Dyspnea is a common, disabling symptom in chronic heart failure, yet the underlying mechanisms remain unknown. The respiratory muscle pump is composed of skeletal muscles whose strength directly influences the pump's performance. Respiratory muscle weakness is important in the dyspnea experienced by some patients with pulmonary disease; however, the role of the respiratory muscle pump in the dyspnea of chronic heart failure has not previously been examined. To assess respiratory muscle strength and its relation to dyspnea during daily activity, we measured maximum inspiratory and expiratory mouth pressures as indices of respiratory muscle strength and the baseline dyspnea index in nine stable, chronic cardiac pump failure patients who had no evidence of primary lung disease, and in nine age- and sex-matched healthy control subjects. The chronic heart failure patients, when compared with their matched control subjects, had reduced inspiratory and expiratory muscle strength, and both inspiratory and expiratory muscle strength were significantly correlated with dyspnea during daily activity (r2 = 0.80, p = 0.001 and r2 = 0.45, p = 0.05, respectively). Inspiratory muscle strength accounted for all of the variance in dyspnea that was correlated with respiratory muscle strength when the relative contributions of inspiratory and expiratory muscle strength were examined. There was no correlation between lung volumes or spirometry and dyspnea in the heart failure patients. These findings indicate that patients with stable chronic heart failure have inspiratory and expiratory muscle weakness and further suggest that the respiratory muscle pump significantly contributes to the dyspnea during the activities of daily living.

with unloading, as did mean Pmus I and pmus E (21 and 44%). 4. The lack of any significant changes in VE, PA,co, or breathing pattern, despite a marked reduction in respiratory muscle load throughout CWHE, indicates that the load on the respiratory muscles has only a minor role in the regulation of ventilation during heavy exercise. 5. The absence of improvement in CWHE duration (control, 11-4 + 1 2 min; unload, 12-6 + 2 1 min, n.s.) with unloading implies that respiratory muscle function does not limit endurance exercise performance during cycling in healthy humans.This study tested the hypothesis that the load on the respiratory muscles is an important determinant of the ventilatory response to heavy exercise in normal humans. We used constant work rate heavy exercise (CWHE) to exhaustion as the ventilatory stimulus and the rationale of the study was as follows. Minute ventilation (VE) and breathing pattern are determined by the intensity and pattern of respiratory muscle contraction (i.e. respiratory muscle output) and the mechanical properties of the respiratory system. The relation between respiratory muscle pressure (Pmus) and VE is illustrated schematically in Fig. 1 (Hussain, Pardy & Dempsey, 1985) previous studies, we have used a linear model to illustrate the Pmus-17E relationsEhip in Fig. 1. A linear model is used to facilitate discussion of concepts raised in this paper but the concepts and questions addressed here do not depend on the linearity (or otherwise) of this relation. The term 'respiratory impedance' will be used in this manuscript as a descriptive term to denote the relation between respiratory muscle pressure generated by the subject (Pmus) and minute ventilation (VE). 'Reducing respiratory impedance' is merely a short-hand way of stating that the 'relation between Pmus and VE was altered such that one gets a higher VE for a given

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PLR accounted for nearly 40% of the TNFi failures in axial SpA patients. Older age, negative HLA-B27, higher baseline disease activity, and treatment with soluble TNF receptors were the independent predictors of the primary nonresponse to TNFi.