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Alpha motoneurons integrate synaptic inputs and neuromodulatory influences to shape firing patterns transmitted to muscle fibres, thereby regulating force production across task demands. Brief high-frequency bursts, or doublets, have been observed in animals and humans for nearly a century and are known to disproportionately enhance muscle force. Despite extensive experimental work, the cellular mechanism underlying delayed depolarisation (DD), which gives rise to motoneuron doublets, remains unresolved. Here, we combine preliminary in vitro mouse recordings, in vivo human motor unit recordings using high-density surface EMG, and ultrafast ultrasound recordings, along with biophysically grounded computational modelling, to identify a unifying mechanism for motoneuron doublet firing and its functional consequences. Preliminary in vitro recordings from mouse spinal motoneurons provided an important experimental constraint that guided our modelling. In voltage-clamp recordings, we observed a brief, spike-locked inward current following the clamped action potential that was abolished by sodium channel block. This inward current transient was temporally distinct from the spike current, absent at subthreshold voltages, and differed from classical somatodendritic persistent inward sodium currents, which activate gradually with depolarisation. The current emerged only following spike generation, including during voltage ramps. These observations suggested a spike-triggered depolarising process and motivated the inclusion of a spike-triggered axonal persistent sodium current (NaP) in the computational model. In parallel, analysis of human motor unit recordings demonstrated that doublet firing is common during voluntary contractions. Initial doublets were observed in 13 of 14 participants performing fast sinusoidal ankle dorsiflexions (5-15% MVC), while repetitive doublets occurred in 18 of 24 participants during steady tibialis anterior contractions (2-25% MVC). The computational model reproduced key features of these human firing patterns, initial doublets during rapid activation, repetitive doublets near recruitment, and spike-frequency adaptation of the high-frequency firings. Systematic manipulation of outward currents by altering calcium-dependent and potassium-mediated outward constraints in the model revealed two firing regimes, corresponding to experimentally described forms of doublet firing: initial and repetitive doublets. In both regimes, removal of axonal NaP abolished doublets, leaving only small subthreshold depolarising humps, indicating that initial and repetitive doublets reflect different operating regimes of a common spike-triggered mechanism. To assess functional relevance, we used motor unit spike trains and triggered on the intramuscular displacement data from ultrafast ultrasound recordings. We found that doublet firings produced disproportionate increases in displacement in single motor units compared to singlet firing of the same unit, yielding a gain greater than unity during voluntary contractions. Taken together, these findings suggest that spike-triggered axonal persistent sodium current is the primary source of the DD, and that neuromodulation may unmask this current to produce force-enhancing doublets.