การออกกำลังกายช่วยป้องกันความเสียหายของ DNA และปัญหาหลอดเลือดที่เกี่ยวข้องกับอายุได้อย่างไร

A recent animal study by researchers from the Department of Internal Medicine at the University of Utah in Salt Lake City investigates the role of DNA damage in blood vessels and the aging cardiovascular system.

They found that increased exercise was associated with reduced DNA damage in cells lining blood vessels. This may help explain how exercise even later in life can reduce the risk of atherosclerosis.

Led by Jisook Lim, PhD, a postdoctoral fellow at the University of Utah, researchers will present their findings at American Physiology Summit - the annual meeting of the American Physiological Society - in Long Beach, Calif. The conference is April 4-7, 2024.

How does exercise protect vascular health as we age?

As we age, the risk of cardiovascular disease and other cardiovascular problems increases. This is usually due to atherosclerosis - the accumulation of fatty substances on the mucous membrane of blood vessels.

As these plaques grow, they narrow blood vessels, increasing the risk of cardiovascular events such as heart attacks or strokes.

Fortunately, physical exercise can significantly reduce the risk of atherosclerosis. Even exercise in the elderly can slow plaque formation and improve cardiovascular outcomes.

However, understanding exactly how exercise benefits cardiovascular health has proven more difficult. A new study focuses on one likely mechanism: DNA damage.

DNA damage and telomeres: key players in aging

As we age, there is a slow loss of function in many aspects of our physiology. Part of this decline is due to DNA damage.

DNA damage occurs for many reasons, and our DNA repair mechanisms become more error prone in older age.

Experts believe that DNA damage plays a central role in the aging process, and it appears to play an important role in the deterioration of our blood vessels as we age.

Telomeres are DNA "caps" at the ends of chromosomes - they protect them from tangling and fraying. For this reason telomere length is an indicator of biological age - shorter length is associated with many age-related diseases, including cardiovascular disease.

Telomeres in cells lining blood vessels are particularly susceptible to damage by a force called "shear stress."

"The higher the blood velocity and the smaller the diameter of the artery, the higher the shear stress," explained Jan Malik, M.D., M.P.H., a professor at the University General Hospital in Prague, Czech Republic, who was not involved in this study.

Although our bodies have systems in place to cope with this stress, when blood vessels are disrupted blood flow is impaired. This disruption increases the friction experienced by the cells lining the blood vessels, which increases the risk of atherosclerosis.

Malik, who has published papers on the topic, told us that "changes in shear stress are critical to the development of atherosclerosis."

An ongoing University of Utah study examined whether exercise can reduce cardiovascular risk by minimizing DNA damage and protecting telomeres.

Higher physical activity is associated with less DNA damage

Researchers at the University of Utah monitored 15 male mice for 4 weeks in a cage with a treadmill wheel. They divided them into three categories depending on how much distance they ran each day:

• swift
• moderate runner
• low-movement.

At the end of the study, the scientists collected tissue from the animals' aorta, the blood vessel through which blood flows from the heart. They studied different sections of the aorta that are subjected to different levels of shear stress.

In particular, they focused on two cell types:

• Endothelial cells lining the inside of blood vessels;
• Vascular smooth muscle cells found in the walls of blood vessels.

They then assessed the cells' DNA damage and evaluated how well their telomeres functioned.

Their analysis showed that increased physical activity was associated with less DNA damage and improved telomere function in endothelial cells but not in vascular smooth muscle cells.

Previous research has also shown that vascular smooth muscle is not damaged to the same extent as endothelial cells, which face the full force of blood flow.

According to the study abstracts, in general, "the amount of aerobic exercise is inversely proportional to DNA damage and telomere dysfunction." This means that the animals that exercised the most had the least amount of damage and dysfunction.

What does this study provide?

This study adds to the growing body of evidence that exercise can provide health benefits by protecting against DNA damage and protecting telomere function.

"By revealing the different responses of aortic regions experiencing different blood flow patterns and cell types to aerobic exercise," Lim explained in a press release, "this study will provide a solid foundation for a detailed and individualized approach to cardiovascular health interventions."

Scientists have been studying the relationship between exercise and telomeres for some time. For example, a 2013 study showed that ultramarathon runners have longer telomeres than healthy control participants.

Other studies have also found a link between physical fitness and telomere length.