<?xml version="1.0"?>
<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=29360"><dc:title>Spinal mechanisms in post-activation potentiation</dc:title><dc:creator>Kalc,	Miloš	(Avtor)
	</dc:creator><dc:creator>Holobar,	Aleš	(Avtor)
	</dc:creator><dc:creator>Kramberger,	Matej	(Avtor)
	</dc:creator><dc:creator>Murks,	Nina	(Avtor)
	</dc:creator><dc:creator>Škarabot,	Jakob	(Avtor)
	</dc:creator><dc:subject>HDsEMG</dc:subject><dc:subject>Ia aﬀerence</dc:subject><dc:subject>soleus</dc:subject><dc:subject>heteroniumous Ia facilitation</dc:subject><dc:subject>spinal reflex</dc:subject><dc:subject>muscle contraction</dc:subject><dc:subject>neural mechanisms</dc:subject><dc:subject>performance enhancement</dc:subject><dc:description>This study invesƟgated the spinal neural mechanisms underlying post‐acƟvaƟon potenƟaƟon in ten16healthy young males (21.9 ± 4.8 years). ParƟcipants performed a 10‐second maximal isometric17plantarﬂexion, aŌer which we measured twitch torque and assessed spinal excitability using the18soleus H‐reﬂex, D1 presynapƟc inhibiƟon and heteronymous Ia facilitaƟon (HF). High‐density surface19EMG was decomposed to track single motor unit responses. The condiƟoning contracƟon increased20twitch torque by 12.2 Nm (p &lt; 0.001) immediately and returning to baseline within nine minutes. This21mechanical potenƟaƟon was accompanied by a 29% reducƟon in H‐reﬂex amplitude (p &lt; 0.001),22which recovered within three minutes. Paradoxically, neurophysiological indices of presynapƟc23inhibiƟon, D1 and HF were signiﬁcantly increased (D1: p&lt;0.017; HF: p&lt;0.001), resulƟng in spinal24facilitaƟon. Single MU analysis revealed increased discharge probability, parƟcularly in higher‐25threshold units indicaƟng overall spinal facilitaƟon. These results demonstrate that post‐acƟvaƟon26potenƟaƟon involves a complex dissociaƟon: H‐reﬂex pathway inhibiƟon along with facilitaƟon of27presynapƟc spinal mechanisms. This paradox can be explained by either post‐acƟvaƟon depression28(caused by depleƟon of neurotransmiƩer at the Ia–motoneuron synapse) or muscle thixotropy, a29contracƟon history‐dependent decrease in muscle spindle sensiƟvity, which reduces the eﬃcacy of30the Ia aﬀerent volley independently of spinal inhibitory mechanisms. Our ﬁndings highlight a31dissociaƟon between spinal presynapƟc facilitaƟon and the decreased H‐reﬂex, underscoring the32need for future studies to explicitly test the roles of post‐acƟvaƟon depression and muscle thixotropy33aŌer condiƟoning contracƟons.</dc:description><dc:date>2026</dc:date><dc:date>2026-05-12 11:59:55</dc:date><dc:type>Neznano</dc:type><dc:identifier>29360</dc:identifier><dc:language>sl</dc:language><dc:rights>© 2026 The Authors.</dc:rights></rdf:Description></rdf:RDF>
