Patients with severe obesity and obstructive sleep apnea (OSA) have been shown to have abnormalities in respiratory muscle function and respiratory control. The present study was done to evaluate diaphragmatic function and the diaphragm fiber-length-compensating reflex in morbidly obese patients with OSA (1). Twelve normal subjects and 13 morbidly obese patients with OSA were studied in recumbent and upright positions. In the normal subjects, the diaphragm fiber-length-compensating reflex operated normally causing the diaphragm's inspiratory EMG to increase when the diaphragm's fibers shortened with assumption of the upright position. However, 8 of the 13 obese patients with OSA showed a decrease rather than an increase in the inspiratory diaphragmatic EMG on assuming the upright posture. Further data indicate greater diaphragmatic efficiency in the upright than in the supine position in a majority of the obese patients, a reversal of the normal response. Two possible explanations of these observations are: an abnormality of central respiratory control in obese patients with OSA and overstretching of the diaphragm in the recumbent obese patient. The observation of reduced maximal transdiaphragmatic pressures in the recumbent position in some of the obese patients with OSA supports the second explanation. Diaphragmatic overstretching may be an important mechanism in the development of hypoventilation in the morbidly obese.