Even though exercise benefits patients suffering from a heart injury or heart attack, the way it does this is apparently unknown. In a major breakthrough, experts from the Emory University School of Medicine found that the ability of the heart to produce and store nitric oxide enables exercise to protect the heart after a heart attack or injury. Nitric oxide is a gas generated within the body that seemingly turns on chemical pathways. These pathways in turn, may relax blood vessels to increase blood flow and activate survival pathways.
While conducting experiments with mice, it was observed that mice which ran on a wheel for four weeks had a blocked coronary artery and the amount of heart muscle damaged by the blockage was less after the exercise period. Even after a week of taking away the wheel, the mice were purportedly protected. It was asserted that voluntary exercise improves levels of an enzyme that produces nitric oxide (eNOS, endothelial nitric oxide synthase).
“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,” commented David Lefer, PhD, professor of surgery at Emory University School of Medicine and director of the Cardiothoracic Research Laboratory at Emory University Hospital Midtown.
The levels of eNOS in heart tissue, nitrite and nitrosothiols in the blood as well as heart tissue allegedly stayed high for a week after exercise ceased. The protective effects of exercise may have not extended beyond four weeks after the exercise period was over. However, the effects lasted when nitrite and nitrosothiols in the heart returned to baseline. Exercise probably failed to protect the heart from a coronary blockage in mice lacking the eNOS enzyme. The results appeared even though these mice didn’t have the ability to exercise like normal mice.
The other molecule that may be crucial for the benefits of exercise is the beta-3-adrenergic receptor. This molecule possibly allows cells to respond to the hormones epinephrine and norepinephrine. All the beneficial effects of voluntary exercise are reportedly lost in mice that are deficient in this receptor. Further investigations are currently underway to determine the potential benefit of beta-3-adrenergic receptor activating drugs after a heart attack.
The research is published online in the journal Circulation Research.