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Resumen Introduccion La fisioterapia respiratoria es parte imprescindible del tratamiento de las patologias hipersecretoras o con compromiso de la capacidad tusigena. Hasta el momento se desconoce el efecto del dispositivo de terapia de oscilacion de alta frecuencia en la pared toracica (HFCWO) sobre la fuerza de los musculos respiratorios y los efectos sobre la mecanica respiratoria y la dinamica de los gases respiratorios. Por ello, el objetivo de este estudio fue describir estos tres aspectos en sujetos sanos. Metodos Se midio la fuerza de los musculos respiratorios en 25 sujetos antes e inmediatamente despues de terapia con HFCWO. Durante la sesion, se midieron continuamente los parametros de ventilacion, la dinamica de los gases respiratorios y la frecuencia cardiaca. Se llevaron a cabo dos sesiones identicas por sujeto, separadas 24 h. Se registraron los sintomas durante la sesion y las molestias experimentadas mediante escala analogica visual (EVA). Resultados La terapia con HFCWO produce un incremento de la ventilacion asociado con una alteracion de la dinamica de los gases respiratorios. Tambien se aumenta la frecuencia cardiaca, sin modificacion de la oxigenacion tisular. No se observaron efectos sobre la fuerza de los musculos respiratorios. Hasta un 20% de los participantes indico molestias importantes (EVA ≥ 5/10) durante la sesion. Conclusiones Durante la aplicacion de HFCWO en sujetos sanos se produce incremento en la ventilacion y ritmo cardiaco. Sin embargo, aparecen efectos indeseables sobre la dinamica de los gases respiratorios y un grado elevado de intolerancia por parte de los voluntarios y no hay efectos sobre la fuerza de los musculos respiratorios.

While the incidence of thrombotic complications in critically ill patients is very high, in patients under non-invasive respiratory support (NIS) is still unknown. The specific incidence of thrombotic events in each of the clinical scenarios within the broad spectrum of severity of COVID-19, is not clearly established, and this has not allowed the implementation of thromboprophylaxis or anticoagulation for routine care in COVID-19. Patients admitted in a semi-critical unit treated initially with NIS, especially Continuous-Positive Airway Pressure (CPAP), were included in the study. The cumulative incidence of pulmonary embolism was analyzed and compared between patients with good response to NIS and patients with clinical deterioration that required orotracheal intubation. 93 patients were included and 16% required mechanical ventilation (MV) after the NIS. The crude cumulative incidence of the PE was 14% (95%, CI 8-22) for all group. In patients that required orotracheal intubation and MV, the cumulative incidence was significantly higher [33% (95%, CI 16-58)] compared to patients that continued with non-invasive support [11% (CI 5-18)] (Log-Rank, p = 0.013). Patients that required mechanical ventilation were at higher risk of PE for a HR of 4.3 (95%CI 1.2-16). In conclusion, cumulative incidence of PE is remarkably higher in critically patients with a potential impact in COVID-19 evolution. In this context, patients under NIS are a very high-risk group for developing PE without a clear strategy regarding thromboprophylaxis.

Sarcopenia is a major comorbidity in chronic obstructive pulmonary (COPD). Whether deficient muscle repair mechanisms and regeneration exist in the vastus lateralis (VL) of sarcopenic COPD remains debatable. In the VL of control subjects and severe COPD patients with/without sarcopenia, satellite cells (SCs) were identified (immunofluorescence, specific antibodies, anti-Pax-7, and anti-Myf-5): activated (Pax-7+/Myf-5+), quiescent/regenerative potential (Pax-7+/Myf-5-), and total SCs, nuclear activation (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling [TUNEL]), and muscle fiber type (morphometry and slow- and fast-twitch, and hybrid fibers), muscle damage (hematoxylin-eosin staining), muscle regeneration markers (Pax-7, Myf-5, myogenin, and MyoD), and myostatin levels were identified. Compared to controls, in VL of sarcopenic COPD patients, myostatin content, activated SCs, hybrid fiber proportions, TUNEL-positive cells, internal nuclei, and muscle damage significantly increased, while quadriceps muscle strength, numbers of Pax-7+/Myf-5- and slow- and fast-twitch, and hybrid myofiber areas decreased. In the VL of sarcopenic and nonsarcopenic patients, TUNEL-positive cells were greater, whereas muscle regeneration marker expression was lower than in controls. In VL of severe COPD patients regardless of the sarcopenia level, the muscle regeneration process is triggered as identified by SC activation and increased internal nuclei. Nonetheless, a lower regenerative potential along with significant alterations in muscle phenotype and damage, and increased myostatin were prominently seen in sarcopenic COPD.

Patients requiring surgery for locally advanced esophagogastric cancer often require neoadjuvant therapy (NAT), which may have a detrimental impact on cardiorespiratory reserve. The aims of this study were to investigate the feasibility and tolerability of a 5-week preoperative high-intensity interval training program after NAT, and to assess the potential effects of the training protocol on exercise capacity, muscle function, and health-related quality of life (HRQL). We prospectively studied consecutive patients with resectable locally advanced esophageal and gastric cancer in whom NAT was planned (chemo- or chemoradiotherapy). Feasibility was assessed with the TELOS (Technological, Economics, Legal, Operational, and Scheduling) components, and data on exercise tolerability (attendance and occurrence of adverse or unexpected events). Exercise capacity was assessed with peak oxygen uptake (VO2peak) in a cardiopulmonary exercise test at baseline, post-NAT, and following completion of a high-intensity interval exercise training (25 sessions). Changes in muscle strength and HRQL were also assessed. Of 33 recruited subjects (mean age 65 years), 17 received chemoradiotherapy and 16 chemotherapy. All the TELOS components were addressed before starting the intervention; from a total of 17 questions considered as relevant for a successful implementation, seven required specific actions to prevent potential concerns. Patients attended a mean of 19.4 (6.4) exercise sessions. The predefined level of attendance (≥15 sessions of scheduled sessions) was achieved in 27 out of 33 (81.8%) patients. Workload progression was adequate in 24 patients (72.7%). No major adverse events occurred. VO2peak decreased significantly between baseline and post-NAT (19.3 vs. 15.5 mL/Kg/min, P

