Persistent Exertional Intolerance After COVID-19

Abstract

Background Some Coronavirus disease 2019 (COVID-19) patients who have recovered from their acute infection after experiencing only mild symptoms continue to exhibit persistent exertional limitation that is often unexplained by conventional investigative studies. Research question What is the patho-physiological mechanism of exercise intolerance that underlies the post-COVID-19 long haul syndrome following COVID-19 in patients without cardio-pulmonary disease? Study Design and Methods This study examined the systemic and pulmonary hemodynamics, ventilation, and gas exchange in 10 post-COVID-19 patients without cardio-pulmonary disease during invasive cardiopulmonary exercise testing (iCPET) and compared the results to 10 age- and sex matched controls. These data were then used to define potential reasons for exertional limitation in the post-COVID-19 cohort. Results Post-COVID-19 patients exhibited markedly reduced peak exercise aerobic capacity (VO 2 ) compared to controls (70±11%predicted vs. 131±45%predicted; p<0.0001). This reduction in peak VO 2 was associated with impaired systemic oxygen extraction (i.e., narrow CaVO 2 /CaO 2 ) compared to controls (0.49±0.1 vs. 0.78±0.1, p<0.0001) despite a preserved peak cardiac index (7.8±3.1 vs. 8.4±2.3 L/min, p>0.05). Additionally, post-COVID-19 patients demonstrated greater ventilatory inefficiency (i.e., abnormal VE/VCO 2 slope: 35±5 vs. 27±5, p=0.01) compared to controls without an increase in dead space ventilation. Interpretation Post-COVID-19 patients without cardiopulmonary disease demonstrate a marked reduction in peak VO 2 from a peripheral rather than a central cardiac limit along with an exaggerated hyper-ventilatory response during exercise.

Reduced exercise capacity, chronotropic incompetence, and early systemic inflammation in cardiopulmonary phenotype Long COVID

“…48 Endothelial and coronary microvascular dysfunction are associated with chronotropic incompetence in the general population [49][50][51] and have been demonstrated in early PASC. [52][53][54] Endothelial dysfunction may be associated with reduced VO2 in PASC; 55 57 preload failure 58 or inadequate stroke volume augmentation, 23,24 and disordered breathing. [58][59][60] Autonomic Function, Sinus Node Function, and Inflammation in PASC Altered autonomic function is the most likely unifying explanation for the constellation of findings we observed.…”

“…Diagnosis of chronotropic incompetence may have prognostic implications: chronotropic incompetence is associated with incident cardiovascular disease, sudden death, and all-cause mortality among men without known coronary artery disease. [88][89][90] Impaired peripheral oxygen extraction (assessed using invasive CPET) may also contribute to exercise limitations in PASC, 57 perhaps via changes in autonomic regulation of microcirculatory function. 91 We did not find differences in VO2/work slope, a noninvasive correlate of measured oxygen extraction.…”

Persistent symptoms in athletes following COVID-19: time to take a breath in the search for answers?

“…The study by Moulson et al employs physiological testing to evaluate the cause of persistent symptoms and specifically utilises cardiopulmonary exercise testing (CPET). In the general population with persistent or long-COVID symptoms, CPET studies have revealed disparate results, with some revealing a high prevalence of hyperventilation±breathing pattern irregularities,7 while others highlight issues in peripheral muscular oxygen extraction 8. In athletes with persistent cardiopulmonary symptoms, Moulson et al 5 found that CPET results were generally reassuring; despite nearly all subjects developing symptoms during testing, there were no contemporaneous cardiac abnormalities detected.…”

Genesen, aber nicht gesund – Long Covid und die Auswirkungen auf die körperliche Leistungsfähigkeit

“…Dennoch zeichnet sich ab, dass Personen mit anhaltenden Symptomen sowohl im Vergleich mit einer gesunden Kontrollgruppe als auch gemessen an ihrer zu erwartenden Leistungsfähigkeit eine reduzierte aerobe Kapazität aufweisen. Unabhängig vom Schweregrad der akuten Covid-19-Erkrankung wurden zum Beispiel eine reduzierte Sauerstoffaufnahme bei Beendigung des Tests und eine Akkumulation von Laktat im arteriellen Blut festgestellt 1 , 8 , 18 , 24 , 26 . Dies geht einher mit einer möglichen Linksverschiebung der Sauerstoffbindungskurve, wodurch die Sauerstoffabgabe von Hämoglobin im Gewebe beeinträchtigt wird, was einen früheren Übergang zum anaeroben Metabolismus erklären könnte 2 .…”

“…Darüber hinaus berichteten Singh et al 24 , dass, verglichen mit einer Kontrollgruppe, Personen mit anhaltender Kurzatmigkeit und Belastungsintoleranz 11 Monate (Mittelwert) nach ihrer Infektion bei maximaler Belastung einen signifikant höheren venösen Sauerstoffgehalt aufwiesen. Zusätzlich dazu gibt es Hinweise, dass Long-Covid-Patient*innen eine geringere mitochondriale Flexibilität aufweisen könnten.…”