Intensity-dependent corticospinal facilitation by repetitive peripheral magnetic stimulation: evidence for a major...

Repetitive peripheral magnetic stimulation (PMS) is increasingly used in neurorehabilitation, yet the optimal intensity for inducing corticospinal facilitation and underlying afferent mechanisms remains unclear. We investigated the intensity-dependent effects of PMS on corticospinal excitability and single motor unit responses, and tested the contribution of group I afferents. Healthy young adults received repetitive PMS over the extensor carpi radialis (ECR) in a crossover design at 0.9 × motor threshold (MT), 1.2 × MT, and high-intensity stimulation individually adjusted to induce maximal wrist dorsiflexion (mean: 1.8 ± 0.3 × MT). Motor-evoked potentials (MEPs) elicited by transcranial magnetic stimulation were recorded from the ECR and flexor carpi radialis (FCR) before and during the intervention (total 15 min). To examine group I afferent contribution, the same high-intensity protocol was applied during upper-arm ischemia after the ECR H-reflex was reduced to <10% of baseline. Sensory-motor input characteristics across stimulation intensities were compared using poststimulus time histograms of ECR single motor unit firings. High-intensity PMS significantly increased ECR MEPs after 9 min, whereas PMS at 1.2 × MT required 15 min. PMS at 0.9 × MT did not induce significant MEP changes, and FCR MEPs remained unaltered. ECR MEPs remained elevated for up to 30 min after 9 min of high-intensity PMS. This enhancement was abolished by ischemia, and suprathreshold PMS elicited a short-latency peak in firing probability, consistent with monosynaptic Ia excitation, whose amplitude increased with stimulation intensity. These findings suggest that repetitive PMS above MT facilitates corticospinal excitability in an intensity-dependent manner and depends on large-diameter group I afferent input, with additional evidence consistent with a substantial Ia component.NEW & NOTEWORTHY Repetitive peripheral magnetic stimulation (PMS) facilitates corticospinal excitability in an intensity-dependent manner and requires suprathreshold intensities. High-intensity PMS acts faster than lower-intensity suprathreshold stimulation, whereas subthreshold stimulation does not significantly modulate corticospinal excitability. This facilitation is abolished by ischemia and linked to short-latency motor unit responses, supporting a major contribution of large-diameter group I afferent input with a substantial Ia component. These findings inform optimization of PMS protocols for neurorehabilitation.