During periods of increased anxiety there is an increase in respiratory frequency which correlates significantly with individual trait anxiety. These changes are observed especially in high trait individuals and occur with no change in V . co 2 or tidal volume, but with a resultant decrease in end tidal CO 2 (P ET CO 2 ).Recent work focusing on human brain activities has suggested that the temporal pole and the amygdala in the limbic system are activated during increased anxiety in high-trait individuals. The activation of these areas participates in the enhancement of respiratory frequency in normal subjects [6].Idiopathic hyperventilation (IH) is a condition of uncertain aetiology that is characterized by sustained arterial and alveolar hypocapnia and a plethora of It is generally agreed that a central pattern generator (CPG) for respiration exists in the lower brainstem; however, respiratory patterns in the awake state are also affected by the higher brain centers to varying degrees, dependent on the arousal level [1], the emotional state [2] and personality trait [3]. In the conscious state, carbon dioxide inhalation modifies the breathing pattern primarily by a stimulation of chemoreceptors. However, the final respiratory output results from a strong interaction between requirements from metabolism and behavior.It is well known that the emotions of fear and anxiety generated in the limbic system cause physiological changes in heart rate, perspiration and respiration [4]. Anxiety increases respiratory frequency and minute ventilation with no change in metabolism [5].Japanese Journal of Physiology Vol. 54, [465][466][467][468][469][470] 2004 Received on August 4, 2004; accepted on October 13, 2004 Correspondence should be addressed to: Ikuo Homma, Department of Physiology II, Showa University School of Medicine, 1-5-8 Hatanodai. Shinagawa-ku, Tokyo 142-8555, Japan. Phone: +81 3 3784 8113, Fax: +81 3 3784 0200, E-mail: ihomma@med.showa-u.ac.jp Abstract: Idiopathic hyperventilation (IH) is a condition of uncertain aetiology characterized by sustained arterial and alveolar hypocapnia and a plethora of symptoms, the most commonly reported being shortness of breath, and breathlessness. We previously reported that anxiety increases respiratory frequency and minute ventilation with no change in metabolism in normal subjects. In this study, we compared the breathing frequency response to 5% and 7% of CO 2 gas mixtures in normal subjects (n = 13) and in subjects with IH (n = 9), taking into account anxiety and breathlessness in order to determine how breathing patterns may vary with changes in the degree of involvement of higher brain centers because of anxiety and the perception of breathlessness. CO 2 produced a significantly higher value in respiratory frequency (f ) in subjects with IH. Subjects with IH also showed lower P ET CO 2 than normal subjects. During the inhalation of room air, a significant correlation between f and trait anxiety scores was observed in normal subjects (r = 0.49) and IH subjects (r = 0...