UBC-Nepal expedition: acclimatization to high-altitude increases spinal motoneurone excitability during fatigue in humans

Abstract

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, MVC) intermittent isometric elbow flexions in N, AH (environmental chamber), and CH (7–14 days at 5050 m) (P_IO_2 = 140, 74, and 76 mmHg, respectively). Each minute of the fatigue protocol, motoneurone (MN) responsiveness was measured with cervicomedullary stimulation delivered 100 ms after transcranial magnetic stimulation (TMS) used to transiently silence voluntary drive. Every two minutes, 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, 95%, respectively) and the end of the protocol (∼82, 90, 90%, P < 0.05). During the fatiguing task, MN excitability in N and AH declined to ∼65 and 40% of the baseline value (P < 0.05). In CH, MN 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.

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