Persistent dyspnea after COVID-19 is not related to cardiopulmonary impairment; a cross-sectional study..., 2022, Beaudry et al

Full title: Persistent dyspnea after COVID-19 is not related to cardiopulmonary impairment; a cross-sectional study of persistently dyspneic COVID-19, non-dyspneic COVID-19 and controls

Background: Up to 53% of individuals who had mild COVID-19 experience symptoms for >3-month following infection (Long-CoV). Dyspnea is reported in 60% of Long-CoV cases and may be secondary to impaired exercise capacity (VO2peak) as a result of pulmonary, pulmonary vascular, or cardiac insult. This study examined whether cardiopulmonary mechanisms could explain exertional dyspnea in Long-CoV.

Methods: A cross-sectional study of participants with Long-CoV (n = 28, age 40 ± 11 years, 214 ± 85 days post-infection) and age- sex- and body mass index-matched COVID-19 naïve controls (Con, n = 24, age 41 ± 12 years) and participants fully recovered from COVID-19 (ns-CoV, n = 14, age 37 ± 9 years, 198 ± 89 days post-infection) was conducted. Participants self-reported symptoms and baseline dyspnea (modified Medical Research Council, mMRC, dyspnea grade), then underwent a comprehensive pulmonary function test, cardiopulmonary exercise test, exercise pulmonary diffusing capacity measurement, and rest and exercise echocardiography.

Results: VO2peak, pulmonary function and cardiac/pulmonary vascular parameters were not impaired in Long- or ns-CoV compared to normative values (VO2peak: 106 ± 25 and 107 ± 25%predicted, respectively) and cardiopulmonary responses to exercise were otherwise normal. When Long-CoV were stratified by clinical dyspnea severity (mMRC = 0 vs mMRC≥1), there were no between-group differences in VO2peak. During submaximal exercise, dyspnea and ventilation were increased in the mMRC≥1 group, despite normal operating lung volumes, arterial saturation, diffusing capacity and indicators of pulmonary vascular pressures.

Interpretation: Persistent dyspnea after COVID-19 was not associated with overt cardiopulmonary impairment or exercise intolerance. Interventions focusing on dyspnea management may be appropriate for Long-CoV patients who report dyspnea without cardiopulmonary impairment.

Open access, https://www.frontiersin.org/articles/10.3389/fphys.2022.917886/full

 

Really seems like "exercise intolerance" should say deconditioning instead. It's definitely not deconditioning, and yet many do have exertion intolerance. So this creates a lot of unnecessary confusion out of what should be simple vocabulary.

I don't know how many times this has to be proven, though, if the medical profession can't accept reality. That this has nothing to do with deconditioning has been obvious nonsense for years, and it's still the default truth, even though there never was any evidence and in fact all data pointed otherwise.

What does it say about a profession that they will hold on dearly to long-debunked hypotheses while refusing to accept evidence that disproves it? That it's not based on science or evidence, that it's heavily political and arbitrary.

 

How would they know from a cross-sectional study, since they didn't measure VO2Peak before COVID?

They also don't seem to understand the regulation of respiratory drive and it's relationship with peripheral afferents.