Whether a deficiency in muscle repair and regeneration may exist in the lower limb muscles of COPD patients remains debatable. We hypothesized that the negative regulator myotastin may inhibit muscle regeneration potential in sarcopenic COPD patients. In vastus lateralis (VL) of control subjects and severe COPD patients with and without sarcopenia, satellite cells (SC) were identified (immunofluorescence, anti-Pax7 and anti-myf5): activated (Pax7+ and myf5+), quiescent/regenerative potential (Pax7+ and myf-5-), and total SC, nuclear activation (TUNEL assay), and muscle fiber type (morphometry, hybrid fibers), muscle damage, muscle regeneration markers (Pax7, myf-5, myogenin, and myoD), and myostatin levels were identified. Compared to control subjects and normal body composition COPD, in the VL of sarcopenic COPD patients, myostatin protein levels, activated SC, hybrid fibers, TUNEL-positive cells, internal nuclei, and total abnormal fraction were significantly increased, while quadriceps muscle strength, numbers of Pax7+ and myf-5- and slow- and fast-twitch muscle fiber areas decreased. In VL of sarcopenic and non-sarcopenic COPD patients, TUNEL-positive cell counts were greater, whereas expression of muscle regeneration markers was lower than in controls. Myostatin may have interfered with the process of muscle cell proliferation early on during the regeneration process, thus leading to poor muscle growth and development following injury in COPD patients with sarcopenia. This may be another relevant mechanism of muscle mass loss in COPD. Method: CIBERES, FIS 18/00075 (FEDER), SEPAR 2018, and unrestricted grant from Menarini SA 2018.

With the 60th anniversary of the CIBA symposium, it is worth evaluating research questions that should be prioritized in the future. Coming research initiatives can be summarized in 10 main areas. (1) From epidemiology the impact of new forms of electronic cigarettes on prevalence and mortality of COPD will be sought. (2) The study of the disease endotypes and its relationship phenotypes will have to be unraveled in the next decade. (3) Diagnosis of COPD faces several challenges opening the possibility of a change in the definition of the disease itself. (4) Patients' classification and risk stratification will need to be clarified and reassessed. (5) The asthma-COPD overlap dilemma will have to be clarified and define whether both conditions represent one only chronic airway disease again. (6) Integrating comorbidities in COPD care will be key in a progressively ageing population to improve clinical care in a chronic care model. (7) Nonpharmacological management have areas for research including pulmonary rehabilitation and vaccines. (8) Improving physical activity should focus research because of the clear prognostic impact. (9). Pharmacological therapies present several challenges including efficacy and safety issues with current medications and the development of biological therapy. (10) The definition, identification, categorization and specific therapy of exacerbations will also be an area of research development. During the next decade, we have a window of opportunity to address these research questions that will put us on the path for precision medicine.

Introduction: Physical activity (PA) is reduced in IPF and related to mortality predictors. This study aims to describe PA in IPF and evaluate its association with clinical parameters, exercise capacity, muscular strength and health-related quality of life (HRQL). Methods: 17 IPF patients were included. Clinical data was collected; pulmonary function tests, 6-minute walk test (6MWT), respiratory and peripheral muscle strength, body mass index and body composition were performed; patients completed dyspnea scale, Hospital anxiety and depression scale and St. George’s Respiratory Questionnaire (SGRQ). GAP index (Gender-Age-Physiology) was calculated. The following PA parameters were measured with accelerometer: steps/day, time on moderate-vigorous PA/day (MVPA), energy expenditure/day (EE) and PA level (PAL). All variables were compared by PA (steps/day) and PA variables were compared by GAP index; correlations were established between PA variables, exercise capacity and muscular strength. Results: Patients performed a median (p25-p75) of 4393(2444-6919) steps/day, 37(22-51) minutes of MVPA, EE of 1384(713-1630) J and a PAL of 1.3(1.2-1.4). Those with lower PA had higher SGRQ score. GAP III patients performed significantly less PA compared to GAP I-II. There was significant correlation between 6MWT distance and all PA variables. Quadriceps strength correlated with MVPA (r=0.486; p=0.048), EE (r=0.647; p=0.005), and PAL (r=0.56;p=0.03); hand-grip correlated with steps/day (r=0.491;p=0.045), MVPA (r=0.531;p=0.028) and EE (r=0.557;p=0.016). Conclusions: IPF patients with lower PA presented worse HRQL. Those in GAP III stage (worst prognosis) performed less PA. Peripheral muscular strength was positively correlated with PA variables.

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.

In patients with chronic obstructive pulmonary disease (COPD), skeletal muscle dysfunction is a major comorbidity that negatively impacts their exercise capacity and quality of life. In the current guidelines, the most recent literature on the various aspects of COPD muscle dysfunction has been included. The Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) scale has been used to make evidence-based recommendations on the different features. Compared to a control population, one third of COPD patients exhibited a 25% decline in quadriceps muscle strength, even at early stages of their disease. Although both respiratory and limb muscles are altered, the latter are usually more severely affected. Numerous factors and biological mechanisms are involved in the etiology of COPD muscle dysfunction. Several tests are proposed in order to diagnose and evaluate the degree of muscle dysfunction of both respiratory and limb muscles (peripheral), as well as to identify the patients' exercise capacity (six-minute walking test and cycloergometry). Currently available therapeutic strategies including the different training modalities and pharmacological and nutritional support are also described.

Neoadjuvant therapy (NAT) carries the risk of toxicity and reduces exercise capacity in patients having surgery for digestive cancer.. Our aim was to evaluate the effect of a 5-week structured exercise-training program (SETP) to improve physical fitness after NAT for locally advanced esophageal and gastric cancer. We also assessed the feasibility and safety of the program. Prospective observational cohort study of consecutive patients with locally advanced esophageal and gastric cancer scheduled for NAT. All patients underwent a CPET before, immediately after NAT, and after 5 weeks of a SETP, before surgery. Patients exercised in a supervised hospital setting, 5 times per week for 5 weeks (25 sessions). Nineteen patients were recruited but 2 were excluded due to complications of the primary tumor during the NAT. The final analysis includes 17 patients (13 men / 4 women) with a mean age of 66 years (range 40-80). Thirteen patients had esophageal / GEJ cancer and 4 had gastric cancer. 68% of patients received chemoradiotherapy (CROSS regime) and 32% chemotherapy (MAGIC scheme). All 17 patients completed at least 80% of the SETP, with an average of 23 sessions. All patients showed deterioration in values of CPET after neoadjuvant therapy, with significant improvement of them after the SETP (Figure 1) In Conclusion, 5-week exercise training program after neoadjuvant treatment improves cardiorespiratory fitness in patients with locally advanced esophagogastric cancer. This benefit may have an impact on the surgical outcome in this group of patients.

