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<metadata xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:dc="http://purl.org/dc/elements/1.1/"><dc:title>Spinal mechanisms in postactivation 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 investigated the spinal neural mechanisms underlying postactivation potentiation in 10 healthy young males (21.9 ± 4.8 yr).Participants performed a 10-s maximal isometric plantarﬂexion, after which we measured twitch torque and assessed spinal excitabilityusing the soleus H-reﬂex, D1 presynaptic inhibition, and heteronymous Ia facilitation (HF). High-density surface EMG was decomposed totrack single motor unit responses. The conditioning contraction increased twitch torque by 12.2 Nm (P &lt; 0.001) immediately and returnedto baseline within 9 min. This mechanical potentiation was accompanied by a 29% reduction in H-reﬂex amplitude (P &lt; 0.001), whichrecovered within 3 min. Paradoxically, neurophysiological indices of presynaptic inhibition, D1, and HF were signiﬁcantly increased (D1:P &lt; 0.017; HF: P &lt; 0.001), resulting in spinal facilitation. Single MU analysis revealed increased discharge probability, particularly inhigher-threshold units, indicating overall spinal facilitation. These results demonstrate that postactivation potentiation involves a complexdissociation; H-reﬂex pathway inhibition along with facilitation of presynaptic spinal mechanisms. This paradox can be explained by eitherpostactivation depression (caused by depletion of neurotransmitter at the Ia-motoneuron synapse) or muscle thixotropy, a contraction his-tory-dependent decrease in muscle spindle sensitivity, which reduces the efﬁcacy of the Ia afferent volley independently of spinal inhibi-tory mechanisms. Our ﬁndings highlight a dissociation between spinal presynaptic facilitation and the decreased H-reﬂex, underscoringthe need for future studies to explicitly test the roles of postactivation depression and muscle thixotropy after conditioning contractions.NEW &amp; NOTEWORTHY This study provides evidence that postactivation potentiation is accompanied by a reduction in soleusH-reﬂex amplitude and a concurrent facilitation of presynaptic spinal mechanisms. By combining global EMG and single motorunit analyses extracted from high-density surface EMG, we reveal a dissociation between spinal disinhibition and reﬂex depres-sion. These ﬁndings suggest that acute postcontraction reﬂex suppression might be mediated by mechanisms other than presyn-aptic inhibition, potentially involving postactivation depression or changes in muscle spindle sensitivity.</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:identifier>UDK: 612.741</dc:identifier><dc:identifier>ISSN pri članku: 0022-3077</dc:identifier><dc:identifier>DOI: 10.1152/jn.00031.2026</dc:identifier><dc:identifier>COBISS_ID: 277837059</dc:identifier><dc:language>sl</dc:language><dc:rights>© 2026 The Authors.</dc:rights></metadata>
