Magnesium, Endurance Athletes & Atrial Fibrillation - Dr. Carolyn Dean MD ND

Magnesium, Endurance Athletes & Atrial Fibrillation

December 17, 2020

In a Medscape blog by an electrophysiology cardiologist called “Endurance Exercise and Heart Disease: Look for Clues in the Genes” it seems the good doctor has stopped looking for a proper reason for heart disease and wants to “blame it on the genes.” I equate that with med school training that told us to blame patients’ symptoms on getting older after they reach age 65.

Yes, when all else fails – blame the genes. Researchers say that gene mutations that code for certain proteins in the tissue of the right ventricle can lead to a form of cardiomyopathy with the unwieldy name, arrhythmogenic right ventricular dysplasia (ARVD). I’m convinced these names are created in a smoke-and-mirrors attempt to make us sound like we know something we don’t.

What medicine doesn’t seem to know, in this case, is that the highest amount of magnesium in the body is found in the heart. Let that fact sink in for a minute!

Here’s what I say a magnesium and athletes in my book, Magnesium Miracle (2017).

When your muscles are engaged in the rapid-fire contraction and relaxation of physical exercise, if there is too much calcium (the initiator of contractions) and too little magnesium (the initiator of relaxation), muscle cramps and a buildup of lactic acid can result.

Too little magnesium is very common in athletes because so much is lost through sweating and instead of replacing with proper mineral electrolytes, including magnesium, you chug down sodium and sugar concoctions that cause brain swelling in the short term and diabetes in the long term.

Even though most athletes and coaches don’t know it, magnesium is one of the most important nutrients athletes can possibly take. Mitochondria in our cells make energy molecules called ATP (adenosine triphosphate), which are created under the influence of magnesium.

Some of the first studies investigating the relationship between magnesium and physical performance were done on animals and showed that decreased exercise capacity can be an early sign of magnesium deficiency. When the animals were given magnesium dissolved in water, their endurance was restored. Most human studies also confirm that both brief and extended exercise deplete magnesium.

A study in the journal Magnesium Research offers an overview of the importance of magnesium to the athlete.[1] The investigators outline the following:

“Magnesium is involved in numerous processes that affect muscle function including oxygen uptake, energy production and electrolyte balance. Thus, the relationship between magnesium status and exercise has received significant research attention. This research has shown that exercise induces a redistribution of magnesium in the body to accommodate metabolic needs. There is evidence that marginal magnesium deficiency impairs exercise performance and amplifies the negative consequences of strenuous exercise (e.g., oxidative stress). Strenuous exercise apparently increases urinary and sweat losses that may increase magnesium requirements by 10-20%. Based on dietary surveys and recent human experiments, a magnesium intake less than 260 mg/day for male and 220 mg/day for female athletes may result in a magnesium-deficient status. Recent surveys also indicate that a significant number of individuals routinely have magnesium intakes that may result in a deficient status. Athletes participating in sports requiring weight control (e.g., wrestling, gymnastics) are apparently especially vulnerable to an inadequate magnesium status. Magnesium supplementation or increased dietary intake of magnesium will have beneficial effects on exercise performance in magnesium-deficient individuals.”

Once the Human Genome Project tanked we realized that genes don’t control us. I say it tanked because researchers predicted they would find at least 100,000 genes that individually controlled all functions in the body. With that knowledge they thought they could “remove bad genes” and along with the genes, bad diseases. That didn’t happen because they only found about 23,000 genes so they had to admit that genes shared the 100,000 tasks in the body and that other influences were afoot.

One of the most important “other” influences is described by the new field of Epigenetics, which is basically the environment that turns genes on and off. And it seems that the biggest influence on genes is magnesium!

After The Genome Project, researchers went into the Proteome Project to identify and quantify proteins. In 2012 this research led to the discovery of the “Human Magnesome” the name given to a set of proteins within the complete makeup of human protein containing multiple binding sites for magnesium ions. Using innovative technology, researchers found that magnesium binding sites are very common in proteins and help direct their structure and function.[2] Only partway through their study they discovered that 27 percent of the human sequences studied (3,751 out of 13,689) carried magnesium binding sites.

Back to the Medscape article: Using the “too cute” byline: “Trials and Fibrillations,” the author’s far-from-cute message ignores magnesium. The article lays out the problem with ARVD and unknowingly identifies magnesium deficiency perfectly saying “Disruption of the architecture of cell-cell coupling sets up a milieu favorable for arrhythmia.”

If the cells are damaged (because of magnesium deficiency) they can’t electrically couple to create the proper heart rhythm (because of magnesium deficiency). How many athletes, how many people have damaged heart cells due to magnesium deficiency making the electrical contracting ability of the heart erratic?

I noticed that other blogs by this author report on the Heart Rhythm Society, which awarded me The Arrhythmia Alliance Outstanding Medical Contribution to Cardiac Rhythm Management Services Award 2012, but he never mentions anything about magnesium. Such remarkable bias against something as simple as magnesium for support of the heart muscle structure and function has reached a level of malpractice. We can only hope that a tipping point is reached with public education so that doctors will have to take note.

The writer of this blog says he can’t figure out why endurance athletes have “mysterious heart disease.” A study on rats that had a genetic predisposition to heart disease developed ARVD when stressed with exercise and the researchers immediately concluded that the genes were at fault. However, it is well known that strenuous exercise diminishes magnesium levels and possibly leads to heart disease by epigenetically turning on the heart disease gene.

Then the writer mentions focal cardiomyopathy, which is heart scarring that can cause arrhythmia. He says that marathoner and Ironman studies find heart enzyme elevations and transient functional impairments of the Right and Left Ventricles. These defects mostly resolve, but some hearts develop persistent scarring. The writer ends by saying that “The answer will be found in the genes.” But it won’t, the answer is in your magnesium levels, but only if they are Ionzied Magnesium blood levels!

The improper testing of magnesium levels in the body was the topic of a study on our product, ReMag published in the journal Nutrients.[3]

The European Heart Journal[4] in their study of 52,000 cross country skiers showed conclusively that endurance athletes are at higher risk for heart arrhythmia but they also failed to recognized the role of magnesium deficiency in creating these symptoms.

I say, why waste any more time and money on useless studies? Do your own experiment and measure Ionized Magnesium or at least RBC Magnesium before and after a race in your athletic patients and see just how much magnesium is lost.

Carolyn Dean MD ND

The Doctor of the Future®

RESOURCES: Along the borders and in the links of my web site you can find my books, writings, and my call-in radio show. Email your questions to:

[1] Nielsen FH, Lukaski HC. Update on the relationship between magnesium and exercise. Magnes Res 2006;19(3):180-9

[2] Piovesan D, et al. The human “magnesome”: detecting magnesium binding sites on human proteins. BMC Bioinformatics 2012. 13(Suppl 14):S10.

[3] Circulating Ionized Magnesium as a Measure of Supplement Bioavailability: Results from a Pilot Study for Randomized Clinical Trial. Nutrients 202012(5), 1245;

[4] Risk of arrhythmias in 52 755 long-distance cross-country skiers: a cohort study, European Heart Journal, Volume 34, Issue 47, 14 December 2013, Pages 3624–3631,

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