RESUMEN
Time to exercise limitation (Tlim) in response to constant work rate (CWR) is sensitive to interventions in chronic obstructive pulmonary disease (COPD). This is particularly true when the pre-intervention test lasts between 3 and 8 min (Tlim3'-8'). There is, however, no simple method to select a work rate which is consistently associated with Tlim3'-8' across the spectrum of COPD severity. We assessed 59 GOLD stages II-IV patients who initially cycled to Tlim at 75% peak. In case of short (<3 min, low-endurance) or long (>8 min, high-endurance) tests, patients exercised after 60 min at 50% or 90%, respectively (CWR50%â75%â90%). Critical mechanical constraints and limiting dyspnea at 75% were reached within the desired timeframe in 27 "mid-endurance" patients (46%). Increasing work rate intensity to 90% hastened the mechanical-ventilatory responses leading to Tlim3'-8' in 23/26 (88%) "high-endurance" patients; conversely, decreasing exercise intensity to 50% slowed those responses leading to Tlim3'-8' in 5/6 (83%) "high-endurance" patients. Repeating the tests at higher (60%) or lower (80%) intensities fail to consistently produce Tlim3'-8' in "low-" and "high-endurance", respectively (p > 0.05). Compared to a fixed work rate at 75%, CWR50%â75%â90% significantly decreased Tlim's coefficient of variation; consequently, the required N to detect 100 s or 33% improvement in Tlim decreased from 82 to 26 and 41 to 14, respectively. This simplified approach to individualized work rate adjustment (CWR50%â75%â90%) might allow greater sensitivity in evaluating interventional efficacy in improving respiratory mechanics and exercise tolerance while simultaneously reducing sample size requirements in patients with COPD.
Asunto(s)
Disnea/fisiopatología , Prueba de Esfuerzo/métodos , Resistencia Física/fisiología , Enfermedad Pulmonar Obstructiva Crónica/fisiopatología , Anciano , Disnea/etiología , Tolerancia al Ejercicio , Femenino , Volumen Espiratorio Forzado , Humanos , Masculino , Persona de Mediana Edad , Enfermedad Pulmonar Obstructiva Crónica/complicaciones , Enfermedad Pulmonar Obstructiva Crónica/terapia , Mecánica Respiratoria , Factores de Tiempo , Capacidad VitalRESUMEN
Rationale: Post-coronavirus disease 2019 (COVID-19) survivors frequently have dyspnoea that can lead to exercise intolerance and lower quality of life. Despite recent advances, the pathophysiological mechanisms of exercise intolerance in the post-COVID-19 patients remain incompletely characterised. The objectives of the present study were to clarify the mechanisms of exercise intolerance in post-COVID-19 survivors after hospitalisation. Methods: This prospective study evaluated consecutive patients previously hospitalised due to moderate-to-severe/critical COVID-19. Within mean±sd 90±10â days of onset of acute COVID-19 symptoms, patients underwent a comprehensive cardiopulmonary assessment, including cardiopulmonary exercise testing with earlobe arterialised capillary blood gas analysis. Measurements and main results: 87 patients were evaluated; mean±sd peak oxygen consumption was 19.5±5.0â mL·kg-1·min-1, and the tertiles were ≤17.0, 17.1-22.2 and ≥22.3â mL·kg-1·min-1. Hospitalisation severity was similar among the three groups; however, at the follow-up visit, patients with peak oxygen consumption ≤17.0â mL·kg-1·min-1 reported a greater sensation of dyspnoea, along with indices of impaired pulmonary function, and abnormal ventilatory, gas-exchange and metabolic responses during exercise compared to patients with peak oxygen consumption >17â mL·kg-1·min-1. By multivariate logistic regression analysis (receiver operating characteristic curve analysis) adjusted for age, sex and prior 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-COVID-19 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.