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This article discusses the concept of acute intermittent hypoxia (AIH) and its potential effects on motoneuronal output. AIH involves alternating periods of hypoxia and normoxia, and animal studies have shown that it can enhance the output of respiratory motoneurones. However, the effects of AIH on human motoneurones are still unclear. The article presents the findings of several studies that have investigated the impact of AIH on motoneuronal output in humans, with mixed results. While some studies have shown potential benefits, others have found no significant changes. The article concludes that more research is needed to fully understand the effects of AIH on motoneuronal function in humans. [Extracted from the article]

Purpose: Acute intermittent hypoxia (AIH) is a safe and non-invasive treatment approach that uses brief, repetitive periods of breathing reduced oxygen air alternated with normoxia. While AIH is known to affect spinal circuit excitability, the effects of AIH on cortical excitability remain largely unknown. We investigated the effects of AIH on cortical excitability within the primary motor cortex. Methods: Eleven healthy, right-handed participants completed two testing sessions: (1) AIH (comprising 3 min in hypoxia [fraction of inspired oxygen ~ 10%] and 2 min in normoxia repeated over five cycles) and (2) normoxia (NOR) (equivalent duration to AIH). Single- and paired-pulse transcranial magnetic stimulations were delivered to the primary motor cortex, before and 0, 25, and 50 min after AIH and normoxia. Results: The mean nadir in arterial oxygen saturation was lower (p < 0.001) during the cycles of AIH (82.5 ± 4.9%) than NOR (97.8 ± 0.6%). There was no significant difference in corticospinal excitability, intracortical facilitation, or intracortical inhibition between AIH and normoxia conditions at any time point (all p > 0.05). There was no association between arterial oxygen saturation and changes in corticospinal excitability after AIH (r = 0.05, p = 0.87). Conclusion: Overall, AIH did not modify either corticospinal excitability or excitability of intracortical facilitatory and inhibitory circuits within the primary motor cortex. Future research should explore whether a more severe or individualised AIH dose would induce consistent, measurable changes in corticospinal excitability. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?Does a single session of repeated bouts of acute intermittent hypoxic breathing enhance the motoneuronal output of the limb muscles of healthy able‐bodied participants?What is the main finding and its importance?Compared to breathing room air, there were some increases in motoneuronal output following acute intermittent hypoxia, but the increases were variable across participants and in time after the intervention and depended on which neurophysiological measure was checked. Acute intermittent hypoxia (AIH) induces persistent increases in output from rat phrenic motoneurones. Studies in people with spinal cord injury (SCI) suggest that AIH improves limb performance, perhaps via postsynaptic changes at cortico‐motoneuronal synapses. We assessed whether limb motoneurone output in response to reflex and descending synaptic activation is facilitated after one session of AIH in healthy able‐bodied volunteers. Fourteen participants completed two experimental days, with either AIH or a sham intervention (randomised crossover design). We measured H‐reflex recruitment curves and homosynaptic post‐activation depression (HPAD) of the H‐reflex in soleus, and motor evoked potentials (MEPs) evoked by transcranial magnetic stimulation (TMS) and their recruitment curves in first dorsal interosseous. All measurements were performed at rest and occurred at baseline, 0, 20, 40 and 60 min post‐intervention. The intervention was 30 min of either normoxia (sham, FiO2${F_{{\rm{i}}{{\rm{O}}_{\rm{2}}}}}$ ≈ 0.21) or AIH (alternate 1‐min hypoxia [FiO2${F_{{\rm{i}}{{\rm{O}}_{\rm{2}}}}}$ ≈ 0.09], 1‐min normoxia). After AIH, the H‐reflex recruitment curve shifted leftward. Lower stimulation intensities were needed to evoke 5%, 50% and 99% of the maximal H‐reflex at 40 and 60 min after AIH (P < 0.04). The maximal H‐reflex, recruitment slope and HPAD were unchanged after AIH. MEPs evoked by constant intensity TMS were larger 40 min after AIH (P = 0.027). There was no change in MEP recruitment or the maximal MEP. In conclusion, some measures of the evoked responses from limb motoneurones increased after a single AIH session, but only at discrete time points. It is unclear to what extent these changes alter functional performance. [ABSTRACT FROM AUTHOR]

