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Exercise protects the heart via nitric oxide
Date:5/4/2011

them from having a coronary artery was blocked; the amount of heart muscle damaged by the blockage was less after the exercise period. Importantly, the mice are still protected a week after the wheel is taken away.

The researchers found that voluntary exercise boosted levels of an enzyme that produces nitric oxide (eNOS, endothelial nitric oxide synthase). Moreover, the levels of eNOS in heart tissue, and nitrite and nitrosothiols in the blood as well as heart tissue, stayed high for a week after exercise ceased, unlike other heart enzymes stimulated by exercise. The protective effects of exercise did not extend beyond four weeks after the exercise period was over, when nitrite and nitrosothiols in the heart returned to baseline.

In mice that lack the eNOS enzyme, exercise did not protect the heart from a coronary blockage, although these mice appeared to lack the ability to exercise as much as normal mice.

Another molecule that appears to be important for the benefits of exercise is the beta-3-adrenergic receptor, which 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 receptor. One of the effects of stimulating the receptor appears to be activating eNOS. Additional animal studies are currently underway in Lefer's lab to determine the potential benefit of beta-3-adrenergic receptor activating drugs following a heart attack.


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Contact: Jennifer Johnson
jennifer.johnson@emory.edu
404-727-5696
Emory University
Source:Eurekalert

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