The purpose of this study was to evaluate patients with adolescent idiopathic scoliosis (AIS) to determine whether a low body mass index (BMI) influences surgery outcomes and satisfaction.There were 39 patients in this prospective 3-year cohort study. The BMI, Cobb angle, the Body Shape Questionnaire 14 (BSQ-14), the Scoliosis Research Society Questionnaire 22 (SRS-22) and eight satisfaction questions results were obtained. Having a BMI greater than or less than 18 kg/m(2) was used as a determiner to allocate patients to groups. As a low BMI is related to the presence of a disturbance in body perception, patients were also dichotomized by using the BSQ-14.All scales were worse in both slimmer patients and the group with a body perception disorder. The group with a BMI18 kg/m(2) obtained a total of 82.31 points in the SRS-22, and it was 93.45 points for the group with a BMI18 kg/m(2) (p = 0.001). In terms of satisfaction, the percentage of patients that would undergo surgery again was 30.8 vs 69.2 % (p = 0.054). Patients with an alteration of physical perception obtained a total SRS-22 of 82.90 points versus 96.10 points in the control group (p0.001). No differences in terms of the Cobb correction (p = 0.29) or the percentage of correction (p = 0.841) were found in any case.The alteration of physical perception and a low BMI negatively affect the outcomes in AIS surgery, regardless of the curve magnitude and the percentage of correction. Considerable care should be taken in recommending surgical correction to these patients.

Nutritional abnormalities are associated with chronic obstructive pulmonary disease with a frequency ranging from 2 to 50%, depending on the geographical area and the study design. Diagnostic tools include anthropometry, bioelectrical impedance, dual energy radioabsortiometry and deuterium dilution, being the body mass and the lean mass indices the most frequently used parameters. While the most important consequences of nutritional abnormalities are muscle dysfunction and exercise limitation, factors implicated include an imbalance between caloric intake and consumption, and between anabolic and catabolic hormones, inflammation, tobacco smoking, poor physical activity, hypoxemia, some drugs and aging/comorbidities. The most important molecular mechanism for malnutrition associated with chronic obstructive pulmonary disease appears to be the mismatching between protein synthesis and breakdown. Among the therapeutic measures proposed for these nutritional abnormalities are improvements in lifestyle and nutritional support, although the use of anabolic drugs (such as secretagogues of the growth hormone) offers a new therapeutic strategy.

Introduccion La disfuncion muscular es una de las manifestaciones sistemicas mas estudiadas en la EPOC. Las alteraciones metabolicas musculares son dificiles de estudiar in vivo, debido a la falta de tecnicas no invasivas. El objetivo fue evaluar sincronicamente la actividad metabolica de diferentes grupos musculares en pacientes con EPOC. Metodos Se incluyeron 39 pacientes y 21 controles (funcion pulmonar normal), candidatos a realizacion de tomografia axial computarizada y por emision de positrones para estadificacion de lesion pulmonar localizada. Tras infusion de 18-fluor-deoxi-glucosa, se captaron imagenes de 2 musculos respiratorios (porciones costal y crural del diafragma, y recto abdominal) y 2 musculos perifericos (cuadriceps y biceps braquial), utilizando como indice de metabolismo glucidico el standard uptake value. Resultados Este indice fue superior en ambas porciones del diafragma comparado con el resto de los musculos en todos los sujetos. Ademas, el diafragma crural y el recto del abdomen mostraban mayor actividad en los pacientes con EPOC que en los controles (1,8 ± 0,7 vs. 1,4 ± 0,8; y 0,78 ± 0,2 vs. 0,58 ± 0,1; respectivamente; p < 0,05). El cuadriceps mostraba una tendencia similar. En los pacientes con EPOC los niveles de captacion de ambos musculos respiratorios y del cuadriceps se correlacionaron directamente con el atrapamiento aereo (r = 0,388; 0,427 y 0,361, respectivamente; p < 0,05). Conclusiones Existe mayor nivel de captacion-utilizacion de glucosa en el diafragma humano respecto de otros musculos en respiracion tranquila. Se confirma cuantitativamente que los pacientes con EPOC tienen incrementado el metabolismo glucidico de sus musculos respiratorios (con tendencia similar para el cuadriceps), en relacion directa con las cargas mecanicas que afrontan.

Chronic obstructive pulmonary disease (COPD) is a complex disorder with extrapulmonary manifestations. Even though there is some knowledge regarding sex differences in the lung disease, little is known about extrapulmonary manifestations. Our aim was to analyze the specific profile of muscle dysfunction, structure, and biology in COPD women. Twenty-one women and 19 men with stable COPD as well as 15 controls were included. Nutritional status, physical activity, lung and muscle function, exercise capacity, and quality of life were assessed. In addition, blood, breath condensate, and quadriceps muscle samples were tested for inflammatory markers. Moreover, fiber phenotype, signs of damage–regeneration, and the expression of key genes linked to myogenesis and inflammation were assessed in the muscle. Inflammatory markers were increased in all body compartments but no correlation was found among them. Muscle dysfunction was present in both COPD groups but was more marked in women. The opposite occurred with the increase in the percentage of type II fibers that was lower in women despite a similar level of airway obstruction as in men. Female COPD also showed higher signs of muscle damage than COPD men who, in contrast, exhibited slightly higher signs of regeneration. We conclude that sex influences muscle phenotype and function in COPD.

