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Resumen: Introducción: La enfermedad pulmonar obstructiva crónica (EPOC) es la patología respiratoria que causa mayor morbimortalidad a nivel mundial. Los parámetros de función pulmonar y las manifestaciones sistémicas se han definido como factores pronósticos, sin embargo, presentan limitaciones. El objetivo ha sido analizar si la fuerza muscular inspiratoria sería un reflejo de la insuflación pulmonar y, por tanto, un factor pronóstico de los pacientes con EPOC. Método: Se seleccionaron pacientes con EPOC que se realizaron previamente una valoración de la fuerza muscular respiratoria no invasiva y una prueba de función pulmonar desde enero de 2015 hasta octubre de 2017. Posteriormente, se revisó la mortalidad hasta el 1 de marzo de 2020. Resultados: Se incluyeron 140 pacientes con EPOC (estadio GOLD I 5%, II 73,4% y III 21,6%) de los cuales un 10% fallecieron durante el seguimiento. La obstrucción bronquial, definida por volumen espiratorio forzado en el primer segundo (FEV1) fue un buen predictor de mortalidad (p = 0,004). La hiperinsuflación pulmonar, definida como relación capacidad inspiratoria/capacidad pulmonar total (CI/CPT) inferior a 25 y CI inferior al 65% de los valores de referencia, incrementaba la mortalidad en los pacientes con EPOC (p = 0,001 y p = 0,06, respectivamente). En la presente cohorte la fuerza de los músculos inspiratorios, valorada mediante la presión nasal durante una inhalación máxima (SNIP) no fue un factor pronóstico (p = 0,629). Conclusión: En los pacientes con EPOC, la hiperinsuflación pulmonar es un factor pronóstico, no así la función muscular inspiratoria. La función muscular inspiratoria de los pacientes de los EPOC no solo depende de la mecánica pulmonar, sino que también de factores intrínsecos de los propios músculos. Abstract: Introduction: Chronic obstructive pulmonary disease (COPD) is the respiratory disease that causes the greatest morbidity and mortality worldwide. Lung function parameters and systemic manifestations have been defined as prognostic factors; however, they have limitations. The aim of this study was to analyze whether inspiratory muscle strength could reflect lung hyperinflation, and therefore serve as a prognostic factor in COPD patients. Method: We selected COPD patients who had performed a non-invasive respiratory muscle strength assessment and lung function testing between January 2015 and October 2017. Mortality was subsequently followed up until March 1, 2020. Results: We included 140 COPD patients (GOLD stage I 5%, II 73.4%, and III 21.6%), of whom 10% died during follow-up. Bronchial obstruction, defined by FEV1, was a good predictor of mortality (p = 0.004). Lung hyperinflation, defined as inspiratory capacity (IC)/total lung capacity less than 25 and IC less than 65% of predicted increased mortality in COPD patients (p = 0.001 and p = 0.06, respectively). In this cohort, inspiratory muscle strength, measured by SNIP, was not a prognostic factor (p = 0.629). Conclusion: In COPD patients, lung hyperinflation is a prognostic factor, but inspiratory muscle function is not. Inspiratory muscle function in COPD patients depends not only on lung mechanics but also on intrinsic muscle factors.

Abstract Background: Loss of muscle mass and function are well-recognized systemic manifestations of chronic obstructive pulmonary disease (COPD). Acute exacerbations, in turn, significantly contribute to upgrade these systemic comorbidities. Involvement of myogenic precursors in muscle mass maintenance and recovery is poorly understood. The aim of the present study was to investigate the effects of the vascular systemic environment from stable and exacerbated COPD patients on the myogenic behavior of human muscle precursor cells (MPC) in vitro. Methods: Serum from healthy controls and from stable and exacerbated COPD patients (before and after Methylprednisolone treatment) was used to stimulate human MPC cultures. Proliferation analysis was assessed through BrdU incorporation assays. MPC differentiation was examined through real-time RT-PCR, western blot and immunofluorescence analysis. Results: Stimulation of MPCs with serum obtained from stable COPD patients did not affect myogenic precursor cell function. The vascular systemic environment during an acute exacerbation exerted a mitotic effect on MPCs without altering myogenic differentiation outcome. After Methylprednisolone treatment of acute exacerbated COPD patients, however, the mitotic effect was further amplified, but it was followed by a deficient differentiation capacity. Moreover, these effects were prevented when cells were co-treated with the glucocorticoid receptor antagonist Mifepristone. Conclusion: Our findings suggest that MPC capacity is inherently preserved in COPD patients, but is compromised after systemic administration of MP. This finding strengthens the concept that glucocorticoid treatment over the long term can negatively impact myogenic stem cell fate decisions and interfere with muscle mass recovery.