RESUMEN
The impact of acute stress on executive processes is commonly attributed to glucocorticoid-induced disruptions of the pFC. However, the occipital cortex seems to express a higher density of glucocorticoid receptors. Consequently, acute stress effects on executive processes could as well be mediated by glucocorticoid (e.g., cortisol)-induced alterations of visual sensory processes. To investigate this alternative route of stress action by demarcating the effects of acute stress and cortisol on executive from those on visual sensory processes, 40 healthy young men completed a standardized stress induction (i.e., the Trier Social Stress Test) and control protocol in two consecutive sessions. In addition, they received either a placebo or hydrocortisone (0.12-mg/kg bodyweight) pill and processed a dual and a partial report task to assess their executive and visual sensory processing abilities, respectively. Hydrocortisone administration improved both partial report and dual-task performance as indicated by increased response accuracies and/or decreased RTs. Intriguingly, the hydrocortisone-induced increase in dual-task performance was completely mediated by its impact on partial report performance (i.e., visual sensory processes). Moreover, RT measures in both tasks shared approximately 26% of variance, which was only in part attributable to hydrocortisone administration (ΔR2 = 8%). By contrast, acute stress selectively impaired dual-task performance (i.e., executive processes), presumably through an alternative route of action. In summary, the present results suggest that cortisol secretion (as mimicked by hydrocortisone administration) may counteract adverse residual stress effects on executive processes by improving visual sensory processes (e.g., the maintenance and amplification of task-relevant sensory information).
RESUMEN
This article seeks to address the prevailing issue of how to measure specific process components of psychobiological stress responses. Particularly the change of cortisol secretion due to stress exposure has been discussed as an endophenotype of many psychosomatic health outcomes. To assess its process components, a large variety of non-compartmental parameters (i.e., composite measures of substance concentrations at different points in time) like the area under the concentration-time curve (AUC) are commonly utilized. However, a systematic evaluation and validation of these parameters based on a physiologically plausible model of cortisol secretion has not been performed so far. Thus, a population pharmacokinetic (mixed-effects stochastic differential equation) model was developed and fitted to densely sampled salivary cortisol data of 10 males from Montreal, Canada, and sparsely sampled data of 200 mixed-sex participants from Dresden, Germany, who completed the Trier Social Stress Test (TSST). Besides the two major process components representing (1) stress-related cortisol secretion (reactivity) and (2) cortisol elimination (recovery), the model incorporates two additional, often disregarded components: (3) the secretory delay after stress onset, and (4) deviations from the projected steady-state concentration due to stress-unrelated fluctuations of cortisol secretion. The fitted model (R2â¯=â¯99%) was thereafter used to investigate the correlation structure of the four individually varying, and readily interpretable model parameters and eleven popular non-compartmental parameters. Based on these analyses, we recommend to use the minimum-maximum cortisol difference and the minimum concentration as proxy measures of reactivity and recovery, respectively. Finally, statistical power analyses of the reactivity-related sex effect illustrate the consequences of using impure non-compartmental measures of the different process components that underlie the cortisol stress response.