Introduction: Patients with Chronic Obstructive Pulmonary Diseases (COPD) have skeletal muscle dysfunction. In these patients, skeletal muscle dysfunction has impact on the quality of life and mortality. However, its relevance is unknown in other chronic respiratory diseases such as bronchiectasis, which shares some deleterious factors with COPD. Accordingly, our aim was to describe the structure and function of skeletal muscle ( vastus lateralis ) in patients with non-cystic fibrosis bronchiectasis (non-CF BCH), valuing its relationship with exercise capacity and physical activity. Methods: 29 patients with non-CF BCH and 8 healthy subjects of similar age were recruited. Anthropometry, body composition (bioimpedance), health-related quality of life (QoL, Quittner9s questionnaire), physical activity (accelerometer), exercise capacity (6 minute walking test), lung function, and respiratory and limb muscle function were assessed in all subjects. In addition, open biopsies of the vastus lateralis were obtained for the analysis of structural signs of muscle damage/regeneration (McGowan technique) and fiber typing. Results: Patients with non-CF BCH showed a moderate obstructive pattern, nutritional disorders (decreased a 13% in fat-free mass index), decreased exercise capacity and physical activity compared to controls. In addition, skeletal muscle strength was also lower in the group of patients, however, no structural alterations were observed in the vastus lateralis . Conclusion: Patients with non-CF BCH have shown skeletal muscle dysfunction that could limit their daily activities and exercise capacity. However, they do not depict changes in the structure of the skeletal muscle.

Introduction: Inspiratory muscle strength is usually assessed thorough the determination of static mouth pressure (PImax). However, since this manoeuvre presents certain problems, alternative techniques have been developed over the last few years. One of the most promising is determination of sniff nasal inspiratory pressure (SNIP). Aim: To evaluate SNIP assessment as an alternative for the evaluation of the inspiratory muscle strength. Methods: Subjects were consecutively included and assigned to one of three different groups: control (8), COPD patients (23) and patients with neuromuscular disorders (21). Different maximal inspiratory pressures were determined: (a) dynamic in the esophagus (maximal sniff Pes, reference variable), (b) PImax, and (c) SNIP. Results: Both SNIP and MIP showed an excellent correlation with Pes (r=0.835 and 0.752, respectively, P

To the Editor: Quadriceps weakness and atrophy is present in approximately 30% of patients with chronic obstructive pulmonary disease (COPD) in secondary care (1, 2). The quadriceps also displays a shift in fiber type so that there are fewer type I (oxidative) fibers and more type II (glycolytic) fibers (3). Pulmonary rehabilitation only partially addresses this fiber shift (4). Muscle mass (5) and strength (6) are both associated with increased mortality, but the prognostic significance of fiber shift is unknown. In a retrospective multicenter analysis of 392 patients from four sites (see Tables E1–E4 in the online supplement), mortality data were collated, as part of audit procedures, on outpatients with stable COPD who had undergone a vastus lateralis biopsy between 1995 and 2013. Data from these subjects have been previously published (e.g., References 2, 4, 5). Fiber proportion, reported as the percentage of type II fibers (type II fiber %), was established by immunohistochemistry. Fiber shift, evaluated as a dichotomous variable, was considered to have occurred when the proportion of type II fibers was greater than 68% (men) or greater than 65% (women) based on normal ranges established from an age-matched healthy population published by Natanek and colleagues (3). Body mass index (BMI), fat-free mass index (FFMI), dominant leg isometric quadriceps maximum voluntary contraction (QMVC and QMVC/BMI), mid-thigh cross-sectional area determined by computed tomography scan (MTCSA), residual volume normalized to total lung capacity (RV/TLC), and percent predicted value for the carbon monoxide transfer factor corrected for hemoglobin (TLCOc), when available, were included in subanalyses. Data were analyzed for the whole dataset and also after splitting the group into those with an FEV1 less than 50% predicted and those with an FEV1 greater than or equal to 50% predicted. Further details on the methodology and statistical analyses are presented in the online supplement. Some of the results of this study have been previously reported in abstract form (7). Patients were followed up for a median of 1,699 days (127–6,601 d); 102 of 392 (26.7%) patients died during follow-up (Table E6). Cohort characteristics are presented in Tables 1 and ​and22 and Tables E1–E5. One hundred fifty-one patients had Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage I/II disease and 241 had GOLD stage III/IV disease. Those who died were older and had a lower FEV1 % predicted, and there was a greater male preponderance (Table E6A). One hundred seventy-seven (45.1%) of the patients had fiber shift. The patients who died had a higher percentage of type II fibers (69.5% [62.2, 76.3%] vs. 66.0% [54.0, 74.2%]; P = 0.002) and a higher proportion of them exhibited fiber shift (58% vs. 41%, P = 0.004). BMI, FFMI, QMVC, MTCSA, and TLCOc were all lower, and RV/TLC higher, in those who died (Table E6B). Table 1. Core Characteristics of the Cohort (n = 392) in Addition to Univariate and Multivariate Analyses Including Type II Fiber Proportion Dichotomized into the Occurrence of Fiber Shift Table 2. Core Characteristics of the Cohort (n = 392) in Addition to Univariate and Multivariate Analyses Including Type II Fiber Proportion as a Continuous Measure In the cohort considered as a whole, both type II fiber % and the presence of fiber shift were univariate predictors of mortality, as were age and FEV1 % predicted (Tables 1 and ​and2).2). In a multivariate analysis including fiber shift as a dichotomous variable, fiber shift was retained, as were age and FEV1 % predicted, Table 1. When age, FEV1 % predicted, and type II fiber % were entered into a multivariate analysis, age and FEV1 % predicted were retained as independent predictors, but the association between fiber type and mortality just missed statistical significance (Table 2). The relationship between FEV1 and fiber proportion is shown in Figure 1A, and survival as a function of fiber shift, adjusted for age and FEV1, is shown in Figure 1B. Additional data regarding other lung function and muscle parameters are presented in Tables E7–E10. FEV1 expressed in liters and TLCOc were also univariate predictors of mortality; however, RV/TLC was not. When including TLCOc in the analysis (n = 209), fiber shift, age, FEV1 % predicted, and TLCOc were all independent predictors of mortality. In other subanalyses, BMI, FFMI, QMVC, QMVC/BMI, and MTCSA were not univariate predictors of mortality. Figure 1. (A) The relationship between type II fiber percentage and FEV1 % predicted (dashed lines demonstrate the 95% confidence interval), and (B) survival curves for those with fiber shift (n = 177) and those without fiber shift (n = 215) after adjusting for ... When limiting the analysis to those with an FEV1 greater than or equal to 50% predicted, age was the only predictor of mortality (hazard ratio [HR], 1.16; 95% CI, 1.07, 1.25; P < 0.0001; Table E11). In a multivariate analysis confined to those with an FEV1 less than 50%, fiber shift was retained as an independent predictor (HR, 1.71; 95% CI, 1.08, 2.71; P = 0.02), as were age (HR, 1.06; 95% CI, 1.03, 1.09; P < 0.0001), and FEV1 % predicted (HR, 0.96; 95% CI, 0.94, 0.99; P = 0.002; Table E12A). In a separate analysis confined to those with an FEV1 less than 50%, type II fiber % was not retained as an independent predictor (HR, 1.014; 95% CI, 0.996, 1.032; P = 0.13), whereas age and FEV1 % predicted were (Table E12B). Fiber shift in the vastus lateralis of patients with COPD was associated with increased mortality, although this association was weaker when lung function and age were included in the analysis. This finding was pronounced in patients with GOLD stage III/IV disease but undetectable in those with GOLD stage I/II disease. The relationship between skeletal muscle atrophy (5) and weakness (6) with mortality has been previously noted in COPD. However, we believe the present analysis is timely because we (3) and others (8) have recently shown that the nature of skeletal muscle involvement in COPD is heterogeneous rather than uniform. No prior study has related quadriceps biopsy appearances to long-term outcome in COPD. Given the known relationship between exercise capacity and survival (9), these data are consistent with our prior studies, which demonstrated a relationship between fiber shift (although not fiber atrophy) and impaired exercise capacity (3) and functional performance (10). Nevertheless, it remains unclear whether fiber shift causes poor exercise tolerance or is a manifestation of exercise intolerance and reduced physical activity, which are both associated with increased mortality in COPD (9, 11). Both concepts can be supported by in vivo models that demonstrate that muscle disuse results in type I to type II fiber shift (12) and that fiber shift toward a type I fiber predominance increases exercise performance (13). Due to the retrospective nature of the current analysis, exercise performance and physical activity data were not available for inclusion in this report, so a causative role for fiber shift in mortality cannot be demonstrated from this study. A prospective study would have been preferable and could also have considered other factors of relevance, including pulmonary rehabilitation over the intervening period. Despite the limitations of the current study, it is doubtful that a prospective study of comparable size and duration will ever be done. Interest in pharmacological management of skeletal muscle dysfunction is growing (14), and addressing fiber shift may eventually become a therapeutic possibility. Further studies to address whether the reversal of fiber shift is of benefit are of value.

