"Exercise not only reduces the risk of a heart attack but protects the heart from injury if a cardiac arrest does occur,” reported The Daily Telegraph. It said that researchers have found that keeping fit helps the heart produce and store nitric oxide, which turns on chemical pathways that relax blood vessels and increase blood flow.
This research was mainly animal research, which looked at how heart attack damage is affected by whether mice have been exercising or not. Its findings suggest that nitric oxide, and other related proteins and chemicals, play a role. The researchers also found that the levels of a chemical made from nitric oxide in the body were higher in trained endurance athletes than non-trained individuals.
The link between exercise and a healthy heart has been demonstrated in previous studies. These findings go some way to helping us understand how one such heart benefit may work. Importantly, this study was predominantly in mice and so its findings would ideally be confirmed by further research in animals, human tissue and in humans if possible.
The study was carried out by researchers from Emory University School of Medicine in Atlanta, and other universities in the USA. Funding was provided by the American Diabetes Association, the National Heart Lung and Blood Institute of the National Institutes of Health, and the Carlyle Fraser Heart Center of Emory University Hospital. The study was published in the peer-reviewed journal Circulation Research.
This was mainly animal research aimed at investigating how exercise might protect the heart from injury. The researchers report that studies in humans have found that exercise is associated with improved survival after heart attacks, but it is not fully understood why. The researchers say that the chemical nitric oxide is thought to play a role. They wanted to assess this theory by looking at how exercise protected against heart injury in mice, and how this was related to various proteins and chemicals linked to nitric oxide production and metabolism.
Animal research is useful in identifying the biological and chemical pathways responsible for certain biological phenomena, as similar experiments could not be performed in humans.
In their experiments, the researchers placed mice in cages with a running wheel for up to four weeks, and monitored how far they ran each day. After this, the running wheel was removed from the cage. Different groups of these mice were then given a simulated heart attack either 24 hours, one week or four weeks after the wheel was removed. Other mice did not have an exercise wheel in their cages (the control group) and were kept in these cages for similar periods to the exercised mice before they were given a simulated heart attack. To simulate a heart attack, the researchers surgically cut off blood flow to a part of the mouse’s heart (similar to what happens in a human heart attack) for 45 minutes, before reversing the procedure. The mice were allowed to recover for 24 hours, after which the researchers examined their hearts to see how much damaged tissue there was.
The researchers were particularly interested in looking at the effects of exercise on the enzyme that makes nitric oxide (called eNOS), a protein that increases eNOS activity called the beta 3-adrenergic receptor (beta 3-AR) and the chemicals that are formed from nitric oxide in the body (called nitrites and nitrosothiols). The beta 3-AR is known to be stimulated by chemicals produced during exercise, and nitrites and nitrosothiols are known to help protect the heart from damage. The researchers carried out various experiments to assess the roles of these proteins and other chemicals, including examining mice that were genetically engineered to lack either eNOS or beta 3-AR.
Finally, the researchers compared the levels of nitrates, nitrites and nitrosothiols in blood samples from seven trained endurance athletes (who exercised for at least 45 minutes on at least three days a week for at least two years) and 16 non-trained individuals of a similar age.
The researchers found that mice that exercised for four weeks before their simulated heart attack had less heart injury than control mice that did not exercise. This heart protection lasted for up to a week after the exercised mice stopped exercising.
This protective effect appeared to be related to eNOS, as mice that were genetically engineered to lack this enzyme did not display the same heart protection from exercise as normal mice. Exercise caused chemical changes in eNOS, making the enzyme generate more nitric oxide, and increasing the storage of the heart-protecting nitrites and nitrosothiols in the heart.
Exercise was found to cause these changes by stimulating the beta 3-adrenergic receptor. This was demonstrated by experiments on mice that lacked this receptor, which did not show increased activity of eNOS in response to exercise, or the protective effects of exercise on the heart after simulated heart attack.
The levels of nitrites and nitrates in the blood of trained endurance athletes and non-trained individuals were similar. However, the trained endurance athletes had higher levels of nitrosothiols in their blood than non-trained individuals.
The researchers concluded that their findings show that exercise in mice protects the heart from greater injury from a simulated heart attack. They say that exercise acts on the beta 3-adrenergic receptor, leading to increased storage of the chemicals formed from nitric oxide in the heart.
This research has studied how regular exercise might reduce the damage to the heart caused by a heart attack. As this study was mainly carried out in mice that were given a simulated heart attack, the results may not be entirely representative of what happens in humans.
The finding of elevated levels of one nitric oxide metabolite in the blood of trained endurance athletes suggests that similar processes may exist in humans, but this will need confirmation in further research.