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

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.

Contraction velocity influence the magnitude and etiology of neuromuscular fatigue during repeated maximal contractions.

This study aimed to compare the magnitude and etiology of neuromuscular fatigue during maximal repeated contractions performed in two contraction modes (concentric vs isometric) and at two contraction velocities (30/s vs 240°/s). Eleven lower limb-trained males performed 20 sets of maximal contractions at three different angular velocities: 0°/s (KE0), 30/s (KE30), and 240°/s (KE240). Cumulated work, number of contraction, duty cycle, and contraction time were controlled. Torque, superimposed and resting twitches, as well as gas exchange, were analyzed. Increasing contraction velocity was associated with greater maximal voluntary torque loss (KE0: -9.8 ± 3.9%; KE30: -16.4 ± 8.5%; KE240: -32.6 ± 6.3%; P < 0.05). Interestingly, the torque decrease was similar for a given cumulated work. Compared with KE0, KE240 generated a greater evoked torque loss (Db100: -24.3 ± 5.3% vs -5.9 ± 6.9%; P < 0.001), a higher O2 consumption (23.7 ± 6.4 mL/min/kg vs 15.7 ± 3.8 mL/min/kg; P < 0.001), but a lower voluntary activation (VA) loss (-4.3 ± 1.6% vs -11.2 ± 4.9%; P < 0.001). The neuromuscular perturbations were intermediate for KE30 (Db100: -10.0 ± 6.8%; VA: -7.2 ± 2.8%). Although the amount of mechanical work cumulated strongly determined the magnitude of torque decrease, the contraction velocity and mode influenced the origin of the neuromuscular fatigue. The metabolic stress and peripheral fatigue increased but reduction of VA is attenuated when the contraction velocity increased from 0°/s to 240°/s.

Cortical current density oscillations in the motor cortex are correlated with muscular activity during pedaling exercise.

Despite modern imaging techniques, assessing and localizing changes in brain activity during whole-body exercise is still challenging. Using an active electroencephalography (EEG) system in combination with source localization algorithms, this study aimed to localize brain cortical oscillations patterns in the motor cortex and to correlate these with surface electromyography (EMG)-detected muscular activity during pedaling exercise. Eight subjects performed 2-min isokinetic (90 rpm) cycling bouts at intensities ranging from 1 to 5 Wkg(-1) body mass on a cycle ergometer. These bouts were interspersed by a minimum of 2 min of passive rest to limit to development of peripheral muscle fatigue. Brain cortical activity within the motor cortex was analyzed using a 32-channel active EEG system combined with source localization algorithms. EMG activity was recorded from seven muscles on each lower limb. EEG and EMG activity revealed comparatively stable oscillations across the different exercise intensities. More importantly, the oscillations in cortical activity within the motor cortex were significantly correlated with EMG activity during the high-intensity cycling bouts. This study demonstrates that it is possible to localize oscillations in brain cortical activity during moderate- to high-intensity cycling exercise using EEG in combination with source localization algorithms, and that these oscillations match the activity of the active muscles in time and amplitude. Results of this study might help to further evaluate the effects of central vs. peripheral fatigue during exercise.