Adolescent idiopathic scoliosis (AIS) can lead to ventilatory restriction, respiratory muscle weakness and exercise limitation. However, both the causes and the extent of muscle dysfunction remain unclear. The aim of our study is to describe muscle weakness and its relationship to lung function and tolerance to exercise in AIS patients. Lung and muscle function, together with exercise capacity, were assessed in 60 patients with pronounced spinal deformity (>40 degrees) and in 25 healthy volunteers. Patients with AIS had only mild to moderate abnormal ventilatory patterns, the most frequent of which were restrictive abnormalities. The function of respiratory and limb muscles and exercise capacity were below normal limits in AIS patients, and were significantly lower than in controls. Exercise capacity was found to correlate with the function of inspiratory, expiratory, upper limb and lower limb muscles which, in addition, were reciprocally interrelated. Multivariate analysis showed that lower limb muscle function is the main contributor to exercise intolerance. There appeared to be no connection between spinal deformity and lung function, muscle function or exercise capacity. We conclude that AIS patients show generalised muscle dysfunction which contributes to the reduction in their exercise capacity, even in the absence of severe ventilatory impairment.

Resumen Introduccion Las acciones locales de las citocinas en los musculos de los pacientes con enfermedad pulmonar obstructiva cronica (EPOC) se hallan sometidas a debate. El objetivo del presente estudio ha sido analizar las relaciones entre su expresion y la activacion genetica de programas de reparacion muscular. Pacientes y metodos Se incluyo en el estudio a 25 pacientes con EPOC grave en situacion estable. Se les realizo una biopsia del musculo intercostal externo, donde se evaluaron los signos de lesion muscular (morfometria), la infiltracion de celulas inflamatorias (inmunohistoquimica) y la expresion de genes seleccionados (tecnica de reaccion en cadena de la polimerasa en tiempo real) correspondientes a las propias citocinas —factor de necrosis tumoral alfa (TNF-α) y sus receptores 1 y 2 (TNFR1 y TNFR2), e interleucinas-1β, 6 y 10—, un marcador panleucocitario (CD18) y moleculas clave en las vias de reparacion-miogenesis (Pax7, M-Caderina y Mio-D). Resultados La expresion de TNFR2 se relaciono directamente con la funcion muscular inspiratoria (representada por la presion inspiratoria maxima sostenible; r=0,496, p Conclusiones La expresion de los receptores del TNF-α guarda una estrecha relacion tanto con la activacion de los programas de miogenesis como con la propia funcion muscular inspiratoria. Este hecho refuerza nuestra hipotesis de que algunas citocinas locales participan en la reparacion de los musculos respiratorios en los pacientes con EPOC.

a b s t r a c t Objective: There is disagreement regarding the local action of cytokines in the respiratory muscles of patients with chronic obstructive pulmonary disease (COPD). The objective of this study was to analyze the relationships between cytokine expression and genetic activation of the mechanisms of muscle repair. Patients and Methods: Twenty-five patients with severe COPD and in stable condition were enrolled in the study. We performed a biopsy of the external intercostal muscle of the patients and analyzed the specimen for signs of muscle lesion (morphometry), infiltration of inflammatory cells (immunohistochemistry), and expression of selected genes (real-time polymerase chain reaction technique) corresponding to the cytokines (tumor necrosis factor α (TNF-α) and its type 1 and 2 receptors (TNFR1 and TNFR2), and interleukin (IL) 1β, IL-6, and IL-10), a pan-leukocyte marker (CD18), and key molecules in the repair- myogenesis pathways (Pax7, M-cadherin, and MyoD). Results: Expression of TNFR2 is directly related to inspiratory muscle function (represented by maximum sustainable inspiratory pressure; r=0.496; P

Resumen La funcion muscular se halla frecuentamente afectada en los pacientes con enfermedad pulmonar obstructiva cronica (EPOC), lo cual condiciona su semiologia y pronostico. La distribucion y la gravedad de esta disfuncion son heterogeneas, por lo que sus causas predominantes parecen en parte especificas del grupo muscular examinado. Es el caso de la sobreactividad y una geometria desfavorable caracteristicas de los musculos respiratorios, frente a la relativa inactividad de los musculos de las extremidades. Tambien hay factores que serian comunes a todos los musculos del organismo. Entre ellos destacarian la inflamacion sistemica, las alteraciones nutricionales, el uso de determinados farmacos, la hipoxia y la presencia de comorbilidad y/o edad avanzada. Sin embargo, mientras que los musculos respiratorios muestran un fenotipo adaptado a su situacion desfavorable, y llegan a compensarla parcialmente, los musculos de las extremidades muestran cambios de tipo involutivo, que contribuirian a la disfuncion. Por tanto, aunque la perdida funcional puede aparecer en diferentes territorios musculares, sus causas, y por tanto sus enfoques terapeuticos, seran diversos, incluidos el soporte nutricional, el entrenamiento y/o el reposo, segun los casos.

