Abstract Introduction Sleep loss has been shown to alter catecholamine (epinephrine, norepinephrine, and dopamine) levels. We investigated the effects of baseline sleep, total sleep deprivation (TSD), and recovery sleep on catecholamine measures and determined whether baseline catecholamine concentrations predicted TSD cognitive performance. Methods We conducted a five-day experiment under highly controlled conditions in 8 healthy adults (ages 28-42; 3 females). Peripheral catecholamine measures via blood samples were collected: 1) after two baseline 8h time-in-bed (TIB) nights (B1, B2); 2) during 39h of TSD and 3) after two recovery nights of 8-10h TIB (R1, R2). Cognitive measures including the Digit Symbol Substitution Test (DSST), which measures cognitive throughput, were collected at 0400h, 1130h, and 1730h during TSD and averaged. Repeated measures ANOVAs evaluated catecholamine measures across condition (baseline, TSD, and recovery). For significant condition effects, post hoc analyses with Bonferroni corrections compared each condition. Furthermore, partial eta-squared (ηp2) estimated effect size with ranges: 0.01-0.06 (small); 0.06-0.14 (medium); and above 0.14 (large). Simple linear regression analyses evaluated whether baseline catecholamine measures predicted TSD cognitive indices. p≤0.05 was significant. Results Epinephrine concentrations demonstrated a significant condition effect, with a large estimate of effect size F(2, 12)=5.295, p=0.022, ηp2=0.469. Post hoc analyses showed that TSD epinephrine levels were significantly greater than recovery epinephrine levels (p=0.026). There were no significant condition effects for norepinephrine or for dopamine concentrations. In addition, higher baseline epinephrine levels significantly predicted higher TSD DSST # correct (r=0.706; β=0.075); by contrast, baseline norepinephrine and dopamine levels did not significantly predict TSD cognitive metrics. Conclusion Our novel results demonstrate that epinephrine levels increased with TSD and significantly declined with recovery sleep in healthy adults. By contrast, TSD or recovery sleep did not significantly modify norepinephrine or dopamine levels. Furthermore, higher epinephrine levels at baseline significantly predicted better TSD cognitive throughput, explaining a high percentage of the variance (49.8%). Our findings underscore the critical impact of sleep loss and recovery on epinephrine regulation and demonstrate that baseline epinephrine levels are biomarkers of TSD cognitive resilience. Support (if any) NASA grants NNX14AN49G; 80NSSC20K0243 (NG)
Goel et al. (Fri,) studied this question.