The fatigue-induced failure of the motor cortex to drive muscles maximally increases in acute hypoxia (AH) compared to normoxia (N) but improves with acclimatization (chronic hypoxia; CH). Despite their importance to muscle output, it is unknown how locomotor motoneurones in humans are affected by hypoxia and acclimatization. Eleven participants performed 16 min of submaximal [25% maximal torque (maximal voluntary contraction, MVC)] intermittent isometric elbow flexions in N, AH (environmental chamber) and CH (7-14 days at 5050 m) (P O = 140, 74 and 76 mmHg, respectively). For each minute of the fatigue protocol, motoneurone responsiveness was measured with cervicomedullary stimulation delivered 100 ms after transcranial magnetic stimulation (TMS) used to transiently silence voluntary drive. Every 2 min, cortical voluntary activation (cVA) was measured with TMS. After the task, MVC torque declined more in AH (∼20%) than N and CH (∼11% and 14%, respectively, P < 0.05), with no differences between N and CH. cVA was lower in AH than N and CH at baseline (∼92%, 95% and 95%, respectively) and at the end of the protocol (∼82%, 90% and 90%, P < 0.05). During the fatiguing task, motoneurone excitability in N and AH declined to ∼65% and 40% of the baseline value (P < 0.05). In CH, motoneurone excitability did not decline and, late in the protocol, was ∼40% higher compared to AH (P < 0.05). These novel data reveal that acclimatization to hypoxia leads to a heightened motoneurone responsiveness during fatiguing exercise. Positive spinal and supraspinal adaptations during extended periods at altitude might therefore play a vital role for the restoration of performance after acclimatization to hypoxia.

The findings do not support the concept that equivocal findings regarding sex differences in central fatigue are related to augmented effects of group III/IV afferent feedback in males compared with females.

Transcranial magnetic stimulation (TMS) of the motor cortex during a maximal voluntary contraction (MVC) permits functionally relevant measurements of muscle group relaxation rate (i.e., when muscles are actively contracting under voluntary control). This study's purpose was twofold: (1) to explore the impact of muscle length on TMS‐induced plantar flexor relaxation rate; and (2) to incorporate ultrasonography to measure relaxation‐induced lengthening of medial gastrocnemius (MG) fascicles and displacement of the muscle–tendon junction (MTJ). Eleven males (24.8 ± 7.0 years) performed 21 brief isometric plantar flexor MVCs. Trials were block‐randomized every three MVCs among 20° dorsiflexion (DF), a neutral ankle position, and 30° plantar flexion (PF). During each MVC, TMS was delivered and ultrasound video recordings captured MG fascicles or MTJ length changes. Peak relaxation rate was calculated as the steepest slope of the TMS‐induced drop in plantar flexor torque or the rate of length change for MG fascicles and MTJ. Torque relaxation rate was slower for PF (−804 ± 162 Nm·s−1) than neutral and DF (−1896 ± 298 and −2008 ± 692 Nm·s−1, respectively). Similarly, MG fascicle relaxation rate was slower for PF (−2.80 ± 1.10 cm·s−1) than neutral and DF (−5.35 ± 1.10 and −4.81 ± 1.87 cm·s−1, respectively). MTJ displacement rate showed a similar trend (P = 0.06), with 3.89 ± 1.93 cm·s−1 for PF compared to rates of 6.87 ± 1.55 and 6.36 ± 2.97 cm·s−1 for neutral and DF, respectively. These findings indicate muscle length affects the torque relaxation rate recorded after TMS during an MVC. Comparable results were obtained from muscle fascicles, indicating ultrasound imaging is suitable for measuring evoked contractile properties during voluntary contraction.

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