Objetivo Los musculos respiratorios de los pacientes con enfermedad pulmonar obstructiva cronica (EPOC) presentan lesiones estructurales, que coexisten con signos de adaptacion. Nuestra hipotesis es que esto solo puede explicarse si se produce simultaneamente la activacion de sus celulas satelite. El proposito del presente trabajo ha sido valorar el numero y la eventual activacion de dichas celulas, asi como la expresion de marcadores de microlesion estructural, ligados a la regeneracion. Pacientes y metodos Se incluyo en el estudio a 8 pacientes con EPOC grave —media ± desviacion estandar del volumen espiratorio forzado en el primer segundo: un 33 ± 9% del valor de referencia— y a 7 controles, a quienes se realizo una biopsia del musculo intercostal externo. La muestra se analizo mediante microscopia optica (fenotipo fibrilar), electronica (celulas satelite) y tecnica de reaccion en cadena de la polimerasa en tiempo real (marcadores de microlesion: factor de crecimiento similar a la insulina de tipo 1, factor de crecimiento mecanico e isoformas de cadenas pesadas de miosina [MyHC] embrionaria e isoformas de perinatal; de presencia y activacion de celulas satelite: Pax-7 y m-caderina, respectivamente; y condicionantes del fenotipo fibrilar: MyHC-I, IIa y IIx). Resultados Los pacientes tuvieron unas fibras mayores que los sujetos sanos (54 ± 6 frente a 42 ± 4 μm2; p Conclusiones Los musculos intercostales de pacientes con EPOC grave muestran signos indirectos de microlesion, acompanados de la activacion de sus celulas satelite. Esto apunta a la presencia de ciclos continuados de lesion y reparacion, lo que podria explicar parcialmente la conservacion de sus propiedades estructurales.

Objetivo La presion asistencial sobre la hospitalizacion convencional es un problema acuciante en los servicios de neumologia. El proposito del estudio ha sido analizar el impacto de un nuevo dispositivo, la unidad neumologica de estancia corta (UNEC), sobre la calidad de la atencion en el servicio de neumologia de un hospital terciario. Material y metodos La UNEC se doto de 4 camas de hospitalizacion convencional, gestionadas por un neumologo especializado. En ella ingresaron solo pacientes con diagnosticos de exacerbacion de enfermedad pulmonar obstructiva cronica (EPOC) o asma bronquial, neumonia extrahospitalaria o sospecha de cancer de pulmon, y prevision de estancia inferior a 4 dias. Se analizo el periodo de puesta en funcionamiento de la unidad (6 meses, de octubre a marzo) frente al mismo periodo del ano anterior, valorandose los distintos indices de calidad asistencial. Resultados Se incluyo a 147 pacientes (79% varones), con una media ± desviacion estandar de edad de 64 ± 17 anos. La estancia media en la UNEC fue de 3,3 ± 1,6 dias—solo un 1,4% de los pacientes supero los 4 dias— y la tasa de reingresos, del 2,7%. No hubo mortalidad. Con la UNEC, la estancia media global en el servicio disminuyo un 30% (de 11,8 ± 4,6 a 8,3 ± 2,6 dias; p Conclusiones La UNEC puede mejorar la eficiencia de la atencion neumologica al disminuir la estancia media hospitalaria y la tasa de reingresos, sin reducir la complejidad de las enfermedades atendidas ni precisar recursos adicionales especificos.

The respiratory muscles of patients with chronic obstructive pulmonary disease (COPD) display evidence of structural damage in parallel with signs of adaptation. We hypothesized that this can only be explained by the simultaneous activation of satellite cells. The aim of this study was to analyze the number and activation of those cells along with the expression of markers of microstructural damage that are frequently associated with regeneration.The study included 8 patients with severe COPD (mean [SD] forced expiratory volume in 1 second, 33% [9%] of predicted) and 7 control subjects in whom biopsies were performed of the external intercostal muscle. The samples were analyzed by light microscopy to assess muscle fiber phenotype, electron microscopy to identify satellite cells, and real-time polymerase chain reaction to analyze the expression of the following markers: insulin-like growth factor 1, mechano growth factor, and embryonic and perinatal myosin heavy chains (MHC) as markers of microstructural damage; Pax-7 and m-cadherin as markers of the presence and activation of satellite cells, respectively; and MHC-I, IIa, and IIx as determinants of muscle fiber phenotype.The patients had larger fibers than healthy subjects (54 [6] vs 42 [4] microm(2); P.01) with a similar or slightly increased proportion of satellite cells, as measured by ultrastructural analysis (4.3% [1%] vs 3.7% [3.5%]; P.05) or expression of Pax-7 (5.5 [4.1] vs 1.6 [0.8] arbitrary units [AU]; P.05). In addition, there was greater activation of satellite cells in the patients, as indicated by increased expression of m-cadherin (3.8 [2.1] vs 1.0 [1.2] AU; P=.05). This was associated with increased expression of markers of microstructural damage: insulin-like growth factor 1, 0.35 (0.34) vs 0.09 (0.08) AU (P.05); mechano growth factor, 0.45 (0.55) vs 0.13 (0.17) AU (P=.05).The intercostal muscles of patients with severe COPD show indirect signs of microstructural damage accompanied by satellite cell activation. This suggests the presence of ongoing cycles of lesion and repair that could partially explain the maintenance of the structural properties of the muscle.

