Am. J. Respir. Crit. Care Med., Volume 161, Number 4, April 2000, 1124-1128

Sleep Deprivation Per Se Does Not Decrease the Hypercapnic Ventilatory Response in Humans

CHRISTINA M. SPENGLER and STEVEN A. SHEA

Circadian, Neuroendocrine, and Sleep Disorders Section, Brigham and Women's Hospital, Boston, Massachusetts

Several studies have found that sleep deprivation reduces the hypercapnic ventilatory response (HCVR). Such results may have been affected by uncontrolled activities or environmental influences during the sleep deprivation period. The current study determined the "pure" effect of sleep deprivation on respiratory control under strictly controlled behavioral and environmental conditions. After 2 d of acclimation in the laboratory, 10 subjects maintained wakefulness (confirmed by EEG), a constant semirecumbent posture, ate regular small meals, had constant interaction with experimenters, and stayed in an environment with constant low light (10 lux) and constant room temperature for 41 consecutive hours. Measurements of HCVR, resting ventilation, O₂ and CO₂ were performed every 2 h. Comparisons were made of six pairs of measurements, with each pair separated by 24 h of sleep deprivation. None of the respiratory variables changed significantly with 24 h of sleep deprivation. Mean HCVR increased by 17% with sleep deprivation (3.12 versus 3.54 L · min¹ · mm Hg¹; not significant). These results show that sleep deprivation per se does not reduce the sensitivity of central chemoreceptors nor change resting ventilation or metabolism. The reduced HCVR after sleep loss found in previous studies may have been affected by uncontrolled activities or environmental influences during sleep deprivation periods.

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