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Oxygenation in the artery during nap sleep
Sleep Medicine 7 (2006) 87 www.elsevier.com/locate/sleep
Letter to the Editor Oxygenation in the artery during nap sleep To the Editor: Respiratory function is suppressed during sleep. Its changes during sleep include reduced rate and depth of ventilation, causing reduction of alveolar-arterial oxygen exchange [1]. The controllers of breathing in sleep differ in rapid eye movement (REM) sleep and non-REM sleep [2]. There is limited information of O2 saturation in the artery (PaO2) in each sleep stage and, therefore, we conducted an investigation of oxygenation during nap. Twenty-five healthy male students underwent three hours of polygraphic study during daytime nap. Their mean age was 23.8G1.1 years. Sleep stages were categorized into three groups: light sleep (stages 1 & 2), deep sleep (stages 3 & 4), and REM sleep. Pulse-oximeter was attached to the second finger of the non-dominant arm to monitor PaO2. The mean PaO2 in waking, light sleep, deep sleep, and REM sleep were 97.0G1.09, 96.4G1.09, 96.4G1.10, and 96.6G1.08, respectively. The mean value of PaO2 in waking was significantly higher than those in other sleep stages. In addition, the mean value of PaO2 in stage REM was significantly higher than those in stages 1C2 or stages 3C4 (p!0.05). In each sleep stage, PaO2 and expired ventilation were positively related, and ventilation in sleeping state was most suppressed during REM sleep in normal subjects [3]. Oxygen consumption during REM sleep is suspected to decrease partly because of decrease in muscle tone. Tabachnik et al. reported an unchanged O2 level during REM sleep compared with non-REM sleep [4] whereas others showed lower values of PaO2 in REM sleep than in non-REM sleep [5]. In our study, PaO2 in non-REM sleep was more suppressed than PaO2 during REM sleep. As we
1389-9457/$ - see front matter q 2005 Elsevier B.V. All rights reserved. doi:10.1016/j.sleep.2005.08.004
studied prolonged daytime sleep, the first sleep cycle of REM sleep was mainly selected.
References [1] West JB. Ventilation-perfusion relationships. Am Rev Respir Dis 1977; 116:919–25. [2] Orem J. Respiration control in sleep. In: Carskadon MA, editor. Encyclopedia of sleep and dreaming. London: Simon & Schuster Macmillan; 1995. p. 520–3. [3] Douglas NJ, White DP, Weil JV, Pickett CK, Martin RJ, Hudgel DW, Zwillich CW. Hypoxic ventilatory response decreases during sleep in normal men. Am Rev Respir Dis 1982;125:286–9. [4] Tabachnik E, Muller NL, Bryan AC, Levison H. Changes in ventilation and chest wall mechanics during sleep in normal adolescents. J Appl Physiol 1981;51:557–64. [5] Muller NL, Francis PW, Gurwitz D, Levison H, Bryan AC. Mechanism of hemoglobin desaturation during rapid-eye-movement sleep in normal subjects and in patients with cystic fibrosis. Am Rev Respir Dis 1980;121:463–9.
Tomoyuki Kawada* Masao Katsumata Hiroko Suzuki Takako Shimizu Department of Hygiene and Public Health, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-Ku, Tokyo 113-8602, Japan E-mail address: [email protected] Received 7 July 2005; Received in revised form 20 July 2005; Accepted 11 August 2005 Available online 23 November 2005
* Corresponding author. Tel.: C81 3 3822 2131; fax: C81 3 5685 3065.
Letter to the Editor Oxygenation in the artery during nap sleep To the Editor: Respiratory function is suppressed during sleep. Its changes during sleep include reduced rate and depth of ventilation, causing reduction of alveolar-arterial oxygen exchange [1]. The controllers of breathing in sleep differ in rapid eye movement (REM) sleep and non-REM sleep [2]. There is limited information of O2 saturation in the artery (PaO2) in each sleep stage and, therefore, we conducted an investigation of oxygenation during nap. Twenty-five healthy male students underwent three hours of polygraphic study during daytime nap. Their mean age was 23.8G1.1 years. Sleep stages were categorized into three groups: light sleep (stages 1 & 2), deep sleep (stages 3 & 4), and REM sleep. Pulse-oximeter was attached to the second finger of the non-dominant arm to monitor PaO2. The mean PaO2 in waking, light sleep, deep sleep, and REM sleep were 97.0G1.09, 96.4G1.09, 96.4G1.10, and 96.6G1.08, respectively. The mean value of PaO2 in waking was significantly higher than those in other sleep stages. In addition, the mean value of PaO2 in stage REM was significantly higher than those in stages 1C2 or stages 3C4 (p!0.05). In each sleep stage, PaO2 and expired ventilation were positively related, and ventilation in sleeping state was most suppressed during REM sleep in normal subjects [3]. Oxygen consumption during REM sleep is suspected to decrease partly because of decrease in muscle tone. Tabachnik et al. reported an unchanged O2 level during REM sleep compared with non-REM sleep [4] whereas others showed lower values of PaO2 in REM sleep than in non-REM sleep [5]. In our study, PaO2 in non-REM sleep was more suppressed than PaO2 during REM sleep. As we
1389-9457/$ - see front matter q 2005 Elsevier B.V. All rights reserved. doi:10.1016/j.sleep.2005.08.004
studied prolonged daytime sleep, the first sleep cycle of REM sleep was mainly selected.
References [1] West JB. Ventilation-perfusion relationships. Am Rev Respir Dis 1977; 116:919–25. [2] Orem J. Respiration control in sleep. In: Carskadon MA, editor. Encyclopedia of sleep and dreaming. London: Simon & Schuster Macmillan; 1995. p. 520–3. [3] Douglas NJ, White DP, Weil JV, Pickett CK, Martin RJ, Hudgel DW, Zwillich CW. Hypoxic ventilatory response decreases during sleep in normal men. Am Rev Respir Dis 1982;125:286–9. [4] Tabachnik E, Muller NL, Bryan AC, Levison H. Changes in ventilation and chest wall mechanics during sleep in normal adolescents. J Appl Physiol 1981;51:557–64. [5] Muller NL, Francis PW, Gurwitz D, Levison H, Bryan AC. Mechanism of hemoglobin desaturation during rapid-eye-movement sleep in normal subjects and in patients with cystic fibrosis. Am Rev Respir Dis 1980;121:463–9.
Tomoyuki Kawada* Masao Katsumata Hiroko Suzuki Takako Shimizu Department of Hygiene and Public Health, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-Ku, Tokyo 113-8602, Japan E-mail address: [email protected] Received 7 July 2005; Received in revised form 20 July 2005; Accepted 11 August 2005 Available online 23 November 2005
* Corresponding author. Tel.: C81 3 3822 2131; fax: C81 3 5685 3065.