Research

May 13, 2011

Exercise protects the heart via nitric oxide

Exercise reduces the risk of a heart attack and protects the heart from injury if a heart attack does occur. For years, doctors have been trying to dissect how this second benefit of exercise works, with the aim of finding ways to protect the heart after a heart attack.

School of Medicine researchers have identified the ability of the heart to produce and store nitric oxide as an important way in which exercise protects the heart from injury.

Nitric oxide, a short-lived gas generated within the body, turns on chemical pathways that relax blood vessels to increase blood flow and activate survival pathways. Both the chemical nitrite and nitrosothiols appear to act as reservoirs for nitric oxide in situations where the body needs it, such as a lack of blood flow or oxygen.

The Emory team's results, spearheaded by John Calvert and David Lefer, strengthen the case for nitrite and nitrosothiols as possible protectants from the damage of a heart attack.

Calvert is assistant professor of surgery at the medical school. Lefer is  professor of surgery and director of the Cardiothoracic Research Laboratory at Emory University Hospital Midtown. Collaborators included scientists at University of Colorado, Boulder, and Johns Hopkins University.

"Our study provides new evidence that nitric oxide generated during physical exercise is actually stored in the bloodstream and heart in the form of nitrite and nitrosothiols. These more stable nitric oxide intermediates appear to be critical for the cardioprotection against a subsequent heart attack," Lefer says.

Timing is key – the benefits of exercise don't last

In experiments with mice, the researchers showed that four weeks of being able to run on a wheel protected the mice from having a blocked coronary artery; the amount of heart muscle damaged by the blockage was less after the exercise period. The mice were still protected a week after the wheel was taken away.

The researchers found that voluntary exercise boosted levels of an enzyme that produces nitric oxide. Moreover, the levels of the enzyme stayed high for a week after exercise ceased, unlike other heart enzymes stimulated by exercise. The protective effects of exercise did not last beyond four weeks after the exercise period was over, the researchers found..

In mice that lack the enzyme, exercise did not protect the heart from a coronary blockage.

Another molecule that appears to be important for the benefits of exercise allows cells to respond to the hormones epinephrine and norepinephrine. All of the beneficial effects of voluntary exercise are lost in mice that are deficient in this molecule. Additional animal studies are currently underway in Lefer's lab to determine the potential benefit drugs that activate this molecule following a heart attack.

The research was supported by the American Diabetes Association, the National Institutes of Health and the Carlyle Fraser Heart Center at Emory University Hospital Midtown.

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