Strength Training Preferentially Enhances Corticospinal Output Compared with High-Intensity Interval Training

Abstract Rostami, M, Lee, A, Frazer, AK, Akalu, Y, Tallent, J, Walker, S, and Kidgell DJ. Strength training preferentially enhances corticospinal output compared to high-intensity interval training. J Strength Cond Res XX(X): 000–000, 2026—Corticospinal responses to motor training are influenced by the specific task, muscle group involved, and contraction type. Yet, the distinct effects of high-intensity interval training (HIIT) and strength exercise ( SE ) on corticospinal excitability and inhibition remain unclear. Although most studies focus on upper-limb muscles not directly engaged in HIIT, this study investigated corticospinal, intracortical, and spinal responses in lower-limb muscles actively involved in both exercises. Eighteen healthy untrained subjects completed a 20-minute high-intensity interval cycling task (HIIT), a single bout of high-intensity SE , and a no-exercise control session on separate days. Corticospinal, intracortical, and spinal responses were assessed using transcranial magnetic stimulation (TMS) and peripheral nerve stimulation at baseline and 5 minutes postexercise. Compared with control, both HIIT and SE significantly increased motor-evoked potential (MEP) amplitude at 130% active motor threshold (AMT) (HIIT: p = 0.006; SE : p < 0.001), with SE inducing substantially greater increases than HIIT ( p < 0.001). At 150% AMT, only SE significantly increased MEP amplitude compared with baseline, control, and HIIT ( p < 0.001). Silent period duration was significantly reduced following SE at 130% AMT ( p = 0.004) and following both HIIT ( p = 0.03) and SE ( p = 0.04) at 150% AMT. Only SE led to significant reduction in short-interval intracortical inhibition ( p = 0.02). Spinal excitability remained unchanged. These findings highlight task-dependent corticospinal plasticity in lower-limb muscles and suggest that SE may be particularly effective for enhancing acute corticospinal excitability, with potential implications for neurorehabilitation programs targeting conditions associated with reduced corticospinal excitability.