Reduced blood oxygen levels induce changes in low-threshold motor unit firing that align with the individual’s tolerance to hypoxia

Abstract

This study aimed to quantify how acute hypoxia impacts firing characteristics of biceps brachii motor units (MUs) during sustained isometric elbow flexions. MU data were extracted from surface electromyography (EMG) during 25% maximal voluntary contractions (MVC) in 10 healthy subjects (age 22 ± 1 yr). Blood oxygen saturation (SpO2) was then stabilized at 80% by reducing 1% of the fraction of inspired oxygen every 3 min for 35 min. MU data were once again collected 1 h and 2 h following the 35-min desaturation phase. Although MVC remained unaffected during 2 h of 80% SpO2, subject-specific changes in MU firing rate were observed. Four of 10 subjects exhibited a decrease in firing rate 1 h postdesaturation (12 ± 11%) and 2 h postdesaturation (16 ± 12%), whereas 6 of 10 subjects exhibited an increase in firing rate 1 h (9 ± 6%) and 2 h (9 ± 4%) postdesaturation. These bidirectional changes in firing rate were strongly correlated to the desaturation phase and the subjects’ SpO2 sensitivity to oxygen availability, where subjects who had decreased firing rates reached the target SpO2 20 min into the desaturation phase ( R2 = 0.90–0.98) and those who had increased firing rates reached the target SpO2 35 min into the desaturation phase ( R2 = 0.87–0.98). It is unlikely that a single mechanism accounted for these subject-specific changes in firing rate. Instead, differences in intrinsic properties of the neurons, afferent input to the motoneurons, neuromodulators, and sympathetic nerve activity may exist between groups. NEW & NOTEWORTHY The mechanisms of compromised motor control when exposed to hypoxia are largely unknown. The current study examined how severe acute hypoxia affects motor unit firing rate during sustained isometric contractions of the bicep brachii. The response to hypoxia was different across subjects, where motor unit firing rate increased for some individuals and decreased for others. This bidirectional change in firing rate was associated with how fast subjects desaturated during hypoxic exposure.

Time course of neuromuscular responses to acute hypoxia during voluntary contractions

“…The emergence of enhanced excitability across the entire protocol suggests that the impact of reduced on corticospinal pathways is substantial during acute hypoxia. Although the present study identified a ubiquitous enhancement in corticospinal excitability, this contrasts with previous hypoxia studies that have identified a 2–3 h delay in motor unit firing changes (McKeown et al., 2019) and corticospinal excitability changes of the lower limb (Rupp et al., 2012). Likewise, adaptations in neural excitability were evident only when performing MVC, which is contrary to previous research examining the lower limb (Rupp et al., 2012).…”

“…A reduction in blood oxygenation can significantly impair the neural activation of muscles across a range of contraction tasks (Billaut et al., 2013; Goodall, Gonzalez‐Alonso, Ali, Ross, & Romer, 2012; McKeown, Simmonds, & Kavanagh, 2019; Ruggiero, Yacyshyn, Nettleton, & McNeil, 2018). Given that descending drive to muscles is modulated by supraspinal and spinal circuits, several studies have profiled these areas of the nervous system in response to acute exposure to hypoxia.…”

“…However, after experiencing 2 h of 80% a subject‐specific response in low‐threshold motor unit activity emerges in healthy individuals. Specifically, participants who desaturate to 80% in a relatively short period (20 min) exhibit decreased motor unit discharge rates compared with those who desaturate more slowly (McKeown et al., 2019). Corticospinal excitability of the quadriceps is also unaffected after 1 h of hypoxic exposure ( 86%) but increased after 3 h (Rupp et al., 2012).…”

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

“…2012; McKeown et al . 2019, 2020). and heart rate were monitored at all times using a pulse oximeter (Model 7500; Nonin Medical Inc., Plymouth, MN, USA) attached to the middle finger of the left hand.…”

“…As sensitivity to altered oxygen availability is quite variable between individuals (Rojas-Camayo et al 2018), F IO 2 was titrated over a 15 min period for each individual at a rate of 0.01 F IO 2 every 1.5 min and remained at the desired F IO 2 that consequently resulted in 80% S pO 2 for the 2 h experimental protocol. This hypoxic stimulus was chosen as previous research has documented hypoxia-induced changes in neuromuscular fatigue at similar S pO 2 levels (75-80%; Goodall et al 2010Goodall et al , 2012Ruggiero et al 2018) and durations of exposure (2-3 h; Rupp et al 2012;McKeown et al 2019McKeown et al , 2020. S pO 2 and heart rate were monitored at all times using a pulse oximeter (Model 7500; Nonin Medical Inc., Plymouth, MN, USA) attached to the middle finger of the left hand.…”