Exercise intolerance in post-COVID19 survivors after hospitalization

Rationale Post-COVID19 survivors frequently have dyspnea that can lead to exercise intolerance and lower quality of life. Despite recent advances, the pathophysiological mechanisms of exercise intolerance in the post-COVID19 patients remain incompletely characterized.

Objectives To clarify the mechanisms of exercise intolerance in post-COVID19 survivors after hospitalization.

Methods Prospective study evaluated consecutive patients previously hospitalized due to moderate-to-severe/critical COVID19. Within 90±10 days (mean±sd) of COVID19 acute symptoms onset, patients underwent a comprehensive cardiopulmonary assessment, including a cardiopulmonary exercise testing with earlobe arterialized capillary blood gas analysis.

Measurements and Main Results Eighty-seven patients were evaluated, their mean±sd peak oxygen consumption were 19.5±5.0 ml kg⁻¹·min⁻¹, and the tertiles were: ≤17.0, 17.1–22.2 and ≥22.3 ml kg⁻¹·min⁻¹. Hospitalization severity was similar among the three groups; however, at the follow-up visit, they reported a greater sensation of dyspnea, along with indices of impaired pulmonary function, and abnormal ventilatory, gas-exchange and metabolic responses during exercise compared to patients with peak oxygen consumption >17 ml kg⁻¹·min⁻¹. By multivariate logistic regression analysis (ROC curve analysis) adjusted for age, sex and pulmonary embolism, a peak dead space fraction of tidal volume ≥29 and a resting forced vital capacity ≤80%predicted were independent predictors of reduced peak oxygen consumption.

Conclusions Exercise intolerance in the post-COVID19 survivors was related to a high dead space fraction of tidal volume at peak exercise and a decreased resting forced vital capacity, suggesting that both pulmonary microcirculation injury and ventilatory impairment could influence aerobic capacity in this patient population.