COVID-19 disrupts the “hit or run” sympathetic nervous system

According to a new study, young people infected with COVID-19 but otherwise healthy have a disrupted “hit or run” response that can last for months.

In a six-month study involving 30 people (16 of whom were infected with COVID-19), the researchers’ findings largely coincide with what many COVID-19 “truckers” report.

Even at rest, the nerves of young COVID-19 survivors worked much harder than those who had not contracted the virus.

In the study, a tiny electrode inserted into the back of the knee found decreased electrical activity in the muscles of people recovering from COVID-19.

These nerves receive messages from the sympathetic nervous system, which controls our “hit or run” response, and in those recovering from the virus, this system appears to be abnormally active.

For example, 16 COVID survivors showed increased sympathetic activity during the transition from lying down to standing up, followed by an exaggerated heart rate response to changes in blood pressure.

It’s worth noting that this is only a small study, but even though the sample was tiny, the results are consistent with recent reports that many truckers — people experiencing COVID-19 symptoms for months on end — are unable to keep their heart rate from spinning out of control while standing.

In other cases, however, the sympathetic nervous system of patients with COVID-19 appears to be underactive.

For example, when young participants dipped their hands into ice water, their muscle nerve activity was lower than normal, and participants reported experiencing significantly less pain than 14 healthy control subjects.

This is not a perfect comparison; it would have been better to test before and after COVID-19 infection to see how their personal physiological responses may have changed over time. But given the surprising nature of this disease, using healthy participants who were not exposed to the virus as controls is our next best option.

The results show that SARS-CoV-2 can somehow disrupt the sympathetic nervous system, causing it to work too intensely at rest and not intensely enough in stressful situations, even in young people who are not as susceptible to severe disease.

“If similar autonomic dysregulation, such as that found in young people, is present in older people after SARS-CoV-2 infection,” the authors write, “it could have significant negative consequences for cardiovascular health.”

But so far, there are only so many “ifs,” and not many answers.

Increased sympathetic nervous system activity at rest is known to increase heart rate and cardiac output, possibly putting strain on the cardiovascular system over time. But this is the first study to examine nervous system activity after the body has been infected with the SARS-CoV-2 virus.

Today, about 200 million people worldwide have survived COVID-19, and if the new results can be confirmed among much larger groups, it means that millions of people may have suffered from an abnormal sympathetic nervous system for months during recovery.

How long these symptoms lasted before they disappeared remains unknown. In the current study, participants were followed for six months, but some people who were treated for long periods of time continued to have high heart rates and other cardiovascular problems long afterward.

The authors are not sure if it is SARS-CoV-2 that disrupts patients’ sympathetic nervous systems to such an extent, but they suspect that oxidative stress and inflammation are to blame.

High levels of sympathetic nerve activity in muscle have been associated with increased arterial stiffness in the past, and interestingly, young adults with COVID-19 showed increased arterial stiffness within three months of testing positive for the virus.

Reduced elasticity can alter oxygen delivery to the head or heart, which in turn can trigger the body’s “beat-or-run” response. On the other hand, inflammation caused by the immune system can also trigger the sympathetic nervous system.

“If, indeed, our [COVID-positive] participants also had increased vascular diameter at rest, then the increased activity [of the muscular sympathetic nervous system] may serve as an acute adaptation to systemic vascular dilation,” the authors suggest.

“Of course, we are limited in these interpretations, given the cross-sectional nature and short time frame of this study.”

It is difficult to draw any conclusions from the findings, but their implications are worrisome. Given the possible health problems that can arise from overactivity of the sympathetic nervous system, it is important to learn more.

The study was published in the Journal of Physiology.

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