Unlike voluntary contractions, stimulated contractions of a hand muscle do not reduce voluntary activation or motoneuronal excitability

Document Type

Journal Article

Publication Title

Journal of Applied Physiology


American Physiological Society


School of Medical and Health Sciences


D’Amico, J. M., Rouffet, D. M., Gandevia, S. C., & Taylor, J. L. (2020). Unlike voluntary contractions, stimulated contractions of a hand muscle do not reduce voluntary activation or motoneuronal excitability. Journal of Applied Physiology, 128(5), 1412-1422. https://doi.org/10.1152/japplphysiol.00553.2019


Voluntary force declines during sustained, maximal voluntary contractions (MVC) due to changes in muscle and central nervous system properties. Central fatigue, an exercise-induced reduction in voluntary activation, is influenced by multiple processes. Some may occur independently of descending voluntary drive. To differentiate the effects associated with voluntary drive from other central and peripheral influences, we measured voluntary activation and motoneuron excitability following fatiguing contractions produced voluntarily or by electrical stimulation. On two separate days, participants performed either a 2-min MVC of adductor pollicis muscle or received 2-min continuous supramaximal electrical stimulation of the ulnar nerve. In study 1 (n = 14), the superimposed twitch elicited by ulnar nerve stimulation during brief MVCs was increased, and, hence, voluntary activation was reduced, up to 240 s after the 2-min MVC [-20 ± 12% (SD), P = 0.002] but not the 2-min stimulated contraction (-4 ± 7%), despite large reductions in MVC force (voluntary, -54 ± 18%; stimulated, -46 ± 16%). In study 2 (n = 12), F-waves recorded from the adductor pollicis were reduced in area for 150 s following the 2-min MVC (-21 ± 16%, P = 0.007) but not after the stimulated contraction (5 ± 27%). Therefore, voluntary activation and motoneuron excitability decreased only when descending voluntary drive was present during the fatiguing task. The findings do not exclude a cortical or brain stem contribution to the reduced voluntary activation but suggest that neither sensory feedback from the fatigued muscle nor repetitive activation of motoneurons underlie the changes, whereas they are consistent with motoneuronal inhibition by released factors linked to voluntary drive. NEW & NOTEWORTHY We demonstrate that reductions in voluntary activation and motoneuron excitability following 2-min isometric maximal contractions in humans occur only when fatigue is produced through voluntary contractions and not through electrically stimulated contractions. This is contrary to studies that suggest that changes in the superimposed twitch and therefore voluntary activation are explained by changes in peripheral factors alone. Thus, the interpolated twitch technique remains a viable tool to assess voluntary activation and central fatigue.