Recent research suggests that recovery sleep (RS) has the potential to restore pain sensitivity and modulation after hyperalgesia due to preceding sleep deprivation. However, it has not yet been systematically examined whether the restoration of these pain parameters is driven by sleep characteristics of RS. Thus, the present study assessed changes in experimental pain during RS after total sleep deprivation (TSD) to test whether RS parameters predicted the restoration of the pain system. Thirty healthy participants completed one night of habitual sleep, one night of TSD and a subsequent recovery night. At-home sleep during baseline and recovery was assessed using portable polysomnography and a questionnaire. Before and after each night pressure pain thresholds (PPTs), temporal pain summation (TSP) and conditioned pain modulation (CPM) were assessed. PPTs decreased after TSD and increased following RS, indicating a restoration of pain sensitivity after hyperalgesia. RS characteristics did not predict this restoration, suggesting other mechanisms (e.g., changes in serotonergic activity) underlying the observed pain changes. TSP indicated a lack of effect of experimental sleep manipulations on excitatory processes whereas CPM lacked sufficient reliability to investigate inhibitory processes. Thus, results indicate moderate effects of sleep manipulations on pain sensitivity, but not on pain modulation. Perspective: This article highlights the potential of recovery sleep to let pain thresholds return to normal following their decrease after a night of total sleep deprivation. In contrast, endogenous pain modulation (temporal pain summation, conditioned pain modulation) was not affected by sleep deprivation and recovery sleep.
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