The purpose of this study was to test the hypothesis that respiratory arrhythmias and apneas induced by α 2 agonists in anesthetized goats are associated with an increase of upper airway expiratory-related activity, rather than a general depression of breathing. Activities of phrenic (Phr) and recurrent laryngeal nerves (RLN) were recorded in response to the α 2 agonists clonidine (0.5–3.0 μg · kg −1 i.v.) or guanabenz (7.0–20.0 μg · kg −1 i.v.) in ten chloralose-anesthetized goats. Injection of either α 2 agonist resulted in respiratory arrhythmias with a greater than seven-fold increase in T e and a 30% reduction in T i. During apneas RLN expiratory-related activity remained tonic until the next Phr burst, consistent with our hypothesis. Cessation of Phr activity during hypocapnia also resulted in a tonic increase of RLN expiratory activity; and injection of NaCN (50 μg · kg −1 i.v.) increased Phr and RLN inspiratory activities, while attenuating RLN expiratory-related activity. Inspiratory and expiratory-related activity of RLN motoneurons appear to be reciprocally modulated by α 2 agonists or changes in central or peripheral chemoreceptor drive. The results indicate that central apneas and respiratory arrhythmias may be associated with α 2-adrenoceptor modulation of laryngeal expiratory-related activity.