Arginine Boosts Exercise Tolerance in Weakened Hearts

Arginine—A Performance Nutrient

Arginine Boosts Exercise
Tolerance in Weakened Hearts

Patients with congestive heart failure showed improved
cardiovascular function during endurance exercise
By Richard P. Huemer, M.D.

e all know about traffic arteries—but where are the traffic veins? Perhaps an artery becomes a vein when you turn around and go the other way. For the moment, let’s think of those highways as veins at rush hour, which means one thing: congestion. And what often happens, eventually, if the congestion becomes chronic and intolerable? The state widens the highway to allow traffic to flow more freely.

Something similar happens in our bodies if our hearts are damaged or weakened. The most common causes for this are a heart attack or impaired circulation in the coronary arteries, a condition that deprives the heart of sufficient blood for its own nourishment. Another common cause is prolonged pumping against excessive resistance, such as that caused by hypertension (high blood pressure). All these factors can be minimized through regular exercise and good diet.

With the heart damaged or weakened, its pumping action becomes increasingly inefficient, and the blood slows down and backs up in our veins, creating congestion. If this chronic condition becomes severe enough, some veins, notably those in the neck, become distended (widened) as a result. This aids in blood flow, but at the expense of loss of tone in the veins, which makes matters worse in the long run.

Congestive Heart Failure: Stalled Blood

The condition we’re talking about is called congestive heart failure (CHF), or just plain heart failure. This term can understandably cause some confusion—it does not mean, as some people think, that the heart simply fails to work (there’s a five-letter word for that). CHF is deemed to exist when the heart’s pumping action can no longer meet the body’s normal demands for oxygen and the other nutrients carried by our blood. It results in reduced exercise tolerance (decreased physical capacity), among other things. A characteristic symptom is shortness of breath during exertion.

It’s not just the veins that become congested. More serious is that fact that the heart itself, as it progressively weakens, becomes more and more congested with blood that should be ejected with each heartbeat, but isn’t. This causes the heart muscle to become distended and enlarged (flabby), making it that much more difficult for it to contract with the force necessary to eject the required amount of blood.

As the condition worsens, the stroke volume—the amount of blood ejected into the aorta with each heartbeat—diminishes. A good measure of the heart’s pumping efficiency (or lack of it) is given by the ejection fraction (EF), defined as the stroke volume divided by the volume of blood contained in the filled left ventricle just before it contracts. In a normal heart, the EF is 0.55 or greater, i.e., the heart’s pumping efficiency is 55% or greater. CHF is characterized by an EF of 0.40 or less; in severe cases, it can be as low as 0.10 or even less.

How Serious Can CHF Be?

A serious complication of CHF is pulmonary edema (excess intracellular fluid in the lungs), caused by congestion in the pulmonary blood vessels. This impairs oxygen exchange in the lungs, resulting in less oxygen and more carbon dioxide in our arterial blood, upon which every cell in our bodies depends for proper nourishment. A symptom of poor oxygenation is cyanosis (bluish skin color).

Yet another major problem with CHF is impaired blood flow to the kidneys, which depresses their vital function. It also causes them to retain more water and salt in an effort to expand the plasma volume and compensate for their reduced blood supply. Excessive fluid retention, however, merely makes the venous congestion worse, thus exacerbating the condition rather than alleviating it. A common symptom of fluid retention is edema of the legs, especially the ankles.

The consequences of CHF become increasingly severe and, eventually, fatal—the ultimate heart failure. So how do we prevent that annoying outcome? There was a clue above, when I mentioned hypertension, as well as regular exercise and good diet. Hypertension has many causes and no cures, but exercise can help control it or reduce it, as can a healthy diet and some dietary supplements. One such supplement is the versatile amino acid arginine, a constituent of most proteins.

How Much Arginine Is Enough?

Considering the relatively high protein content of the typical American diet, one might suppose that dietary intake of arginine, plus our bodies’ own internal production of it, would ensure that a deficiency hardly ever occurred. (Among the foods that tend to be rich in arginine are turkey, chicken, nuts, fish, chocolate, and garlic.) There are, however, some situations, especially in various disease states, in which there is insufficient arginine to accomplish a certain metabolic task (which is a good way to define deficiency).

One such situation occurs when blood vessels need to dilate but cannot do so adequately because their rate of production of nitric oxide (NO) is insufficient for the purpose. NO is best known as a poisonous gas (and an industrial and automotive air pollutant). Paradoxically, however, it is also a natural, beneficial neurotransmitter and signaling molecule that plays a fundamental role in the cardiovascular system, where it acts as a vasodilator (a dilator of blood vessels), both at rest and during exercise. In so doing, it modulates the structure and tone of our blood vessels and helps regulate blood pressure.

Arginine Produces NO Benefits (read that carefully)

Arginine is the only natural source of NO in our bodies. The NO molecules are formed in various places, including the brain, but here we are interested in their formation in the inner lining of our blood vessels, called the endothelium, which consists of a single layer of smooth, flat, tightly packed cells. When NO molecules are produced in our endothelial cells, they quickly diffuse into the underlying arterial muscle cells, causing them to relax—that’s vasodilation.