Respiratory muscle dysfunction is a common problem in patients with chronic obstructive pulmonary disease (COPD) and has mostly been related to pulmonary hyperinflation [1, 2]. Associated diaphragm shortening and deleterious changes in the muscle force-length relationship cause a reduction in the muscles’ capacity to generate pressure, placing them at a mechanical disadvantage [1, 3]. Specifically, both inspiratory muscle strength and mechanical efficiency may be reduced in COPD patients [1, 4–6], although, at iso-volume, the contractile strength of the diaphragm in COPD is preserved or may even be improved in some cases [7]. The ratio between transdiaphragmatic pressure and electrical diaphragm activity has been used as a measure of respiratory muscle efficiency [8, 9]. However, in clinical practice, it is complex to measure this parameter directly, as invasive measures are required and these are uncomfortable for patients [4]. During contraction, respiratory muscle fibres vibrate laterally [10]. These vibrations are related to the mechanical activation of these muscles and can be non-invasively recorded through accelerometers positioned on the surface of the skin, proximal to the muscles: this is called respiratory muscle mechanomyogram (MMG) [11–13]. The analysis of the mechanical activation of inspiratory muscles through the MMG might be a useful alternative approach for assessing respiratory muscles function in patients with COPD [13, 14]. MMG reflects the mechanical counterpart of the neural activity measured by electromyography. Respiratory muscle MMG provide some advantages over surface diaphragmatic electromyography with regards to simplicity of use. First of all, MMG recording is easy and simple to implement: MMG is acquired using a small accelerometer attached to the skin surface, whereas electromyography typically uses three electrodes. Secondly, as it is a mechanical signal, MMG is not susceptible to bioelectrical interference. Furthermore, the signal to noise ratio of MMG is typically higher than that of the electromyography, requiring less amplification and electrical shielding. In addition, the MMG recording does not require skin preparation and it is not influenced by changes in the skin impedance. The aim of the present study was to noninvasively evaluate the mechanical activation of inspiratory muscles and its efficiency (EMMG) during tidal volume breathing in patients with severe-to-very severe COPD. With this in mind, we investigated the peak inspiratory mouth pressure (IPpeak) and respiratory muscle MMG acquired under both quiet breathing (QB) and maximal voluntary ventilation (MVV) conditions during an incremental respiratory flow protocol.

Fundamento y objetivo El objetivo del presente estudio fue evaluar de forma prospectiva los efectos de una exacerbacion clinica de la enfermedad pulmonar obstructiva cronica (EPOC) sobre la funcion muscular esqueletica periferica y respiratoria Pacientes y metodo Se selecciono a 49 pacientes (todos varones con una edad media [DE] de 63 [11] anos), asignados a 3 cohortes para el analisis: a) pacientes con EPOC hospitalizados por exacerbacion de su enfermedad en sala convencional; b) pacientes hospitalizados en sala convencional por otra enfermedad pulmonar o nodulo pulmonar, y c) pacientes con EPOC en fase estable (ambulatorios). Se realizaron mediciones secuenciales mediante antropometria, bioquimica serica y bioimpedancia corporal. En la cohorte de pacientes con EPOC agudizada se evaluaron los cambios en la funcion de los musculos perifericos (fuerza y resistencia de las manos dominante y no dominante), asi como de los musculos inspiratorios y espiratorios Resultados Se evaluo a los pacientes durante un periodo medio de 6 (2) dias. Los pacientes con EPOC exacerbada mostraron un deterioro funcional muscular, progresivo y global, expresado como disminucion de la presion espiratoria maxima del 17% (12%), de la fuerza maxima de la mano dominante del 6% (9%) y de la no dominante del 7% (8%), asi como de la resistencia anaerobica de la mano dominante del 28% (26%) y de la no dominante del 23% (16%). Estos cambios tuvieron una tendencia lineal. La bioimpedancia corporal expreso una perdida media de masa magra del 7% (6%) (p Conclusiones La agudizacion de la EPOC se asocia a un deterioro agudo y global de la funcion de los musculos esqueleticos espiratorios y perifericos. Es posible que estos cambios esten relacionados con una perdida aguda de masa muscular (proteolisis). Esta disfuncion muscular no se detecta si se evalua unicamente la funcion muscular inspiratoria, probablemente por la coexistencia de factores mecanicos transitorios

Epigenetic mechanisms regulate muscle mass and function in models of muscle dysfunction and atrophy. We assessed whether quadriceps muscle weakness and atrophy are associated with a differential expression profile of epigenetic events in patients with advanced COPD (chronic obstructive pulmonary disease). In vastus lateralis (VL) of sedentary severe COPD patients (n=41), who were further subdivided into those with (n=25) and without (n=16) muscle weakness and healthy controls (n=19), expression of muscle-enriched miRNAs, histone acetyltransferases (HATs) and deacetylases (HDACs), growth and atrophy signalling markers, total protein and histone acetylation, transcription factors, small ubiquitin-related modifier (SUMO) ligases and muscle structure were explored. All subjects were clinically evaluated. Compared with controls, in VL of all COPD together and in muscle-weakness patients, expression of miR-1, miR-206 and miR-27a, levels of lysine-acetylated proteins and histones and acetylated histone 3 were increased, whereas expression of HDAC3, HDAC4, sirtuin-1 (SIRT-1), IGF-1 (insulin-like growth factor-1) were decreased, Akt (v-akt murine thymoma viral oncogene homologue 1) expression did not differ, follistatin expression was greater, whereas myostatin expression was lower, serum reponse factor (SRF) expression was increased and fibre size of fast-twitch fibres was significantly reduced. In VL of severe COPD patients with muscle weakness and atrophy, epigenetic events regulate muscle differentiation rather than proliferation and muscle growth and atrophy signalling, probably as feedback mechanisms to prevent those muscles from undergoing further atrophy. Lysine-hyperacetylation of histones may drive enhanced protein catabolism in those muscles. These findings may help design novel therapeutic strategies (enhancers of miRNAs promoting myogenesis and acetylation inhibitors) to selectively target muscle weakness and atrophy in severe COPD.

The aim of the present study was to measure bilateral asynchrony in patients suffering from Chronic Obstructive Pulmonary Disease (COPD) performing an incremental inspiratory load protocol. Bilateral asynchrony was estimated by the comparison of respiratory movements derived from diaphragm mechanomyographic (MMGdi) signals, acquired by means of capacitive accelerometers placed on left and right sides of the rib cage. Three methods were considered for asynchrony evaluation: Lissajous figure, Hilbert transform and Motto's algorithm. Bilateral asynchrony showed an increase at 20, 40 and 60% (values of normalized inspiratory pressure by their maximum value reached in the last inspiratory load) while the very severe group showed and increase at 20, 40, 80, and 100 % during the protocol. These increments in the phase's shift can be due to an increase of the inspiratory load along the protocol, and also as a consequence of distress and fatigue. In summary, this work evidenced the capability to estimate bilateral asynchrony in COPD patients. These preliminary results also showed that the use of capacitive accelerometers can be a suitable sensor for recording of respiratory movement and evaluation of asynchrony in COPD patients.

