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Biomedical Bulletin
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Arginine Increases Exercise Capacity
Patients with congestive heart failure benefit from improved vascular function

hink of a garden hose and a fire hose. Now think of your arteries. When you’re resting, a nice little “garden hose” will do nicely to serve your body’s needs. But when you’re exercising, you want that thing to expand to fire-hose capacity in order to meet your muscles’ demands for more oxygen and glucose to power their contractions. Your heart beats faster to increase the blood flow, and your arteries need to dilate accordingly. When they do, they act as a kind of safety valve, protecting your heart from having to work too hard, and protecting themselves (and the tissues they supply) from being damaged by excessive blood pressure. And by facilitating increased blood flow to your muscles, they enhance your exercise capacity.

Arginine Is the Source of Nitric Oxide

What makes this system work is the layer of smooth, flat, tightly packed endothelial cells that line the inner walls of your arteries; this layer is called the vascular endothelium. In normal, healthy people, it makes the adjacent layer of muscle cells contract or relax to accommodate the body’s changing needs for blood and the precious nutrients it carries. This trick is accomplished by means of a signaling molecule, nitric oxide (NO), that is produced from the amino acid arginine. The chemical reaction that produces NO is catalyzed by the enzyme nitric oxide synthase (NOS).

Thus, nitric oxide acts as the body’s natural vasodilator (a dilator of blood vessels). It plays a crucial role not just in regulating blood pressure but also in facilitating erections, among other things. Inadequate production of NO can be a serious problem, because it leads to endothelial dysfunction, which is common in the elderly. This condition can lead to hypertension, impotence, and other ills, and it can exacerbate congestive heart failure (CHF), a condition in which a weakened heart muscle is unable to maintain adequate blood circulation in the peripheral tissues and the lungs. And, of course, endothelial dysfunction impairs exercise capacity, even in the absence of CHF.

41% Improvement with Arginine

Researchers in Poland investigated whether oral administration of arginine would improve exercise capacity in 17 patients with mild to moderate CHF.1 The patients received 3 g of arginine or placebo 3 times daily (9 g/day total) for 7 days. Testing was done on a treadmill according to a standard protocol, and the patients were asked to exercise until fatigue or dyspnea (difficulty in breathing) forced them to stop. After a 7-day washout period, the arginine and placebo regimens were reversed, and the tests were repeated—thus all the patients served as their own controls.

Whereas the controls had an average exercise duration of 70 seconds on the treadmill, the arginine treatment yielded an average duration of 99 seconds—a 41% improvement. The researchers attributed this effect primarily to improved peripheral vasodilation caused by increased NO production.

A secondary objective of this study was to look for evidence of antioxidant activity in arginine—but none was found. There have, however, been reports of antioxidant effects of arginine (including one report, coincidentally, by another Polish group).*


*See the sidebar “Arginine Boosts Antioxidant Status” in the article “Healthy Arteries—Good for the Heart, and Another Part” in the June 2004 issue. See also “Take Arginine to Heart” in the February 2004 issue.


Arginine Uptake Is Reduced in CHF

An Australian research team became interested in a more fundamental question, namely, what role does arginine play in the pathophysiology of congestive heart failure?2 They were intrigued by a scientific paradox: although nitric oxide synthase levels are sometimes elevated in the heart muscle of patients with CHF, nitric oxide levels are apparently reduced, contrary to what one would expect. (It is well known that NO levels are deficient in the vascular endothelium in CHF patients, leading to endothelial dysfunction, a consistently observed feature of this debilitating disease—but the role of NO in the heart muscle is a different matter, and a controversial one.)

The researchers studied the effects of infusing radioactively labeled arginine into the circulation of seven patients with moderate to severe CHF. By measuring the subsequent distribution of this “hot” arginine in the blood, the coronary vascular endothelium, and the heart muscle, they inferred that the rate of uptake of arginine by the patients’ heart-muscle cells was substantially reduced, and the rate of clearance of arginine from the patients’ blood was also reduced. In other words, arginine was not entering the cells at the normal rate, presumably because of a CHF-related breakdown in the molecular transport mechanism.

Our Need for Arginine Increases with Age

Endothelial dysfunction promotes not just hypertension, but also the formation of blood clots and of atherosclerotic plaque deposits, which further restrict blood flow and can lead to a heart attack. Nitric oxide is considered to be antiatherogenic, i.e., it helps prevent atherosclerosis. And since it has long been known that endothelial dysfunction increases with age, the importance of having adequate compensatory supplies of arginine, the precursor of NO, also increases with age, even when there are no symptoms of cardiovascular disease.

References

  1. Bednarz B, Jaxa-Chamiec T, Gebalska J, Herbaczynska-Cedro K, Ceremuzynski L. L-Arginine supplementation prolongs exercise capacity in congestive heart failure. Kardiol Pol 2004;60(4):348-53.
  2. Kaye DM, Parnell MM, Ahlers BA. Reduced myocardial and systemic L-arginine uptake in heart failure. Circ Res 2002;91:1198-1203.

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