Patients with type 2 diabetes may frequently present inspiratory muscle weakness. In these patients, IMT improves inspiratory muscle function with no consequences in functional capacity or autonomic modulation.

Activity-related dyspnoea is a key cause of physical impairment in cardiovascular and respiratory diseases [1]. Despite remarkable diagnostic advances in the past decades, discriminating "the heart" versus "the lungs" as a cause of exertional dyspnoea remains a challenge for cardiologists and pulmonologists. This state of affairs is not surprising if one considers that the respiratory neural drive, a key correlate of exertional dyspnoea, is characteristically increased in heart and lung diseases [2]. The differentiating feature, however, is the relative contribution of lung mechanical abnormalities as they are, by definition, more pronounced in the respiratory than in the cardiac patient [3]. Cardiopulmonary exercise testing (CPET) has long been advocated as the test of choice to determine the primary source of exercise limitation in these patients. In real life, however, there is substantial overlap in the physiological abnormalities underlying cardiovascular and respiratory diseases. It follows that CPET remains largely underused to untangle such a complex conundrum [4]. This scenario is partially explained by the fact that the interpretation of CPET in dyspnoeic patients remains heavily focused on physiological constructs. Although those physiological variables are important to objectively determine the biological basis of dyspnoea, it is surprising that little attention, if any, has been given to the symptom per se as an auxiliary diagnostic tool.In this context, the burden of exertional dyspnoea can be readily quantified by expressing its severity (e.g. 0-10 Borg category-ratio scale) as a function of work rate (WR). The relationship between dyspnoea and ventilation (V′ E ), however, is more complex and may present with some discriminating features. Thus, if the ventilatory pump is free of major mechanical constraints (e.g. cardiocirculatory diseases), the increased drive to breathe can be largely translated into an equally high V′ E [5]. In other words, the intensity and trajectory of dyspnoea as a function of V′ E may not differ substantially from the pattern observed in normal subjects. Conversely, if the mechanical constraints typical of respiratory diseases preclude the ventilatory pump to "respond" to an increased drive, dyspnoea is expected to increase at a faster rate than V′ E [6]. Owing to the fact that such constraints further increase beyond a certain critical intensity [7], it is conceivable that they could be identified by a sudden upward inflection of dyspnoea against V′ E . To the authors' knowledge, such theoretical constructs have not yet been put under scrutiny with the specific objective of discriminating cardiovascular versus respiratory disease as a cause of exertional dyspnoea.In a proof-of-concept study, we enrolled two groups of patients: those in whom the cardiocirculatory derangements dominate over the lung mechanical abnormalities (chronic heart failure (CHF) with reduced left ventricular ejection fraction, n=14) and vice versa (COPD, n=14). The control group consisted of 10 age-a...

Introduction Inspiratory muscle weakness (IMW) is a potential cause of exertional dyspnea frequently under‐appreciated in clinical practice. Cardiopulmonary exercise testing (CPET) is usually requested as part of the work‐up for unexplained breathlessness, but the specific pattern of exercise responses ascribed to IMW is insufficiently characterized. Objectives To identify the physiological and sensorial responses to progressive exercise in dyspneic patients with IMW without concomitant cardiorespiratory or neuromuscular diseases. Methods Twenty‐three subjects (18 females, 55.2 ± 16.9 years) complaining of chronic daily life dyspnea (mMRC = 3 [2‐3]) plus maximal inspiratory pressure < the lower limit of normal and 12 matched controls performed incremental cycling CPET. FEV1/FVC<0.7, significant abnormalities in chest CT or echocardiography, and/or an established diagnosis of neuromuscular disease were among the exclusion criteria. Results and Conclusion Patients presented with reduced aerobic capacity (peak V̇O2: 79 ± 26 vs 116 ± 21 %predicted), a tachypneic breathing pattern (peak breathing frequency/tidal volume = 38.4 ± 22.7 vs 21.7 ± 14.2 breaths/min/L) and exercise‐induced inspiratory capacity reduction (‐0.17 ± 0.33 vs 0.10 ± 0.30 L) (all P < .05) compared to controls. In addition, higher ventilatory response (ΔV̇E/ΔV̇CO2 = 34.1 ± 6.7 vs 27.0 ± 2.3 L/L) and symptomatic burden (dyspnea and leg discomfort) to the imposed workload were observed in patients. Of note, pulse oximetry was similar between groups. Reduced aerobic capacity in the context of a tachypneic breathing pattern, inspiratory capacity reduction and preserved oxygen exchange during progressive exercise should raise the suspicion of inspiratory muscle weakness in subjects with otherwise unexplained breathlessness.