Emotion regulation is essential for adaptive behavior and mental health. Strategies applied to alter emotions are known to differ in their impact on psychological and physiological aspects of the emotional response. However, emotion regulation outcome has primarily been assessed via self-report, and studies comparing regulation strategies with regard to their peripheral physiological mechanisms are limited in number. In the present study, we therefore aimed to investigate the effects of different emotion regulation strategies on pupil dilation, skin conductance responses, and subjective emotional responses. Thirty healthy females were presented with negative and neutral pictures and asked to maintain or up- and downregulate their upcoming emotional responses through reappraisal or distraction. Pupil dilation and skin conductance responses were significantly enhanced when viewing negative relative to neutral pictures. For the pupil, this emotional arousal effect manifested specifically late during the pupillary response. In accordance with subjective ratings, increasing negative emotions through reappraisal led to the most prominent pupil size enlargements, whereas no consistent effect for downregulation was found. In contrast, early peak dilations were enhanced in all emotion regulation conditions independent of strategy. Skin conductance responses were not further modulated by emotion regulation. These results indicate that pupil diameter is modulated by emotional arousal, but is initially related to the extent of mental effort required to regulate automatic emotional responses. Our data thus provide first evidence that the pupillary response might comprise two distinct temporal components reflecting cognitive emotion regulation effort on the one hand and emotion regulation success on the other hand.

While aging and stress are both known to affect cognitive functions, little is known on whether and how age modulates stress effects on executive functions and their neural correlates. The current study investigated the effect of acute stress on response inhibition and error processing and their underlying cortical processes in younger and older healthy men, using EEG. Forty-nine participants (30 young) were stressed with the Trier Social Stress Test (16 young, 9 older) or underwent a friendly control procedure (14 young, 10 older) and subsequently performed a Go/No-Go task with two levels of task difficulty while performance (reaction time, error rate), stimulus-locked (N2, P3) and response-locked (Ne, Pe) ERPs were measured. Previous results on age-related cognitive deficits were replicated, with slower responses and reduced and delayed N2 and P3 components, as well as reduced Ne and Pe components in older participants. Independent of age, acute stress improved response inhibition, reflected in higher accuracy for compatible trials and enhanced inhibition-related components (N2, P3 and N2d, P3d of the difference waves No-Go minus Go), and improved error processing, reflected in enhanced error-related components (Ne, Pe and Ne_d, Pe_d of the difference waves error minus correct trial). Our findings indicate that acute stress leads to a reallocation of cognitive resources, strengthening inhibition and error processing in young and older healthy men to a similar degree. Neural generators of the analyzed ERPs are mainly part of the salience network, which is upregulated immediately after stress. This offers an explanation as to why response inhibition, in contrast to other executive functions, improves after acute stress.

The current study investigated the influence of acute stress and the resulting cortisol increase on response inhibition and its underlying cortical processes, using EEG. Before and after an acute stressor or a control condition, 39 healthy men performed a go/no-go task while ERPs (N2, P3), reaction times, errors, and salivary cortisol were measured. Acute stress impaired neither accuracy nor reaction times, but differentially affected the neural correlates of response inhibition; namely, stress led to enhanced amplitudes of the N2 difference waves (N2d, no-go minus go), indicating enhanced response inhibition and conflict monitoring. Moreover, participants responding to the stressor with an acute substantial rise in cortisol (high cortisol responders) showed reduced amplitudes of the P3 of the difference waves (P3d, no-go minus go) after the stressor, indicating an impaired evaluation and finalization of the inhibitory process. Our findings indicate that stress leads to a reallocation of cognitive resources to the neural subprocesses of inhibitory control, strengthening premotor response inhibition and the detection of response conflict, while concurrently diminishing the subsequent finalization process within the stream of processing.

Nutritional state (i.e., fasting or nonfasting) may affect the processing of interoceptive signals, but mechanisms underlying this effect remain unclear. We investigated 16 healthy women on two separate days: when satiated (standardized food intake) and after an 18-h food deprivation period. On both days, heartbeat-evoked potentials (HEPs) and cardiac and autonomic nervous system activation indices (heart rate, normalized low frequency heart rate variability [nLF HRV]) were assessed. The HEP is an EEG pattern that is considered an index of cortical representation of afferent cardiovascular signals. Average HEP activity (R wave +455-595 ms) was enhanced during food deprivation compared to normal food intake. Cardiac activation did not differ between nutritional conditions. Our results indicate that short-term food deprivation amplifies an electrophysiological correlate of the cortical representation of visceral-afferent signals originating from the cardiovascular system. This effect could not be attributed to increased cardiac activation, as estimated by heart rate and nLF HRV, after food deprivation.

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