ISLAMABAD, APRIL 06 (ONLINE): DNA damage is one of the driving forces behind aging, including age-related damage to blood vessels.
\nA new study in mice investigates links between DNA damage, exercise, and heart health.
\nThe scientists conclude that increased physical activity is linked to reduced DNA damage, including sections of DNA called telomeres, which are associated with biological aging.<\/p>\n
A recent animal study from researchers in 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 is linked to reduced DNA damage in the cells that line blood vessels. This may help explain how exercise, even later in life, can reduce the risk of developing atherosclerosis.<\/p>\n
Led by Jisok Lim, PhD, a postdoctoral fellow at the University of Utah, the researchers will present their findings at the American Physiology Summit \u2014 the annual meeting of the American Physiological Society \u2014 in Long Beach, CA. The conference runs between ??April 4\u20137, 2024.How does exercise protect vascular health as we age?
\nOur risk of heart disease and other cardiovascular problems increases as we age. Commonly, this is due to atherosclerosis \u2014 a build-up of fatty substances on the lining of blood vessels.<\/p>\n
As these plaques grow, they narrow the vessels, increasing the risk of cardiovascular events like heart attacks or strokes.
\nThankfully, exercise can significantly reduce the risk of atherosclerosis. Even exercise during older age can slow plaque buildup and improve cardiovascular outcomes.<\/p>\n
However, understanding precisely how exercise benefits cardiovascular health has proven more challenging. The new study focuses on one of the likely mechanisms: DNA damage.<\/p>\n
DNA damage and telomeres: Key players in aging
\nAs we age, there is a slow loss of function across many aspects of our physiology. Part of this decline is due to damaged DNA.<\/p>\n
DNA damage occurs for many reasons, and our DNA repair mechanismsTrusted Source become more prone to errors later in life.<\/p>\n
Experts consider DNA damage central to the aging processTrusted Source, and it appears to play an important part in the declining health of our blood vessels with age.<\/p>\n
TelomeresTrusted Source are DNA \u201ccaps\u201d on the ends of chromosomes \u2014 they protect them from becoming tangled or frayed. For this reason, telomere length is an indicator of biological age, with shorter lengths associated with many age-related diseases, including cardiovascular disease.<\/p>\n
Telomeres in cells that line blood vessels are particularly sensitive to damage by a force called \u201cshear stress.\u201d<\/p>\n
\u201cThe higher the blood velocity and the smaller the arterial diameter, the higher the shear stress,\u201d explained Jan Malik, MuDr, a professor at General University Hospital in Prague, Czech Republic, not involved in this reasearch, in an interview with Medical News Today.<\/p>\n
Although our bodies have systems in place to handle this stress, when there are irregularities in blood vessels, blood flow is disruptedTrusted Source. This disruption increases the friction experienced by the cells lining blood vessels, which raises the risk of atherosclerosis.<\/p>\n
Malik, who has published papers on the topic, told us that \u201cshear stress alterations are crucial for the development of atherosclerosis.\u201d<\/p>\n
The current study from the University of Utah investigated whether exercise might reduce cardiovascular risk by minimizing DNA damage and protecting telomeres.<\/p>\n
Higher physical activity tied to less DNA damage
\nThe University of Utah scientists observed 15 male mice for 4 weeks in a cage with a running wheel. They assigned them to three categories based on how far they ran each day:<\/p>\n
high-running
\nmoderate-running
\nlow-running.
\nAt the end of the study, the scientists collected tissue from the animals\u2019 aortas \u2014 the blood vessel that carries blood from the heart. They looked at different sections of the aorta, which are exposed to varying levels of shear stress.<\/p>\n
In particular, they focused on two types of cells:<\/p>\n
endothelial cells, which line the inside of blood vessels.
\nvascular smooth muscle cells, which sit within blood vessel walls.
\nThen, they evaluated the cells\u2019 DNA damage and assessed how well their telomeres functioned.<\/p>\n
Their analysis showed that increased physical activity was associated with less DNA damage and better telomere function in endothelial cells but not vascular smooth muscle cells.<\/p>\n
Previous studies have also shown that vascular smooth muscle does not become damaged to the same extent as endothelial cells, which face the full force of blood flow.<\/p>\n
According to the conference abstract, overall, \u201cthe volume of aerobic exercise was inversely associated with DNA damage and telomere dysfunction.\u201d This means that animals that exercised most had the least damage and dysfunction.<\/p>\n
What does this study bring to the table?
\nThis study adds to the growing evidence that exercise may benefit health by defending against DNA damage and protecting telomere function.<\/p>\n
\u201cBy revealing the varied responses of aortic regions experiencing different blood flow patterns and cell types to aerobic exercise,\u201d explained Lim in a press release, \u201cthis research will provide a firm ground on a detailed and customized approach to interventions for cardiovascular health.\u201d<\/p>\n
Scientists have been studying the relationship between exercise and telomeres for some time. For instance, a 2013 studyTrusted Source found that ultra-marathon runners had longer telomeres than healthy control participants.<\/p>\n
Other studies have also identified an association between physical fitness and longer telomeres.<\/p>\n
Study did not account for sex differences
\nWhile the study yielded interesting results, it also had sizeable limitations. First and foremost, it was conducted on just 15 mice. While animal studies are a vital part of the scientific process, we must be cautious when extrapolating findings from mice to humans.<\/p>\n
MNT spoke with Yegor Yegorov, PhD, a professor at Engelhardt Institute of Molecular Biology in Moscow, Russia. He explained that while the mouse model is useful, atherosclerosis occurs in different partsTrusted Source of the vasculature in humans and mice.<\/p>\n
Similarly, he told us that \u201cthe telomere biology of mice is very different from that of humans.\u201d<\/p>\n
Another issue is how the researchers categorized the mice: They split the mice into three groups depending on how much or how little they exercised voluntarily.<\/p>\n
There may have been physiological differences between these mice that explain their different levels of activity.<\/p>\n
As Yegorov explained, \u201c[i]t is not clear what is primary: the initial good condition of the mice, allowing them to run a lot and [apparently] enjoy it, or the effect of running on health.\u201d<\/p>\n
Additionally, they only used male mice. In humans, some researchTrusted Source suggests that that females have a lower risk of cardiovascular disease until menopause. So, studies in female animals may yield different results.<\/p>\n
It is also worth mentioning that this study has not yet been peer-reviewed or published in a specialist journal. Yegorov noted certain contradictions in the study abstract, and \u201cfor a correct assessment\u201d of the study, he would like to read a full paper.<\/p>\n
However, overall, Malik told MNT that \u201cthis study brings a new little stone into the mosaic of our understanding of atherosclerosis and other [diseases of civilisation].\u201d<\/p>\n","protected":false},"excerpt":{"rendered":"
ISLAMABAD, APRIL 06 (ONLINE): DNA damage is one of the driving forces behind aging, including age-related damage to blood vessels. A new study in mice investigates links between DNA damage, exercise, and heart health. The scientists conclude that increased physical activity is linked to reduced […]<\/p>\n
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