In modern fast-paced societies, subjective time pressure has become a common psychological stressor that may impair inhibitory control, a core component of executive function. Inhibitory control consists of two subprocesses—interference control and response inhibition—yet how time pressure differentially affects these processes and their neural mechanisms remains insufficiently understood. This study manipulated subjective time pressure and employed the Flanker task (interference control) and the Go/NoGo task (response inhibition) to examine behavioral performance, event-related potentials (ERPs), and time–frequency oscillations. Forty healthy adults completed both time-pressure and no time pressure conditions. ERP analyses focused on the P1, N1, P2, N2, and P3 components, while time–frequency analyses were performed both across the full frequency range (3–30 Hz) and within specific frequency bands (θ and β), using cluster-based permutation tests. Behaviorally, time pressure reduced accuracy, especially in incongruent Flanker trials and NoGo trials, while accelerating overall reaction times. ERP results showed enhanced N2 and P3 amplitudes in the Flanker task. In the Go/NoGo task, time pressure led to reduced P2, but increased N2 and P3. Time–frequency analysis revealed higher theta power during early control and increased beta power during later inhibition under time pressure. Taken together, the behavioral, ERP, and oscillatory findings suggest that subjective time pressure is associated with alterations in inhibitory control, with distinct patterns observed for interference control and response inhibition. Specifically, interference control under time pressure was characterized by enhanced late-stage neural activity without corresponding oscillatory changes, whereas response inhibition was accompanied by modulations in both early and late neural processes, involving enhanced N2 and P3 components as well as increased θ and β band activity. These findings suggest that time pressure may affect interference control and response inhibition through partially distinct neurocognitive mechanisms, rather than a single unified pathway.
Ding et al. (Thu,) studied this question.