Exercise protects the heart via nitric oxide
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It’s well known that exercise is good for the heart and that it helps protect the heart from injury during a heart attack.
What was not known was how, until Emory researchers recently found that the nitric oxide produced during exercise is a key factor in this cardiovascular benefit.
Nitric oxide, a short-lived gas generated within the body, turns on chemical pathways that relax blood vessels to increase blood flow. Both the chemicals nitrite and nitrosothiol, where nitric oxide is attached to proteins, appear to act as convertible reservoirs for nitric oxide in situations where the body needs it, such as when a lack of blood flow or oxygen occurs. The team’s findings strengthen the case for nitrite and nitrosothiols as possible protectants from damage from a heart attack, says Emory thoracic surgery researcher David Lefer.
The timing of exercise also matters since exercise’s benefits don’t last.
The researchers found that exercise boosted levels of the eNOS (endothelial nitric oxide synthase) enzyme that produces nitric oxide. The levels of eNOS in heart tissue and nitrite and nitrosothiol levels in blood and heart tissue stayed high for a week after exercise ceased, unlike other heart enzymes stimulated by exercise. The protective effects did not extend beyond four weeks after exercise ended, when nitrite and nitrosothiol in the heart returned to baseline.
In mice that lack the eNOS enzyme, exercise did not protect the heart from a coronary blockage. In addition, mice that lacked the beta-3-adrenergic receptor, which allows cells to respond to the hormones epinephrine and norepinephrine, had no beneficial effects from exercise, but stimulating this receptor appears to activate eNOS. Additional animal studies are currently under way in Lefer’s lab to determine the potential benefit of drugs that activate the beta-3-adrenergic receptor following a heart attack.
