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Work with mice has shown that the elevated levels of nitric oxide produced during exercise protect the heart from injury during a heart attack.
Exercise reduces the risk of heart attack by maintaining the heart muscle and the blood vessels that feed it. Exercise also reduces the damage caused by a heart attack if one does occur, but the mechanism for this protection was not understood.
Now experiments with mice has shown that voluntary exercise (in a wheel) generated nitric oxide which was stored as nitrite and compounds called nitrosothiols in the bloodstream and heart.
These stable, but relatively short-lived compounds gave protection from a heart attack. Mice given the option to exercise for four weeks were still protected one week after exercise, but not four weeks after the exercise ended. In mice that lacked the enzyme system that produces nitric oxide (eNOS), exercise gave no protection from heart attack.
Research is now underway to see whether activating the eNOS pathway immediately after a heart attack reduces damage to the heart.
Last edited: 11 January 2022 13:16
