Akira Umeda1, Kazuya Miyagawa2, Atsumi Mochida2, Hiroshi Takeda2, Kotaro Takeda3, Yasumasa Okada4, David Gozal5. 1. Department of Respiratory Medicine, International University of Health and Welfare (IUHW) Shioya Hospital, Japan. Electronic address: umeda@iuhw.ac.jp. 2. Department of Pharmacology, School of Pharmacy, International University of Health and Welfare, Japan. 3. Faculty of Rehabilitation, School of Healthcare, Fujita Health University, Japan. 4. Department of Internal Medicine, National Hospital Organization Murayama Medical Center, Japan. 5. Department of Child Health, MU Women's and Children's Hospital, University of Missouri, USA.
Abstract
BACKGROUND AND OBJECTIVE: Body weight of patients with obstructive sleep apnea after initiation of nasal continuous positive airway pressure appears to increase. We hypothesized that intermittent hypoxia (IH) will decrease energy expenditure (EE), and that normoxic recovery will lead to body weight gains. METHODS: C57BL/6 J male mice were exposed to either 12 h/day of mild IH (alternating FIO2-10-11% and 21%; 640 s cycle), or severe IH (FIO2-6-7%-21%; 180 s cycle) or sham IH daily for 4 or 8 weeks. After exposures, EE was evaluated while mice were kept under normoxia for 5 weeks and organ histology was evaluated. RESULTS: EE was not decreased by IH. However, visceral white adipocyte size after normoxic recovery was significantly increased in severe IH in an intensity-dependent manner. CONCLUSION: Our hypothesis that IH would decrease EE was not corroborated. However, IH and normoxic recovery seem to promote severity-dependent enlargement of visceral adipocytes, likely reflecting altered energy preservation mechanisms induced by IH.
BACKGROUND AND OBJECTIVE: Body weight of patients with obstructive sleep apnea after initiation of nasal continuous positive airway pressure appears to increase. We hypothesized that intermittent hypoxia (IH) will decrease energy expenditure (EE), and that normoxic recovery will lead to body weight gains. METHODS: C57BL/6 J male mice were exposed to either 12 h/day of mild IH (alternating FIO2-10-11% and 21%; 640 s cycle), or severe IH (FIO2-6-7%-21%; 180 s cycle) or sham IH daily for 4 or 8 weeks. After exposures, EE was evaluated while mice were kept under normoxia for 5 weeks and organ histology was evaluated. RESULTS: EE was not decreased by IH. However, visceral white adipocyte size after normoxic recovery was significantly increased in severe IH in an intensity-dependent manner. CONCLUSION: Our hypothesis that IH would decrease EE was not corroborated. However, IH and normoxic recovery seem to promote severity-dependent enlargement of visceral adipocytes, likely reflecting altered energy preservation mechanisms induced by IH.