High-intensity physiological activation disrupts the neural signatures of conflict processing
Metadatos
Mostrar el registro completo del ítemAutor
Avancini, Chiara; Ciria Pérez, Luis Fernando; Alameda, Clara; Palenciano Castro, Ana Francisca; Canales Johnson, Andrés; A. Bekinschtein, Tristan; Sanabria Lucena, DanielEditorial
Springer Nature
Fecha
2024-12-05Referencia bibliográfica
Avancini, C. et. al. Commun Biol 7, 1625 (2024). [https://doi.org/10.1038/s42003-024-06851-w]
Patrocinador
Spanish Ministry of Science and Innovation toDaniel Sanabria (PID2019-105635GBI00); panish Ministry for Science and Innovation awarded to Chiara Avancini (FJC2020-046310-I); Regional Government of Andalusia awarded to Luis F. Ciria (DOC_00225); Ministry of Universities awarded to Clara Alameda (FPU21/00388); UK Research and Innovation (UKRI) under the UK government’s Horizon Europe funding guarantee (EP/Y029100/1); FONDECYT Regular (1240899) research grantResumen
Physiological activation fluctuates throughout the day. Previous studies have shown that during
periods of reduced activation, cognitive control remains resilient due to neural compensatory
mechanisms. In this study, we investigate the effects of high physiological activation on both
behavioural and neuralmarkers of cognitive control.We hypothesize that while behavioural measures
of cognitive control would remain intact during periods of high activation, there would be observable
changes in neural correlates. In our electroencephalography study, we manipulate levels of
physiological activation through physical exercise. Although we observe no significant impact on
behavioural measures of cognitive conflict, both univariate and multivariate time-frequency markers
prove unreliable under conditions of high activation. Moreover, we observe no modulation of wholebrain
connectivity measures by physiological activation. We suggest that this dissociation between
behavioural and neural measures indicates that the human cognitive control system remains resilient
even at high activation, possibly due to underlying neural compensatory mechanisms.