. Volek JS, et al. L-Carnitine L-Tartrate supplementation favorably affects markers of recovery from exercise stress. Am J Physiol Endrocrinol Metab (2002) E474-E482.
36. Dragan G et al. Phsiologie (1987) 24(1):23-28.
37. Swart I el al. Nutr Res (1997) 17:405
38. Karlic H et al Nutrition (2004) 20:709
39. Galloway SDR et al. FASEB  J (2004) 18(4-5):502.5.