Severe acute hypoxia impairs recovery of voluntary muscle activation after sustained submaximal elbow flexion

Abstract

The purpose of this study was to determine how severe acute hypoxia alters neural mechanisms during, and following, a sustained fatiguing contraction. Fifteen participants (25 ± 3.2 years, 6 female) were exposed to a sham condition and a hypoxia condition where they performed a 10-min elbow flexor contraction at 20% of maximal torque. For hypoxia, peripheral blood oxygen saturation (SpO2) was titrated to 80% over a 15-min period and maintained for 2 hr. Maximal voluntary contraction (MVC) torque, EMG root mean square (EMGRMS), voluntary activation, rating of perceived muscle fatigue, and corticospinal excitability (motor evoked potential) and inhibition (silent period duration) were then assessed before, during, and for 6 min after the fatiguing contraction. No hypoxia-related effects were identified for neuromuscular variables during the fatigue task. However, for recovery, voluntary activation assessed by motor point stimulation of biceps brachii was lower for hypoxia than sham at 4 min (sham: 89% ± 7%; hypoxia: 80% ± 12%; P = 0.023) and 6 min (sham: 90% ± 7%; hypoxia: 78% ± 11%; P = 0.040). Similarly, voluntary activation (P = 0.01) and motor evoked potential area (P = 0.002) in response to transcranial magnetic stimulation of the motor cortex were 10% and 11% lower during recovery for hypoxia compared to sham, respectively. Although an SpO2 of 80% did not affect neural activity during the fatiguing task, motor cortical output and corticospinal excitability were reduced during recovery in the hypoxic environment. This was likely due to hypoxia-related mechanisms involving supraspinal motor circuits.