4. Discussion
The current study aimed to determine the underlying physiological
processes and cognitive mechanisms of stress-related impairment of
creativity from a neuroendocrine perspective. We explored the effects of
HPA axis and SAM axis activation on creativity under stress through an
experimental study using reliable biomarkers. Importantly, the mediating
role of cognitive flexibility in the physiological response associated
with creative processing has been corroborated. In Model 1, we assessed
concurrent effects of stress on HPA activation (measured through
salivary cortisol), cognitive flexibility, and creativity. In Model 2
and Model 3, the concurrent effects of stress on cognitive flexibility,
creativity and SAM activation were investigated. SAM activation was
responded to by the activity of dopamine (measured through eye blink
rate) and noradrenaline (measured through pupil diameter). Results
demonstrated that stress facilitated HPA and SAM activation, which
impaired cognitive flexibility, leading to reduced creative performance.
Through testing the serial mediation models in this study, a more
comprehensive framework was constructed based on the changes in hormones
and neurotransmitters under stress.