augmentin q

COVID-19 may mess with the body’s fight-or-flight response, a small new study suggests.

The coronavirus can infect many different organs in the body, including the brain. Previous studies have found that in rare cases, SARS-CoV-2 infections can lead to a variety of forms of brain damage including deadly inflammation, Live Science previously reported. In some cases, the virus has also been linked to “brain fog” and other psychiatric issues in patients, according to another Live Science report. 

But there’s still much that’s unknown about the subtle impacts a typical COVID-19 infection may have on the nervous system. In the new study, researchers recruited a small group of young adults in the U.S. who were recovering or had recovered from COVID-19, to examine whether the coronavirus triggers changes in the sympathetic nervous system.

The sympathetic nervous system —  which regulates involuntary body functions such as blood pressure, how long does accutane remain in system pupil dilation and body temperature — drives the body’s fight-or-flight response. In the face of danger, such as an approaching wild animal, the sympathetic nervous system will trigger the release of hormones to increase alertness and heart rate, which sends extra blood to the muscles, according to Live Science.

“‘Fight-or-flight’ is a great mechanism in situations of high stress,” such as when a bear is chasing you, said study senior author Abigail Stickford, an assistant professor of health and exercise science at the Appalachian State University in North Carolina. “But when that system is chronically elevated or stimulated, it’s not so great.”

Stickford and her team recruited 16 previously healthy young adults who had tested positive for SARS-CoV-2 more than two weeks prior to visiting the lab and had mild cases. The researchers recorded nerve activity using electrodes, blood pressure and heart rate while the participants were resting and while the participants were sticking their hand into an ice water bath — a heart test known as a “cold pressor test.” They compared their results to healthy young adult controls who weren’t infected. 

The researchers found that young adults recovering from SARS-CoV-2 infections had elevated sympathetic activity while resting compared to healthy controls. But they had no difference in heart rate, blood pressure and sympathetic nerve activity during the cold pressor test. That means that their fight-or-flight response was more active when it didn’t have to be during rest, but the system was still able to respond properly to a threat.

They also found that when the participants were asked to perform an “orthostatic challenge,” or quickly stand from a sitting or lying down position, the participants recovering from SARS-CoV-2 infections had higher sympathetic nerve activity and a greater increase in heart rate compared to healthy controls.

Many experts speculate that COVID-19 impacts the sympathetic nervous system, based on heart rate data from those infected and reports of symptoms including racing heartbeat and cognitive changes, so the results weren’t “entirely surprising,” Stickford told Live Science in an email. “However, these participants were very young, healthy, and with mild symptoms, so in that regard, it was surprising.”

The authors say that if the results hold true in older individuals who get COVID-19, “there may be substantial adverse implications for cardiovascular health.”

Just SARS-CoV-2 or all viruses?

No one knows why or how the virus triggers changes in the sympathetic nervous system, but the virus triggers inflammation, which in turn is linked to elevated sympathetic nervous system activity, Stickford said. 

Still, that doesn’t mean that other viruses aren’t causing these changes as well.

Dr. Igor Vaz, from the University of Miami’s Department of Medicine, who was not involved in the research, thinks that the results would have been more robust if the control group hadn’t been healthy individuals but individuals recovering from a different viral infection, such as the flu. “Using the control group as healthy individuals misses the opportunity to show that” these complications are due exclusively to SARS-CoV-2, and not just because people are recovering from a viral infection, he wrote in a “letter to the editor,” which was published in response to the study. 

In a response to the letter, the authors acknowledged that comparisons with other infections would have given more insight into the exact impact of SARS-CoV-2 on the nervous system, but that their “study design was the most appropriate starting place,” given various limitations such as access to patient populations.

—11 (sometimes) deadly diseases that hopped across species

—14 coronavirus myths busted by science

—The deadliest viruses in history 

The biggest limitation of the study is that the researchers don’t know what the participants’ nervous system activity looked like prior to their COVID-19 diagnosis, Stickford said. But it’s likely that the changes to the fight-or-flight response in this young, healthy population is temporary, Stickford added. As viral load decreases, inflammation in the body decreases, and “we would expect the [sympathetic nervous system] activity to also decline a bit,” she said. 

The researchers are continuing to track these participants, none of whom developed “long COVID,” a phenomenon whereby symptoms continue for months after a person is infected. 

Had these participants developed long COVID, “there would likely be more to the story,” as people who suffer from long COVID continue to display symptoms that suggest a dysfunction of the nervous system.

The findings were published on June 26 in The Journal of Physiology.

Originally published on Live Science.

Yasemin Saplakoglu

Yasemin is a staff writer at Live Science, covering health, neuroscience and biology. Her work has appeared in Scientific American, Science and the San Jose Mercury News. She has a bachelor’s degree in biomedical engineering from the University of Connecticut and a graduate certificate in science communication from the University of California, Santa Cruz.

Source: Read Full Article