Acute intermittent hypoxia (AIH) elicits long‐term facilitation (LTF) of respiration. Although LTF is observed when CO2 is elevated during AIH in awake humans, the influence of CO2 on corticospinal respiratory motor plasticity is unknown. Thus, we tested the hypotheses that acute intermittent hypercapnic‐hypoxia (AIHH): (1) enhances cortico‐phrenic neurotransmission (reflecting volitional respiratory control); and (2) elicits ventilatory LTF (reflecting automatic respiratory control). Eighteen healthy adults completed four study visits. Day 1 consisted of anthropometry and pulmonary function testing. On Days 2, 3 and 4, in a balanced alternating sequence, participants received: AIHH, poikilocapnic AIH, and normocapnic‐normoxia (Sham). Protocols consisted of 15, 60 s exposures with 90 s normoxic intervals. Transcranial (TMS) and cervical (CMS) magnetic stimulation were used to induce diaphragmatic motor‐evoked potentials and compound muscle action potentials, respectively. Respiratory drive was assessed via mouth occlusion pressure (P0.1), and minute ventilation measured at rest. Dependent variables were assessed at baseline and 30–60 min after exposures. Increases in TMS‐evoked diaphragm potential amplitudes were observed following AIHH vs. Sham (+28 ± 41%, P = 0.003), but not after AIH. No changes were observed in CMS‐evoked diaphragm potential amplitudes. Mouth occlusion pressure also increased after AIHH (+21 ± 34%, P = 0.033), but not after AIH. Ventilatory LTF was not observed after any treatment. We demonstrate that AIHH elicits central neural mechanisms of respiratory motor plasticity and increases resting respiratory drive in awake humans. These findings may have important implications for neurorehabilitation after spinal cord injury and other neuromuscular disorders compromising breathing. Key points: The occurrence of respiratory long‐term facilitation following acute exposure to intermittent hypoxia is believed to be dependent upon CO2 regulation – mechanisms governing the critical role of CO2 have seldom been explored.We tested the hypothesis that acute intermittent hypercapnic‐hypoxia (AIHH) enhances cortico‐phrenic neurotransmission in awake healthy humans.The amplitude of diaphragmatic motor‐evoked potentials induced by transcranial magnetic stimulation was increased after AIHH, but not the amplitude of compound muscle action potentials evoked by cervical magnetic stimulation.Mouth occlusion pressure (P0.1, an indicator of neural respiratory drive) was also increased after AIHH, but not tidal volume or minute ventilation.Thus, moderate AIHH elicits central neural mechanisms of respiratory motor plasticity, without measurable ventilatory long‐term facilitation in awake humans. [ABSTRACT FROM AUTHOR]

Acute intermittent hypoxia, carotid body, diaphragm, long-term facilitation, motoneuron, motor-evoked potential, phrenic, transcranial magnetic stimulation Initially observed with episodic electrical stimulation of the carotid sinus nerve, this phenomenon was then extensively demonstrated in rodent experiments via protocols of brief, episodic exposures to periods of hypoxia (i.e. acute intermittent hypoxia; AIH). Keywords: acute intermittent hypoxia; carotid body; diaphragm; long-term facilitation; motoneuron; motor-evoked potential; phrenic; transcranial magnetic stimulation EN acute intermittent hypoxia carotid body diaphragm long-term facilitation motoneuron motor-evoked potential phrenic transcranial magnetic stimulation 3017 3019 3 07/04/22 20220701 NES 220701 Pioneering experiments revealed that intermittent stimulation of afferent neurons from the carotid bodies elicits long-lasting increased activity of respiratory nerves, a phenomenon known as respiratory long-term facilitation (LTF). [Extracted from the article]

