Increased breathlessness in post-COVID syndrome despite normal breathing patterns in a rebreathing challenge, 2025, von Werder et al.

SNT Gatchaman

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Increased breathlessness in post-COVID syndrome despite normal breathing patterns in a rebreathing challenge
von Werder, Dina; Aubele, Maria; Regnath, Franziska; Tebbe, Elisabeth; Mladenov, Dejan; von Rheinbaben, Victoria; Hahn, Elisabeth; Schäfer, Daniel; Biersack, Katharina; Adorjan, Kristina; Stubbe, Hans C; Bogaerts, Katleen; Jörres, Rudolf A; Nowak, Dennis; Van den Bergh, Omer; Glasauer, Stefan; Lehnen, Nadine

Severe symptoms in the absence of measurable body pathology are a frequent hallmark of post-COVID syndrome. From a Bayesian Brain perspective, such symptoms can be explained by incorrect internal models that the brain uses to interpret sensory signals. In this pre-registered study, we investigate whether induced breathlessness perception during a controlled CO2 rebreathing challenge is reflected by altered respiratory measures (physiology and breathing patterns), and propose different computational mechanisms that could explain our findings in a Bayesian Brain framework. We analysed data from 40 patients with post-COVID syndrome and 40 healthy participants.

Results from lung function, neurological and neurocognitive examination of all participants were within normal limits on the day of the experiment. Using a Bayesian repeated-measures ANOVA, we found that patients’ breathlessness was strongly increased (BF10,baseline=8.029, BF10,rebreathing=11636, BF10, recovery=43662) compared to controls. When excluding patients who hyperventilated (N = 8, 20%) during the experiment from the analysis, differences in breathlessness remained (BF10,baseline=1.283, BF10,rebreathing=126.812, BF10,recovery=751.282). For physiology and breathing patterns, all evidence pointed towards no difference between the two groups (0.307 > BF10 < 0.704).

In summary, we found intact breathing patterns and physiology but increased symptom perception in patients with post-COVID syndrome.

Web | PDF | Nature Scientific Reports | Open Access
 
It’s pretty clear they have an agenda: they are essentially saying that the perception of breathlessness is caused by anxiety and overly cautious internal models.
Internal models
Our results thus suggest that the cause of heightened symptoms in patients is not directly related to breathing physiology but rather to differences in processing and incorporating interoceptive breathing signals into symptom perception due to incorrect internal models or overly cautious cost-functions.

It is currently unclear where and how internal models for interoception are represented and maintained in the brain, but there is evidence that brain areas like the anterior insula51 play an important role. There have been several findings of brain changes concerning the structural as well as functional connectivity in patients with post-COVID52,53, some of them pertaining to brain areas that are thought to be involved in interoceptive processing.

Pathological changes in these brain areas could lead to problems in correctly maintaining and adapting internal models. Similarly, internal models and cost functions can be adapted by experience. For example, experiencing a persistent immune reaction due to viral reservoirs or social or emotional stress and anxiety, can lead to an adaptation of internal models that assume a high risk for aversive bodily stressors and thus the development of incorrect priors.

Anxiety and depression are known risk factors for developing post-COVID symptoms54,55 and there is a close link between anxiety and respiratory-related interoception that is especially strong at higher levels involving meta-cognitive processes of interoception with different activities in the anterior insula in individuals with low versus high anxiety51.
 
Obviously the conclusions are silly, but the fact that there will be zero examinations for years of baselessly asserting that "breathing patterns", which even reading about doesn't actually clarify anything and is obviously unrelated, must be the problem is itself a major problem.

There was never any basis for it. Not a smidge of evidence. And yet it was asserted again and again, especially from breathing specialists, which really puts their expertise into question.

Because research like this doesn't even matter. Most of the people who have been asserting it will not change their minds, they probably won't even know about the study, and if they did they'd probably just disagree, with some waffling about whatever the hell they're trying to make up about internal models and cost functions and other nonsense.
Anxiety and depression are known risk factors for developing post-COVID symptoms
And they don't even know that correlation, especially out of asking overlapping questions, absolutely does not support either direction of causality, certainly not the least plausible one. Because from the way they are describing it, coughing is a risk factor for respiratory diseases. Which it obviously isn't, but being back-asswards is how they do it.

The lack of any adaptation is the most infuriating part. 5 years of garbage research and absolutely zero progress has been made. Still the same garbage ideas as ever, produced the same way and going nowhere, nothing has been learned, no process or institution has adapted anything, it's all completely stagnant.

But, sure, whatever, it's not symptoms that matter, it's symptoms perception. Garbage.
 
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