Spinal mechanisms in postactivation potentiation: facilitation of presynaptic inhibition contrasts H-reflex amplitude...

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 excitability using the soleus H-reflex, D1 presynaptic inhibition, and heteronymous Ia facilitation (HF). High-density surface EMG was decomposed to track single motor unit responses. The conditioning contraction increased twitch torque by 12.2 Nm (P < 0.001) immediately and returned to baseline within 9 min. This mechanical potentiation was accompanied by a 29% reduction in H-reflex amplitude (P < 0.001), which recovered within 3 min. Paradoxically, neurophysiological indices of presynaptic inhibition, D1, and HF were significantly increased (D1: P < 0.017; HF: P < 0.001), resulting in spinal facilitation. Single MU analysis revealed increased discharge probability, particularly in higher-threshold units, indicating overall spinal facilitation. These results demonstrate that postactivation potentiation involves a complex dissociation; H-reflex pathway inhibition along with facilitation of presynaptic spinal mechanisms. This paradox can be explained by either postactivation depression (caused by depletion of neurotransmitter at the Ia-motoneuron synapse) or muscle thixotropy, a contraction history-dependent decrease in muscle spindle sensitivity, which reduces the efficacy of the Ia afferent volley independently of spinal inhibitory mechanisms. Our findings highlight a dissociation between spinal presynaptic facilitation and the decreased H-reflex, underscoring the need for future studies to explicitly test the roles of postactivation depression and muscle thixotropy after conditioning contractions.NEW & NOTEWORTHY This study provides evidence that postactivation potentiation is accompanied by a reduction in soleus H-reflex amplitude and a concurrent facilitation of presynaptic spinal mechanisms. By combining global EMG and single motor unit analyses extracted from high-density surface EMG, we reveal a dissociation between spinal disinhibition and reflex depression. These findings suggest that acute postcontraction reflex suppression might be mediated by mechanisms other than presynaptic inhibition, potentially involving postactivation depression or changes in muscle spindle sensitivity.