Original Article

Journal of Cerebral Blood Flow & Metabolism (2009) 29, 1421–1428; doi:10.1038/jcbfm.2009.57; published online 13 May 2009

Dynamic changes in brain bioenergetics during obstructive sleep apnea

This work was supported by the Australian National Health and Medical Research Council (Grant #253792 and fellowships to CR and RRG) and NewSouth Global, UNSW.

Caroline Rae1,2, Delwyn J Bartlett3, Qiao Yang3, David Walton4, Angela Denotti3, Toos Sachinwalla4 and Ronald R Grunstein3

  1. 1Prince of Wales Medical Research Institute, Randwick, New South Wales, Australia
  2. 2Brain Sciences, The University of New South Wales, New South Wales, Australia
  3. 3NHMRC Centre for Sleep Medicine, Woolcock Institute of Medical Research, University of Sydney, New South Wales, Australia
  4. 4Rayscan Imaging, Goulburn St, Liverpool, New South Wales, Australia

Correspondence: Professor C Rae, Prince of Wales Medical Research Institute, Barker St, Randwick, NSW 2031, Australia. E-mail: c.rae@unsw.edu.au

Received 18 January 2009; Revised 7 March 2009; Accepted 20 April 2009; Published online 13 May 2009.

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Abstract

Repetitive collapse of the upper airway during obstructive sleep apnea/hypopnea (OSA) exposes the brain of sufferers to frequent, transient, hypoxic episodes. The loss of cerebrovascular reactivity in sleep, and particularly in OSA, means that physiologic compensatory mechanisms may not ensure adequate brain oxygen levels. This 31P magnetic resonance spectroscopy study, of 13 males with severe, untreated OSA undertaken after overnight sleep deprivation, represents the first, seconds time-scale analysis of human brain bioenergetics during transient hypoxia and demonstrates that a moderate degree of oxygen desaturation during sleep has significant effects on brain bioenergetic status. Oxygen desaturation >10% of sleeping baseline resulted in decreases in brain adenosine triphosphate levels (P<0.01), and increases in inorganic phosphate (P<0.0001) with no concomitant changes in phosphocreatine or brain pH. This indicates that the mechanism of adenosine triphosphate depletion in these patients is different to that observed in normoxic, awake working brain. These data show that the buffering capacity of phosphocreatine and the creatine kinase system is not active in mild transient hypoxia and that cerebrovascular compensatory mechanisms are not adequate to prevent decrements in brain high-energy phosphates in OSA. Transient hypoxia experienced during sleep may impair brain function more than previously thought.

Keywords:

cerebral circulation, magnetic resonance spectroscopy, mitochondria, sleep, transient hypoxia

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