Dyspnea in Post-COVID Syndrome following Mild Acute COVID-19 Infections: Potential Causes and Consequences..., 2022, Wirth & Scheibenbogen

Full title: Dyspnea in Post-COVID Syndrome following Mild Acute COVID-19 Infections: Potential Causes and Consequences for a Therapeutic Approach

Abstract

Dyspnea, shortness of breath, and chest pain are frequent symptoms of post-COVID syndrome (PCS). These symptoms are unrelated to organ damage in most patients after mild acute COVID infection. Hyperventilation has been identified as a cause of exercise-induced dyspnea in PCS. Since there is a broad overlap in symptomatology with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), causes for dyspnea and potential consequences can be deduced by a stringent application of assumptions made for ME/CFS in our recent review papers.

One of the first stimuli of respiration in exercise is caused by metabolic feedback via skeletal muscle afferents. Hyperventilation in PCS, which occurs early on during exercise, can arise from a combined disturbance of a poor skeletal muscle energetic situation and autonomic dysfunction (overshooting respiratory response), both found in ME/CFS. The exaggerated respiratory response aggravating dyspnea does not only limit the ability to exercise but further impairs the muscular energetic situation: one of the buffering mechanisms to respiratory alkalosis is a proton shift from intracellular to extracellular space via the sodium–proton-exchanger subtype 1 (NHE1), thereby loading cells with sodium. This adds to two other sodium loading mechanisms already operative, namely glycolytic metabolism (intracellular acidosis) and impaired Na+/K+ATPase activity. High intracellular sodium has unfavorable effects on mitochondrial calcium and metabolism via sodium–calcium-exchangers (NCX). Mitochondrial calcium overload by high intracellular sodium reversing the transport mode of NCX to import calcium is a key driver for fatigue and chronification. Prevention of hyperventilation has a therapeutic potential by keeping intracellular sodium below the threshold where calcium overload occurs.

Open access, https://www.mdpi.com/1648-9144/58/3/419/htm

 

This is a bit odd, or maybe poorly phrased. Dyspnea doesn't need to be triggered by exertion in many cases, it can persist without any exertion at all. It almost seems like it's written backwards, that dyspnea with an exercise trigger could be a cause of some hyperventilation. Or anyway it seems to take the consequence and attribute it as a cause, which I don't understand is standard practice because it's so faulty and self-defeating.

There is way too much focus on exercise, which is obscuring the fact that it's usually about exertion, and even that exertion isn't even needed for most symptoms. It's post-exertional symptom exacerbation, the belief seems to be that the symptoms are otherwise not there until triggered by vigorous exercise. Hence most physicians keep thinking it in terms of people basically feeling fine, going for a run and being out of breath a bit more than usual.

There is such a huge problem of basic communication here and it's just the same old circle of failure. It's like people speaking two languages with many interpretation faults and one side only cares that their way of talking is respected, even if it completely loses all relevant meaning in communication with the others.