A reduced total lung capacity associated with a normal or decreased lung recoil pressure at full inflation (Pel max) has been noted in patients with valvular heart lesions. In order to investigate the mechanism underlying this inappropriately low Pel max, we measured respiratory mechanics in a group of 15 patients with mitral valve disease uncomplicated by other illness. The total lung capacity was 81 percent of control. The static pressure-volume curve of the long intersected the normal one in the vicinity of functional residual capacity (i.e., the recoil pressure was increased at large lung volumes and diminished at low lung volumes), and both expiratory compliance and Pel max were significantly decreased. In 13 of the 15 patients, the minimal (inspiratory) pleural pressure-volume curve was shifted so that the pressures generated by the inspiratory muscles were less negative than normal at any given lung volume. The decrease in Pel max was proportional to the alteration in muscle pressures. These findings indicate (1) that patients with mitral valve disease have compromised function of the inspiratory muscles, and (2) that this alteration is responsible for the low Pel max. Respiratory muscle weakness contributes to the restriction of lung volume in patients with pulmonary vascular congestion and is probably implicated in cardiac dyspnea.