Effects of short-term sleep deprivation on hormonal counter-regulation against hypoglycaemia

Aims: Increasing evidence suggests that sleep loss has a strong influence on glucose metabolism. We tested the hypothesis that short-term sleep deprivation affects hormonal counter-regulation against hypoglycemia.

Methods: Stepwise hypoglycemic clamps (blood glucose 75, 65, 55, 45mg/dl) were performed in 10 young healthy men on 3 different days separated by at least 2 weeks. On the night preceding the experiments, subjects once had to stay awake the entire night (sleep deprivation), once were allow to sleep during the first half of the night (3.5h sleep), and once were allowed to sleep regularly (7h sleep). The order of condition was balanced across subjects.

Results: Morning basal levels of epinephrine, norepinephrine, and growth hormone did not differ between the 3 conditions and the same was true for the hypoglycemia-induced increase of these hormones (all p>0.15). In contrast, basal levels of ACTH and cortisol after 3.5h sleep were significant lower than after 7h sleep (both p<0.05), while levels of these hormone after total sleep deprivation were found to be intermediated. Based on lower basal levels, the increase in ACTH and cortisol during hypoglycemia was significant greater after 3.5h sleep than after 7h sleep (both p<0.001). The increase in cortisol concentrations during hypoglycemia was also higher after total sleep deprivation than after 7h sleep (<0.001). Before as well as throughout the hypoglycemic clamps, glucagon levels were distinctly lower after 3.5h sleep and total sleep deprivation than after 7h sleep (both p<0.05).

Conclusion: Data show a reduced morning basal secretory activity of the pituitary-adrenal axis after sleep deprivation during the second part of the night (i.e. after 3.5h sleep), but not after total night sleep deprivation. Based on lowered basal levels, the counter-regulatory response of this axis is enhanced after 3.5h sleep. In contrast, short-time sleep deprivation does not appear to affect counterregulatory responses of epinephrine, norepinephrine, and growth hormone to hypoglycemia.