MyoMax

MITOCHONDRIAL SUPPORT

MyoMax is a high-dose, 100% soy-free vitamin K2 (MK-7) supplement formulated to support healthy mitochondrial function.

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At a Glance

What is MyoMax

MyoMax is a high-dose, 100% soy-free vitamin K2 (MK-7) supplement formulated to support healthy mitochondrial function. This formula includes 300 mcg of vitamin K2 with calcium pyruvate to support ATP production. *This formula is safe for patients taking anticoagulants like warfarin.

Why MyoMax?
  • 40-50% increase in ATP production within mitochondria
  • 12% increase in cardiac output
  • Improves aerobic capacity from cellular level
  • Extends duration of peak fitness by 20-30%
  • Increases efficiency in training and sports performance

MyoMax® has been clinically demonstrated to improve cardiovascular performance in healthy adults in a manner unlike any other ingredient in the market. Cardiovascular performance was measured as a change in V02max, and specifically cardiac output. These end-points were measured as part of a double-blind, placebo-controlled University study as well as an initial, pilot trial.

The results are impressive and the researching professor has described the effect of 8 weeks of supplementation with MyoMax® as being equivalent to 6 months of high intensity interval training. Another component that determines an athlete’s ability to perform is mitochondrial function and ATP production. MyoMax® has been shown to increase mitochondrial function and ATP production.

One of the main reasons that aerobic athletic performance declines with age is that the body becomes less effective at utilizing oxygen. The maximal ability to utilize oxygen can be measured by VO2max, an assessment of how much oxygen your body can use per kilogram of body weight. As a result, a high VO2max will indicate that a person can effectively utilize oxygen, which is often seen in well-trained endurance athletes.

Unfortunately, after the age of 30, VO2max will begin to decline. For non-athletes, VO2max tends to decline by about 10% every decade. However, athletes who continue their rigorous training can reduce the decline to only 5% every decade. The main reason that VO2max declines with age is because the maximal heart rate (max HR) decreases as well.

Cardiac output is defined as the volume of blood pumped, per minute, by each ventricle of the heart. Of all the measures of cardiovascular performance, cardiac output likely has the biggest impact. It is a direct measure of the body’s ability to deliver oxygen to starving muscles. An increase in cardiac output without an increase in heart rate is favored as this demonstrates increased capacity of the ventricles and the vascular system and not just on the frequency of the heartbeat.

Because cardiac output is the product of stroke volume and maximal heart rate, a decrease in max HR will directly decrease cardiac output, and in turn, oxygen delivery to the muscles. This translates to a lower VO2max and decreased athletic endurance with age. Fortunately, vitamin K2 appears to improve cardiac output by maintaining healthy mitochondrial function.

In the aforementioned University study, the group receiving MyoMax® saw more than a 13% increase in cardiac output and a steady increase at all exercise stages. With over a 13% increase in cardiac output in just 8 weeks of supplementation using MyoMax®, an athlete can experience a significant change in performance at every heart rate zone, including maximum capacity. With over 900 more liters of oxygenated blood pumping through the body in a single 24 hour period, athletes can experience a significant improvement in recovery.

As the “powerhouse” organ, we heavily depend on our hearts for optimal muscle and body tissue function. Adequate intake of vitamin K2-7 has shown to lower the risk of vascular damage because it activates what is called matrix GLA protein (MGP). MGP prevents calcium from depositing in vessel walls and joint spaces.

Vitamin K2-7 is the driver that takes free calcium from the blood, deposits from the arteries, and joint spaces sending it to the bones – thus improving cardiovascular health and bone health. In recent studies, the supplementation of Vitamin K2-7 improved cardiac output by 22% at resting heart rate and 13% at maximum heart rate. This is the definition of performance enhancement. Clinical trials have demonstrated 6-weeks of Vitamin K2-7 supplementation has the ability to increase strength, endurance, cardiovascular, and bone health.

In vitro studies using advanced mitochondrial tissue culture systems have shown that MyoMax® has the capability to increase ATP production in each cell. The increase in ATP production yields higher energy output efficiency, as more energy can be produced per molecule of glucose or fatty acid. In addition to increased ATP production, MyoMax® has been shown, in both in vitro and in vivo studies, to decrease muscle cramping and improve muscle contraction.

Dosing Instructions

Take 2 capsules daily with a meal, or as directed by your healthcare practitioner.
*THESE STATEMENTS HAVE NOT BEEN EVALUATED BY THE FOOD AND DRUG ADMINISTRATION. THESE PRODUCTS ARE NOT INTENDED TO DIAGNOSE, TREAT, CURE OR PREVENT ANY DISEASE.

Research

Tanaka H, Seals DR.

Endurance exercise performance in Masters athletes: age-associated changes and underlying physiological mechanisms. J Physiol. 2008;586(1):55-63.

McFarlin BK, Henning AL, Venable AS.

Oral Consumption of Vitamin K2 for 8 Weeks Associated with Increased Maximal Cardiac Output During Exercise. Altern Ther Health Med. 2017;23(4):26-32.

Vos M, Esposito G, Edirisinghe JN, et al.

Vitamin K2 is a mitochondrial electron carrier that rescues pink1 deficiency. Science. 2012;336(6086):1306-10.

Kulkarni VK, Upase DP, Dound YA, et al.

The effect of vitamin K2-7 in peripheral neuropathy due to Vitamin B12 deficiency and/or diabetes mellitus: A Preliminary Study. Indian Practitioner. 2013;66(10):625-629.

Georgieva E, Ivanova D, Zhelev Z, et al.

Mitochondrial dysfunction and redox imbalances as a diagnostic marker of “free radical diseases”. Anticancer Res. 2017;37(10):5373-5381.

Seyfried TN.

Cancer as a mitochondrial metabolic disease. Front Cell Dev Bio. 2015;3(43):1-12.

Ganguly G, Chakrabarti S, Chatterjee U, Saso L.

Proteinopathy, oxidative stress and mitochondrial dysfunction: cross talk in Alzheimer’s disease and Parkinson’s disease. Drug Des Devel Ther. 2017;11:797-810.

Gao F, Yang J, Wang J, et al.

Mitophagy in Parkinson’s Disease: Pathogenic and Therapeutic Implications. 2017;8:527.

Sureshbabu A, Bhandari V.

Targeting mitochondrial dysfunction in lung diseases: emphasis on mitophagy. Front Physiol. 2013;4:Article 384.

Paradies G, Paradies V, Ruggiero FM, et al.

Oxidative stress, cardiolipin and mitochondrial dysfunction in nonalcoholic fatty liver disease. World J Gastroenterol. 2014;20(39):14205-14218.

Auger C, Alhasawi A, Contavadoo M, et al.

Dysfunctional mitochondrial bioenergetics and the pathogenesis of hepatic disorders. Front Cell Dev Bio. 2015;3:40.

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