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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dc="http://purl.org/dc/elements/1.1/"><rdf:Description rdf:about="https://dirros.openscience.si/IzpisGradiva.php?id=31913"><dc:title>Catecholaminergic contributions to inhibitory controlfollowing physical fatigue</dc:title><dc:creator>Arenales Arauz,	Y. L.	(Avtor)
	</dc:creator><dc:creator>Omejc,	Nina	(Avtor)
	</dc:creator><dc:creator>Díaz,	María Alejandra	(Avtor)
	</dc:creator><dc:creator>Habay,	Jelle	(Avtor)
	</dc:creator><dc:creator>Vanderborght,	Bram	(Avtor)
	</dc:creator><dc:creator>De Pauw,	Kevin	(Avtor)
	</dc:creator><dc:creator>Roelands,	Bart	(Avtor)
	</dc:creator><dc:creator>Marušič,	Uroš	(Avtor)
	</dc:creator><dc:subject>brain neurotransmission</dc:subject><dc:subject>cognitive control</dc:subject><dc:subject>EEG</dc:subject><dc:subject>event‐related potentials</dc:subject><dc:subject>physical fatigue</dc:subject><dc:description>Acute physical fatigue can impair cognitive control, yet its underlying neurochemical mechanisms remain unclear. This studyinvestigated whether catecholaminergic modulation influences behavioral and neural markers of inhibitory control followingphysical fatigue. Eighteen healthy, recreationally active adults (9 males, 9 females; 23.4 ± 2.2 years) completed a randomized,triple‐blind, placebo‐controlled crossover study. On separate visits, participants received methylphenidate (MPH; 20 mg; adopamine and noradrenaline reuptake inhibitor), reboxetine (REB; 8 mg; a noradrenaline reuptake inhibitor), or placebo.Physical fatigue was induced by repeated bilateral leg extensions to task failure. Cognitive performance was assessed before andafter physical fatigue using a Go/No‐Go task with electroencephalographic recording. Behavioral outcomes included reactiontime and accuracy, while event‐related potentials measured neural stages of response execution and inhibition (N2 and P3).Mixed‐effects models were used for statistical analysis. For No‐Go trials, a significant MPH × Time interaction was observed foraccuracy (p = 0.008), with improved post‐fatigue performance following MPH administration (p = 0.048). At the neural level,MPH was associated with shorter fronto‐central No‐Go N2 latency (p = 0.038) and altered fatigue‐related changes in No‐Go P3latency (p = 0.047). REB did not produce comparable behavioral or neural effects. These findings provide pharmacologicalevidence that catecholaminergic mechanisms contribute to inhibitory control following physical fatigue. The differential effectsof MPH and REB suggest that selective noradrenergic enhancement alone is insufficient to maintain inhibitory control followingphysical fatigue. Instead, the findings implicate broader dopaminergic and noradrenergic mechanisms, potentially involvingalterations in the temporal dynamics of inhibitory processing.</dc:description><dc:date>2026</dc:date><dc:date>2026-08-18 09:32:11</dc:date><dc:type>Neznano</dc:type><dc:identifier>31913</dc:identifier><dc:language>sl</dc:language><dc:rights>© 2026 The Author(s). European Journal of Sport Science published by Wiley‐VCH GmbH on behalf of European College of Sport Science</dc:rights></rdf:Description></rdf:RDF>
