Techniques developed in this laboratory to measure intrinsic laryngeal muscle electrical activity and laryngeal airway resistance in humans will be combined with fiberoptic measurements of glottic aperture to determine 1) the physiologic and pathophysiologic factors that control respiratory- related intrinsic laryngeal muscle activity , and 2) the net effect of changes in intrinsic laryngeal muscle activity on the respiratory function of the larynx. Protocols in normal adult humans will examine the hypotheses that the larynx actively brakes exhalation during quiet breathing in wakefulness but not in NREM sleep. Intrinsic laryngeal muscle activity, laryngeal airway resistance and vocal cord position will be compared during wakefulness and sleep. The loss of all intrinsic laryngeal muscle activity throughout expiration in NREM sleep, accompanied by differences between wakefulness and sleep in glottic aperture at end expiration and in laryngeal airway resistance during expiration would support the hypothesis that the larynx actively brakes exhalation during quiet breathing in wakefulness. The possibility that another expiratory brake substitutes for the loss of the active laryngeal brake in NREM sleep will be examined by measuring postinspiratory activity of the diaphragm and anterior scalene muscles during wakefulness and sleep. The effect of induced changes in respiratory mechanics on intrinsic laryngeal muscle activity, laryngeal airway resistance and vocal cord position will determine whether neural afferents tracking changes in lung volume reflexly modulate motor output to the larynx helping to regulate lung volume during and at the end of exhalation. Another protocol in normal subjects will determine the electromechanical relationships of the posterior cricoarytenoid muscle by simultaneously recording the muscle's electrical activity, laryngeal airway resistance, and vocal cord position during NREM sleep. Other protocols will examine the effect of pathologic states on respiratory-related laryngeal function. Studies in asthmatics will determine the changes in respiratory related intrinsic laryngeal muscle activity associated with the known paradoxical narrowing of the vocal cords in expiration during induced bronchospasm. Studies in subjects with interstitial lung disease will determine if pathologic decreases in lung volume are associated with an increase in laryngeal braking in expiration. Studies will also be performed to determine the role of the larynx in the pathophysiology of COPD.
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