• J C Weavil, S K Sidhu, T S Mangum, R S Richardson, and M Amann.
• Department of Exercise and Sport Science, University of Utah, Salt Lake City, Utah;
• Am. J. Physiol. Regul. Integr. Comp. Physiol. 2015 Jun 15; 308 (12): R998-1007.

AbstractWe investigated the role of exercise intensity and associated central motor drive in determining corticomotoneuronal excitability. Ten participants performed a series of nonfatiguing (3 s) isometric single-leg knee extensions (ISO; 10-100% of maximal voluntary contractions, MVC) and cycling bouts (30-160% peak aerobic capacity, W peak). At various exercise intensities, electrical potentials were evoked in the vastus lateralis (VL) and rectus femoris (RF) via transcranial magnetic stimulation (motor-evoked potentials, MEP), and electrical stimulation of both the cervicomedullary junction (cervicomedullary evoked potentials, CMEP) and the femoral nerve (maximal M-waves, M max). Whereas M max remained unchanged in both muscles (P > 0.40), voluntary electromyographic activity (EMG) increased in an exercise intensity-dependent manner for ISO and cycling exercise in VL and RF (both P < 0.001). During ISO exercise, MEPs and CMEPs progressively increased in VL and RF until a plateau was reached at ∼ 75% MVC; further increases in contraction intensity did not cause additional changes (P > 0.35). During cycling exercise, VL-MEPs and CMEPs progressively increased by ∼ 65% until a plateau was reached at W peak. In contrast, RF MEPs and CMEPs progressively increased by ∼ 110% throughout the tested cycling intensities without the occurrence of a plateau. Furthermore, alterations in EMG below the plateau influenced corticomotoneuronal excitability similarly between exercise modalities. In both exercise modalities, the MEP-to-CMEP ratio did not change with exercise intensity (P > 0.22). In conclusion, increases in exercise intensity and EMG facilitates the corticomotoneuronal pathway similarly in isometric knee extension and locomotor exercise until a plateau occurs at a submaximal exercise intensity. This facilitation appears to be primarily mediated by increases in excitability of the motoneuron pool.

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