Researchers make new discovery about how exercise protects against cardiovascular disease

A study by researchers at Massachusetts general hospital (MGH) has identified a new molecular link between exercise and inflammation that could lead to new ways of treating cardiovascular disease.

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As well as highlighting the importance of regular physical activity, the findings suggest that further focus on how exercise dampens inflammation could lead to new approaches to prevent heart attack and strokes.

Regular physical activity is associated with overall health benefits, including lower blood pressure, improved blood sugar regulation, and healthier cholesterol levels. It also promotes the dilation of the heart’s arteries and can help the sympathetic nervous system, which regulates heart rate, be less reactive.

Risk factors for cardiovascular disease are not fully understood

There are certain risk factors for cardiovascular disease that are not fully understood."

Matthias Nahrendorf, Center for Systems Biology, Massachusetts general hospital

Specifically, the team wanted to find out more about the role chronic inflammation plays since it contributes to the formation of atherosclerotic plaques.

For the study, the team assessed the effect that physical activity has on bone marrow activity - in particular, the effect on hematopoietic stem and progenitor cell (HSPC) activity. These HSPCs have the ability to turn into any type of blood cell, including leukocytes – white blood cells that trigger inflammation.

Leukocytes combat infection by removing foreign invaders. However, “when these cells become overzealous, they start inflammation in places where they shouldn't, including the walls of arteries," explains Nahrendorf.

Comparing running mice with inactive mice

As reported in the journal Nature Medicine, the team examined two groups of mice. In one group, the mice were housed in cages that contained treadmills, while mice in the other group were housed in cages without treadmills. Some of the mice in cages with treadmills ran as far as six miles.

After a period of six weeks, the mice that ran on treadmills had significantly lower levels of HSPC activity and reduced levels of leukocytes, compared with the mice that did not run.

The team also found that the reduced leukocyte level did not make the running mice any more susceptible to infection than the inactive mice.

What was responsible for lowering HSPC activity?

Nahrendorf says the reason for the lower HSPC level among the running mice is that they produced less of the hormone leptin. Leptin is produced by fat tissue, and it helps to regulate appetite, but it also instructs HSPCs to be more active and produces more leukocytes.

Next, the team conducted two large studies involving humans. They found that levels of leptin and leukocytes were raised in people who had sedentary lifestyles and cardiovascular diseases associated with chronic inflammation.

This study identifies a new molecular connection between exercise and inflammation that takes place in the bone marrow and highlights a previously unappreciated role of leptin in exercise-mediated cardiovascular protection,"

Michelle Olive, program officer at the National Heart, Lung, and Blood Institute Division of Cardiovascular Sciences

As well as highlighting the importance of following recommendations about physical activity, the research “adds a new piece to the puzzle of how sedentary lifestyles affect cardiovascular health,” she says.

The team thinks that future studies focusing on how exercise dampens inflammation could lead to novel strategies for preventing heart attack and stroke.  

"We hope this research will give rise to new therapeutics that approach cardiovascular disease from a completely new angle," concludes Nahrendorf.

 

Source:

Study helps explain why exercise guards against heart disease. Eurekalert. Available from: https://www.eurekalert.org/pub_releases/2019-11/mgh-she110619.php

Sally Robertson

Written by

Sally Robertson

Sally first developed an interest in medical communications when she took on the role of Journal Development Editor for BioMed Central (BMC), after having graduated with a degree in biomedical science from Greenwich University.

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