Maximal human motor unit firing rates decline in response to nonvolitional induced torque loss: further evidence for peripheral feedback inhibition

The purpose was to assess whether voluntary descending drive is obligatory to reduce maximal motor unit (MU) firing rates following high-intensity muscle fatiguing activation. Maximal MU firing rates were compared following a sustained 60-s maximal voluntary contraction (MVC) and separately following 60 s of maximal tetanic peripheral nerve stimulation (decaying rate 40 to 20 Hz) at high torque levels (initial torque ∼81% MVC). In ten participants, grouped firing rates of 2,290 MUs from the tibialis anterior were recorded with intramuscular tungsten microelectrodes. Baseline MU firing rates during dorsiflexion MVC were 40 ± 11.5 Hz. Immediately (∼2 s) after both tasks, MVC torque (<i>P</i> = 0.08) and maximal MU firing rates (<i>P</i> = 0.14) were depressed equally (all ∼30%, <i>P</i> < 0.001). After 10 min of rest, MVC torque recovered to baseline values following both tasks (<i>P</i> ≥ 0.17) and maximal firing rates recovered similarly (<i>P</i> = 0.12) in both tasks throughout recovery and returned to ∼95% of baseline values (<i>P</i> ≤ 0.02) by 10 min. Furthermore, there were negative correlations (all <i>P</i> ≤ 0.003) between MU firing rates with both electrically evoked doublet half-relaxation time (<i>r</i> = -0.48, <i>r</i> = -0.38) and contraction time (<i>r</i> = -0.39, <i>r</i> = -0.38) during recovery from both fatiguing tasks. These results indicate that factors related to voluntary activation of descending pathways are not directly responsible for the frequently observed reduction of maximal MU firing rates after sustained high-intensity activation. On the contrary, with nonvolitional induced contractile failure, firing rates declined similarly to the voluntary task, providing novel support for peripheral feedback mechanisms as the primary regulator of firing rate during this fatiguing task.<b>NEW & NOTEWORTHY</b> Maximal motor unit firing rates similarly decline and recover following 60 s of sustained maximal voluntary contraction or tetanic peripheral nerve stimulation at high torque levels. Therefore, voluntary activation of descending tracts is not an obligatory contributor to reduction of maximal firing rates after sustained high-intensity activation. On the contrary, with nonvolitional induced contractile failure (i.e., electrical stimulation), firing rates declined similarly to voluntary fatigue, providing novel support for peripheral feedback mechanisms that inhibit MU firing rate.