Corticospinal, reticulospinal, and motoneuronal contributions to fatigability during a sustained contraction of the elbow flexors

Synaptic input to the motoneuron pool is altered during fatiguing muscle contractions. In humans, the corticospinal tract is often studied, with equivocal findings regarding its role in the reduction of force. To date, the involvement of the reticulospinal tract during states of fatigue has not been explored. Fourteen participants (28 ± 6 years, nine males) visited the laboratory twice, first for a familiarisation, then for an experimental trial. Participants completed a 5‐min sustained elbow flexor contraction at an intensity eliciting 40% of the EMG recorded during a maximal isometric voluntary contraction (MVC). Before, during and after the contraction, transcranial magnetic stimulation and electrical cervicomedullary stimulation were used to elicit motor evoked potentials (MEPs) and cervicomedullary evoked potentials during the silent period (SP‐CMEPs), respectively, with CMEPs also being evoked in combination with a startling acoustic sound (CMEPcon). Electrical stimulation of the brachial plexus was used to evoke maximal compound action potentials of the elbow flexors (Mmax). The 5‐min contraction induced a 53% loss of force (P < 0.001), with no change in background EMG (∼4% Mmax, P = 0.293). Neither MEP amplitude (P = 0.246) nor CMEPcon ratio (P = 0.489) was altered during the contraction, whereas CMEP and SP‐CMEP amplitudes were reduced by ∼20% and 50%, respectively (P < 0.001) and remained depressed post‐task. The results suggest that neither corticospinal nor reticulospinal tract excitability was altered during a 5‐min constant‐EMG task at 40% maximal EMG. Instead, the aetiology of the neural contribution to fatigability appeared to be primarily related to the loss of motoneuron excitability.