Mechanism of hemoglobin desaturation during rapid-eye-movement sleep in normal subjects and in patients with cystic fibrosis

Am Rev Respir Dis. 1980 Mar;121(3):463-9. doi: 10.1164/arrd.1980.121.3.463.


To assess the mechanism of the decrease in hemoglobin O2 saturation during rapid-eye-movement sleep, we studied 5 normal subjects 22 to 30 yr of age and 20 patients with cystic fibrosis 9 to 29 yr of age. The largest decrease in arterial O2 saturation, as monitored with an ear oximeter during sleep, occurred during rapid-eye-movement sleep, with a mean +/- SEM decrease of 2 +/- 0.31% in the normal subjects and 7.4 +/- 1.3% in the patients in both groups. Rapid-eye-movement sleep was associated with a significant loss of intercostal and diaphragmatic tonic muscle activity (p < 0.01), as monitored with surface electrodes, and a decrease in the baseline position of the rib cage and abdomen, as recorded by magnetometers (p < 0.01). This suggests a decrease in functional residual capacity, which was accompanied by a consistently lower arterial O2 saturation during rapid-eye-movement sleep. Short periods (< 20 s) of inhibition of phasic respiratory muscle activity during rapid-eye-movement sleep were followed by further decreases in arterial O2 saturation. We conclude that the desaturation during rapid-eye-movement sleep in all subjects was mainly due to a decrease in functional residual capacity, leading to airway closure in the dependent lung regions. The hemoglobin desaturation was further aggravated by transient periods of hypoventilation.

MeSH terms

  • Adolescent
  • Adult
  • Child
  • Cystic Fibrosis / blood*
  • Cystic Fibrosis / physiopathology
  • Diaphragm / physiology
  • Diaphragm / physiopathology
  • Electromyography
  • Female
  • Hemoglobins / metabolism*
  • Humans
  • Intercostal Muscles / physiology
  • Intercostal Muscles / physiopathology
  • Male
  • Oximetry
  • Oxygen / blood*
  • Sleep / physiology
  • Sleep, REM / physiology*


  • Hemoglobins
  • Oxygen