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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.

In COPD patients who are limited due to dyspnoea, magnetic neuromuscular stimulation of the quadriceps constitutes a feasible training method for the lower limbs, with positive effects on the muscle function, effort capacity and perception areas.

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Lung cancer (LC) has become one of the leading causes of preventable death in the last few decades. Cigarette smoking (CS) stays as the main etiologic factor of LC despite that many other causes such as occupational exposures, air pollution, asbestos, or radiation have also been implicated. Patients with chronic obstructive pulmonary disease (COPD), which also represents a major cause of morbidity and mortality in developed countries, exhibit a significantly greater risk of LC. The study of the underlying biological mechanisms that may predispose patients with chronic respiratory diseases to a higher incidence of LC has also gained much attention in the last few years. The present review has been divided into three major sections in which different aspects have been addressed: (I) relevant etiologic agents of LC; (II) studies confirming the hypothesis that COPD patients are exposed to a greater risk of developing LC; and (III) evidence on the most relevant underlying biological mechanisms that support the links between COPD and LC. Several carcinogenic agents have been described in the last decades but CS remains to be the leading etiologic agent in most geographical regions in which the incidence of LC is very high. Growing evidence has put the line forward the implications of COPD and especially of emphysema in LC development. Hence, COPD represents a major risk factor of LC in patients. Different avenues of research have demonstrated the presence of relevant biological mechanisms that may predispose COPD patients to develop LC. Importantly, the so far identified biological mechanisms offer targets for the design of specific therapeutic strategies that will further the current treatment options for patients with LC. Prospective screening studies, in which patients with COPD should be followed up for several years will help identify biomarkers that may predict the risk of LC among these patients.

Bronchial asthma is one of the most prevalent respiratory conditions. Although it is defined as an inflammatory disease, the current guidelines for both diagnosis and follow-up of patients are based only on clinical and lung function parameters. Current research is focused on finding markers that can accurately predict future risk, and on assessing the ability of these markers to guide medical treatment and thus improve prognosis. The use of noninvasive methods to study airway inflammation is gaining increasing support. The study of eosinophils in induced sputum has proved useful for the diagnosis of asthma; however, its clinical implementation is complex. Some studies have shown that the measurement of exhaled nitric oxide (FeNO) may also be useful to establish disease phenotypes and improve control. Others have found that the measurement of pH and certain markers of oxidative stress, cytokines and prostanoids in exhaled breath condensate (EBC) may also be useful as well as the measurement of the temperature of exhaled breath and the analysis of volatile organic compounds (VOCs). In conclusion, since asthma is an inflammatory disease, it seems appropriate to try to control it through the study of airway inflammation using noninvasive methods. In this regard, the analysis of induced sputum cells has proved very useful, although the clinical implementation of this technique seems difficult. Other techniques such as temperature measurement, the analysis of FeNO, the analysis of the VOCs in exhaled breath, or the study of certain biomarkers in EBC require further study in order to determine their clinical applicability.

For decades, chronic obstructive pulmonary disease (COPD) has been considered a relentlessly progressive disease in which the deterioration of lung function is associated with an increase in symptoms, interrupted only by periods of exacerbation. However, this paradigm of COPD severity based on FEV1 has been challenged by currently available evidence. So far, three main approaches, though with contradictory aspects, have been proposed in order to address the complexity of COPD as well as to develop appropriate diagnostic, prognostic and therapeutic strategies for the disease: 1) the use of independent, clinically relevant variables, 2) the use of multidimensional indices, and 3) disease approaches based on clinical phenotypes. Multivariable systems seem superior to FEV1 in predicting prognosis and defining disease severity. However, selection of variables available from current literature must be confronted with issues of medical practice. Future evidence will be needed to reveal their effective relationship with disease long-term prognosis and to demonstrate the most adequate cutoff values to be used in clinical settings. Multidimensional scores provide a good prognostic instrument for the identification of patients with a particular degree of disease severity. Clinical phenotyping can help clinicians identify the patients who respond to specific pharmacological interventions; however, there is some controversy about the phenotypes to select and their long-term implications. Although these approaches are not perfect, they represent the first step towards patient-centered medicine for COPD. In the near-future, these different approaches should converge towards one new field to focus on the better management of COPD patients.