Epigenetic events are differentially expressed in the lungs and airways of patients with chronic obstructive pulmonary disease (COPD). Moreover, epigenetic mechanisms are involved in the skeletal (peripheral) muscle dysfunction of COPD patients. Whether epigenetic events may also regulate respiratory muscle dysfunction in COPD remains unknown. We hypothesized that epigenetic mechanisms would be differentially expressed in the main inspiratory muscle (diaphragm) of patients with COPD of a wide range of disease severity compared to healthy controls. In diaphragm muscle specimens (thoracotomy due to lung localized neoplasms) of sedentary patients with mild-to-moderate and severe COPD, with preserved body composition, and sedentary healthy controls, expression of muscle-enriched microRNAs, histone acetyltransferases (HATs) and deacetylases (HDACs), total DNA methylation and protein acetylation, small ubiquitin-related modifier (SUMO) ligases, muscle-specific transcription factors, and muscle structure were explored. All subjects were also clinically evaluated: lung and muscle functions and exercise capacity. Compared to healthy controls, patients exhibited moderate airflow limitation and diffusion capacity, and reduced exercise tolerance and transdiaphragmatic strength. Moreover, in the diaphragm of the COPD patients, muscle-specific microRNA expression was downregulated, while HDAC4 and myocyte enhancer factor (MEF)2C protein levels were higher, and DNA methylation levels, muscle fiber types and sizes did not differ between patients and controls. In the main respiratory muscle of COPD patients with a wide range of disease severity and normal body composition, muscle-specific microRNAs were downregulated, while HDAC4 and MEF2C levels were upregulated. It is likely that these epigenetic events act as biological adaptive mechanisms to better overcome the continuous inspiratory loads of the respiratory system in COPD. These findings may offer novel therapeutic strategies to specifically target respiratory muscle dysfunction in patients with COPD.

The breathing pattern is probably the first type of study to yield information on respiratory function.1 Its most simple parameter, the respiratory rate (RR or f) may be determined simply by observing the patient, and forms part of the vital signs that are typically recorded in numerous clinical situations.2 The RR and the tidal volume (VT) constitute the basic variables of simple spirometry, and they can be recorded using a simple spirometer such as a Tyssot type device. From these 2 variables we can then calculate at least 2 others: the minute ventilation (V . E or V . I, depending on whether the recording is made during expiration or inspiration), calculated as the RR × V · T; and the total time of the respiratory cycle (TTOT), calculated as 60/RR. To go any further requires instruments that measure the duration of each part of the cycle and the intermediate periods of apnea. In the past, the so-called water spirometer was common; the respiratory times and volumes were recorded by means of the displacement of a rotating cylinder in a tank full of water. However, the instrument now most widely used is the pneumotachometer, which is usually integrated into a spirometer. There are various types of pneumotachometer, including particularly the Fleisch type (which uses the pressure differences on either side of a membrane)3 and, more recently, instruments based on a turbine, ultrasound emission, or the so-called hot-wire devices.4,5 The traditional pneumotachometer calculates the air volume from the flow (volume/ time) and enables the duration of each phase of respiration to be recorded, making it possible to obtain the inspiratory (TI) and expiratory times. Part of the relevance of these variables comes from the information they provide on the duration of contractile muscle activity. For example, the longer the TI, the more difficult it will be to maintain a given inspiratory effort. Using the variables mentioned above, a further 2 variables can be calculated: the ratios VT/TI and TI/TTOT. The first of these is an indicator of the speed at which the air volume is attained; it is therefore an expression of flow but also of central ventilatory drive. Its limitation is that, as the signal is recorded in the mouth, this drive has already been affected by a whole series of factors derived from the respiratory apparatus itself. In comparison with the TI alone, the TI/TTOT ratio enables us to predict more accurately how long a given ventilatory pattern can be maintained. If study of the breathing pattern is combined with measurements made with other devices, more sophisticated variables can be determined, progressively increasing the physiological information about the individual. For example, the addition of respiratory gas analyzers permits oxygen consumption (V . O2), carbon dioxide production (V . CO2), and the dead space (VD/VT) to be calculated; measurement of esophageal pressure enables us to calculate the intrinsic positive end-expiratory pressure (PEEPi), equivalent to the pressure at which flow initiates after a period of generation of “ineffective” inspiratory pressure. Measurement of the dead space is not an irrelevant variable, as it represents the difference between the V . E of the breathing pattern and the effective alveolar ventilation, which is what is really involved in gas exchange in the lungs. One of the main problems when measuring anything more complex than the RR is the need to attach some device to the patient’s face.6,7 Thus, when using the pneumotachometer, a face mask, endotracheal tube, ventilator tubing, or mouthpiece is required (or must be taken advantage of if the clinical situation means that the patient already has such a device in place).3,6 This has its drawbacks, as such an action can lead to changes that mean we will not be evaluating the patient’s natural pattern. Furthermore, care must be taken to minimize the dead space derived from the device used. In a radically different approach, the breathing pattern is determined from changes in the volume of the thoracic and, sometimes, abdominal cavities. There are many techniques based on this principle, from belts containing mercury or air, to magnetometers and inductive plethysmography.8-12 Some of these techniques also allow us to measure changes that occur in the functional residual capacity in certain situations (for example, during exercise). Respiratory magnetometers and inductive plethysmography are the most widely used techniques. Magnetometry is based on the placement of 2 pairs of devices that emit an alternating electromagnetic field, and their corresponding receivers (one on the chest and one on the abdomen).11 Inductive plethysmography uses 2 elastic belts (thoracic and abdominal) with an electrical resistance; changes in the voltage are proportional to the cross-sectional area of the thoracic and abdominal cavities.7 However, calibration to achieve a reliable VT is problematic with both methods, and the magnetometers * Corresponding author. E-mail address: jgea@imim.es (J. Gea).