Experimental partial-night sleep restriction increases pain sensitivity, but does not alter inflammatory plasma biomarkers.

Objectives: Disturbed sleep and chronic pain are public health concerns. Sleep disturbances seem to influence inflammation and may contribute to the increased pain sensitivity after sleep restriction (SR), such as after night work. The primary objective of this study was to determine the effects of SR on pain sensitivity and on relevant markers of inflammation. A secondary objective was to determine if SR affected pain sensitivity and inflammatory responses differently in men and women.

Methods: A paired crossover design with block randomization was applied. Subjects were instructed to follow their habitual sleep (HS) rhythm for two nights (HS condition) and to delay their bedtime to shorten their sleep with 50% for two nights (SR condition). Thirty-nine healthy volunteers between 19 and 44 years old participated (21 women). Experimental pain sensitivity was tested with heat-, electrical-, and pressure pain thresholds (PPTs); electrical temporal summation threshold; pinprick pain; suprathreshold heat pain tolerance; and rating of suprathreshold heat and cold pain. The following markers of inflammation were measured in plasma from a blood sample taken between 10:00 and 12:00: C-reactive protein, fractalkine, tumor necrosis factor, interleukin -8, and monocyte chemoattractant protein-1.

Results: Most subjects did not comply with the SR instructions. Total sleep time during SR was on average 2.6 h shorter than during HS. Therefore, the SR condition was re-defined to be "at least 40% reduction in the time in bed (TIB) the last night." The HS condition was re-defined to "at least 85% of normally reported TIB." SR produced higher suprathreshold heat pain sensitivity and cold pressor pain, compared to HS, but no significant change in electrical pain threshold, electrical temporal summation threshold, PPT, or any of the measured immune parameters. Sex-stratified analyses indicated that the effect on heat pain only occurred in women and that the effect on cold pressor pain was significant only in men.

Conclusions: The present findings indicate that heat and cold pressor pain were rated higher following SR, whereas pain thresholds remained unchanged. We did not find an effect of SR on biomarkers of inflammation. The findings should be cautiously interpreted given the poor adherence to the SR condition.