Promoting vasodilation improves circulation, which allows oxygen and other nutrients to be distributed more efficiently throughout the body. That, in turn, improves our exercise tolerance, which depends on abundant nourishment of muscle cells during exertion. This could be of great benefit to patients with congestive heart failure, who are known to suffer dysfunction of the arginine-NO pathway, as well as to patients with other cardiovascular diseases, such as peripheral arterial disease, coronary artery disease, and pulmonary hypertension.

A team of researchers in Strasbourg, France, investigated whether a 6-week regimen of arginine supplementation (6 g twice daily) might enhance exercise tolerance in patients with chronic, stable CHF.1 They enrolled ten middle-aged (average age 54) patients with an average ejection fraction of 0.26 (26% pumping efficiency). The patients’ condition was such that they were comfortable at rest but had slight limitation of physical activity. Six were in the treatment group, and four served as controls. All patients performed a 30-minute endurance test on a stationary exercise bicycle at the beginning and end of the 6-week test period so that the researchers could assess their progress, if any.

Arginine Reduced Heart Rate and Lactate

“If any” proved to be substantial. Hemodynamic, respiratory, and metabolic functions measured at rest, during exercise, and during the postexercise recovery period showed that the patients who received arginine did indeed have improved exercise tolerance compared with the controls (who showed no improvement).

The principal benefit of arginine treatment was seen in peak heart rate during exercise: it decreased by an average of 8 beats/min over the 6-week period. Also improved were the patients’ exercise-induced blood lactate levels, which decreased by 24%. Lower lactate levels (which were seen at rest as well as during and after exercise) indicate improved oxygen availability and hence a reduction in muscular stress during exercise.

Blood pressure in the arginine-treated patients remained unchanged over the 6-week period, but because the heart rate had decreased, so had the product of the heart rate times the systolic blood pressure; this product is considered to be a good reflection of cardiac burden during exercise.

Of particular interest to the researchers was the fact that the heart-rate and lactate-level benefits observed in this study were very similar to those obtained from 6 weeks of physical training in cardiac patients following heart transplantation. They suggested that arginine supplementation might be useful as a therapeutic adjunct to physical training in CHF patients.

Don’t Just Sit There

The next time you’re crawling along, bumper-to-bumper, on a busy traffic “vein” at rush hour, wishing there were more lanes to accommodate all those cars, you’ll have plenty of time to think about the analogy between that situation and the one inside patients with congestive heart failure. It’s not a pretty picture, but at least you’ll know that, for the patients, there is something that can be done right away to help alleviate the congestion and make things flow a little more smoothly. It’s called arginine.


  1. Doutreleau S, Mettauer B, Piquard F, Rouyer O, Schaefer A, Lonsdorfer J, Geny B. Chronic L-arginine supplementation enhances endurance exercise tolerance in heart failure patients. Int J Sports Med 2006;27(7):567-72.

The Arginine Paradox

There used to be a standing joke among scientists that the laws of aerodynamics prove that a bumblebee can’t fly, because it’s too large and heavy an insect to be lifted by such small, delicate wings. But because bumblebees don’t know that, they fly.

It only goes to show that, at any time in history, there are paradoxes in the natural world that we have not yet been able to figure out. Throughout history, many people have cited things they couldn’t understand as being evidence of the supernatural. Scientists, on the other hand, have sought to explain them by working harder at understanding nature, knowing that science is where the answers ultimately lie. Over time, the “supernatural” phenomena yield, one by one, to our persistent inquiry and become part of our common knowledge.

Currently, scientists have hypotheses, but no definitive answers, regarding something called the arginine paradox. It seems that arginine, not knowing any better, does something that it “can’t” do, according to our conventional understanding of cellular biochemistry. Here’s a synopsis.

The enzyme that catalyzes the synthesis of nitric oxide (NO) from arginine in our endothelial cells is called endothelial nitric oxide synthase (eNOS). Because there is usually an ample amount of arginine in our blood—and, therefore, in our cells, where the arginine winds up—the eNOS molecules are “saturated,” meaning that they have all the arginine molecules they can handle at any given moment. Theoretically, therefore, adding more arginine could not increase the rate of production of NO—the excess arginine in our cells would just hang around, so to speak, feeling useless.

But here’s the thing: adding more arginine does increase the rate of NO production, thereby facilitating the vasodilation that our blood vessels often need. Scientists are not really sure how to explain it, and consumers, by and large, don’t really care, as long as it works—which it definitely does.

Hanging around in our cells, by the way, is something that NO cannot do, because it’s a highly reactive free radical (one that can be either beneficial or harmful, depending on the conditions). It can survive for no more than a few seconds in our cells before reacting with something. Thus we never have a supply of NO to fall back on when it’s needed—it must always be made on demand.

Now, if only we knew whether the arginine paradox occurs in bumblebees—maybe that’s what enables them to fly …

Dr. Richard P. Huemer received his M.D. from UCLA and did postdoctoral research in cancer immunology at CalTech. He has specialized in orthomolecular medicine for most of his career, has written and lectured extensively on alternative medicine, and has served on the editorial boards of professional journals. His published books include The Roots of Molecular Medicine: A Tribute to Linus Pauling and, with coauthor Jack Challem, The Natural Health Guide to Beating the Supergerms.

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