Abstract
Cortisol and C-reactive protein (CRP) typically change during total sleep deprivation (TSD) and psychological stress; however, it remains unknown whether these biological markers can differentiate robust individual differences in neurobehavioral performance and self-rated sleepiness resulting from these stressors. Additionally, little is known about cortisol and CRP recovery after TSD. In our study, 32 healthy adults (ages 27–53; mean ± SD, 35.1 ± 7.1 years; 14 females) participated in a highly controlled 5-day experiment in the Human Exploration Research Analog (HERA), a high-fidelity National Aeronautics and Space Administration (NASA) space analog isolation facility, consisting of two baseline nights, 39 h TSD, and two recovery nights. Psychological stress was induced by a modified Trier Social Stress Test (TSST) on the afternoon of TSD. Salivary cortisol and plasma CRP were obtained at six time points, before (pre-study), during [baseline, the morning of TSD (TSD AM), the afternoon of TSD (TSD PM), and recovery], and after (post-study) the experiment. A neurobehavioral test battery, including measures of behavioral attention and cognitive throughput, and a self-report measure of sleepiness, was administered 11 times. Resilient and vulnerable groups were defined by a median split on the average TSD performance or sleepiness score. Low and high pre-study cortisol and CRP were defined by a median split on respective values at pre-study. Cortisol and CRP both changed significantly across the study, with cortisol, but not CRP, increasing during TSD. During recovery, cortisol levels did not return to pre-TSD levels, whereas CRP levels did not differ from baseline. When sex was added as a between-subject factor, the time × sex interaction was significant for cortisol. Resilient and vulnerable groups did not differ in cortisol and CRP, and low and high pre-study cortisol/CRP groups did not differ on performance tasks or self-reported sleepiness. Thus, both cortisol and CRP reliably changed in a normal, healthy population as a result of sleep loss; however, cortisol and CRP were not markers of neurobehavioral resilience to TSD and stress in this study.
Highlights
Chronic sleep deprivation is an important public health concern associated with many adverse health outcomes and clinical disorders such as anxiety, depression, immune dysfunction, Alzheimer’s disease, cardiovascular disease, obesity, cancer, and overall morbidity and mortality (Ferrie et al, 2007; Gallicchio and Kalesan, 2009; Mullington et al, 2009; Phan and Malkani, 2019; Al-Rashed et al, 2021)
During the 5day experiment (Figure 1), neurobehavioral test battery (NTB) resilient and vulnerable groups did not differ in actigraphic sleep onset latency, wake after sleep onset, or total sleep time, F(1) = 0.000–3.755, p = 0.062–0.992 (Table 1 shows actigraphic data divided by the 3-min Psychomotor Vigilance Test (PVT) resilient-vulnerable grouping), except that the Digit Symbol Substitution Test (DSST) resilient and the Karolinska Sleepiness Scale (KSS) vulnerable groups had significantly shorter onset latencies at B1 than the DSST vulnerable and KSS resilient groups, F(1) = 4.380–4.588, p = 0.041–0.045, and the DSST vulnerable group had a significantly shorter onset latency at R1 than the DSST resilient group, F(1) = 6.491, p = 0.016
Cortisol and C-reactive protein (CRP) levels significantly changed across our study, which included two commonly experienced stressors, total sleep deprivation (TSD) and psychological stress
Summary
Chronic sleep deprivation is an important public health concern associated with many adverse health outcomes and clinical disorders such as anxiety, depression, immune dysfunction, Alzheimer’s disease, cardiovascular disease, obesity, cancer, and overall morbidity and mortality (Ferrie et al, 2007; Gallicchio and Kalesan, 2009; Mullington et al, 2009; Phan and Malkani, 2019; Al-Rashed et al, 2021). The effects of sleep deprivation on cortisol, a hypothalamic–pituitary–adrenal (HPA) axis marker, and C-reactive protein (CRP), an inflammatory marker, remain inconsistent: some studies report no change in cortisol (Vgontzas et al, 2004; Frey et al, 2007; van Leeuwen et al, 2009; Pejovic et al, 2013; Honma et al, 2020) or CRP (Faraut et al, 2011; Irwin et al, 2016; Choshen-Hillel et al, 2021), while others report decreases in cortisol (Åkerstedt et al, 1980) or CRP (Frey et al, 2007; Baek et al, 2020), or increases in cortisol (Leproult et al, 1997; Wright et al, 2015; Baek et al, 2020; Choshen-Hillel et al, 2021; Lamon et al, 2021) or CRP (Meier-Ewert et al, 2004; van Leeuwen et al, 2009). Studies have found that both acute and prolonged stress increase cortisol (Jönsson et al, 2010; Allen et al, 2014) and CRP (Eraly et al, 2014; Kennedy et al, 2014), other studies reported no change in CRP (La Fratta et al, 2018; Szabo et al, 2020)
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