Acute intermittent hypoxia (AIH) is a strategy to improve motor output in humans with neuromotor impairment. A single AIH session increases the amplitude of motor evoked potentials (MEP) in a finger muscle (first dorsal interosseous), demonstrating enhanced corticospinal neurotransmission. Since AIH elicits phrenic/diaphragm long-term facilitation (LTF) in rodent models, we tested the hypothesis that AIH augments diaphragm MEPs in humans. Eleven healthy adults (7 males, age = 29 ± 6 years) were tested. Transcranial and cervical magnetic stimulation were used to induce diaphragm MEPs and compound muscle action potentials (CMAP) recorded by surface EMG, respectively. Stimulus-response curves were generated prior to and 30–60 min after AIH. Diaphragm LTF was assessed by measurement of integrated EMG burst amplitude and frequency during eupnoeic breathing before and after AIH. Following baseline measurements, AIH was delivered from an oxygen generator connected to a facemask under poikilocapnic conditions (15 one minute episodes of 9% inspired oxygen with one minute room air intervals). There were no detectable changes in MEP (−1.5 ± 12.1%, p = 0.96) or CMAP (+0.1 ± 7.8%, p = 0.97) amplitudes across the stimulus-response curve. At stimulation intensities approximating 50% of the difference between minimum and maximum baseline amplitudes, MEP and CMAP amplitudes were also unchanged (p > 0.05). Further, no AIH effect was observed on diaphragm EMG activity during eupnoea post-AIH (p > 0.05). We conclude that unlike hand muscles, poikilocapnic AIH does not enhance diaphragm MEPs or produce diaphragm LTF in healthy humans. • Acute intermittent hypoxia (AIH) increases motor evoked potential (MEP) amplitude in a finger muscle, demonstrating enhanced corticospinal neurotransmission. • We examined AIH effects on diaphragm MEPs induced by transcranial magnetic stimulation in healthy young adults. • After a single AIH session, no detectable changes in MEP amplitudes were observed. • Differences between AIH effects on respiratory and non-respiratory motor systems are discussed. [ABSTRACT FROM AUTHOR]

Paired corticospinal-motoneuronal stimulation (PCMS) elicits spinal synaptic plasticity in humans with chronic incomplete cervical spinal cord injury (SCI). Here, we examined whether PCMS-induced plasticity could be potentiated by acute intermittent hypoxia (AIH), a treatment also known to induce spinal synaptic plasticity in humans with chronic incomplete cervical SCI. During PCMS, we used 180 pairs of stimuli where corticospinal volleys evoked by transcranial magnetic stimulation over the hand representation of the primary motor cortex were timed to arrive at corticospinal-motoneuronal synapses of the first dorsal interosseous (FDI) muscle ~1–2 ms before the arrival of antidromic potentials elicited in motoneurons by electrical stimulation of the ulnar nerve. During AIH, participants were exposed to brief alternating episodes of hypoxic inspired gas (1 min episodes of 9% O 2) and room air (1 min episodes of 20.9% O 2). We examined corticospinal function by measuring motor evoked potentials (MEPs) elicited by cortical and subcortical stimulation of corticospinal axons and voluntary motor output in the FDI muscle before and after 30 min of PCMS combined with AIH (PCMS+AIH) or sham AIH (PCMS+sham-AIH). The amplitude of MEPs evoked by magnetic and electrical stimulation increased after both protocols, but most after PCMS+AIH, consistent with the hypothesis that their combined effects arise from spinal plasticity. Both protocols increased electromyographic activity in the FDI muscle to a similar extent. Thus, PCMS effects on spinal synapses of hand motoneurons can be potentiated by AIH. The possibility of different thresholds for physiological vs behavioral gains needs to be considered during combinatorial treatments. [ABSTRACT FROM AUTHOR]