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Background: Electrical stimulation of the upper airway dilator muscles is an emerging treatment for obstructive sleep apnoea (OSA). Whereas invasive hypoglossal nerve stimulation (HNS) is an accepted treatment alternative to continuous positive airway pressure (CPAP), transcutaneous electrical stimulation (TES) may be a potential non-invasive alternative. Patients and Methods: A systematic review and meta-analysis (CRD42017074674) on the effect of HNS or TES on the apnoea-hypopnoea index (AHI) and the Epworth Sleepiness Scale (ESS) in OSA was conducted. Random-effects models were used. Heterogeneity and between study variance were assessed by I2 and τ2, respectively. Results: Of 41 identified clinical trials (n=1853), 20 (n=895) interventional trials could be pooled in the meta-analysis (15 HNS [n=808], 5 TES [n=87]). Middle aged (mean±SD 56.9±5.5years), overweight (body mass index, BMI 29.1±1.5kg/m2) patients with severe OSA (AHI 37.5±7.0h-1) were followed-up for 6.9±4.0month (HNS) and 0.2±0.4months (TES), respectively. The AHI improved by -23.5 (95% Confidence Interval, CI -27.0, -20.0) h-1 (p Conclusion: Invasive and transcutaneous electrical stimulation reduce OSA severity by a clinically relevant margin and improve associated symptoms.

The magnitude of tidal volume (VT) depends on neural respiratory drive overcoming respiratory resistance. We hypothesized that the ratio of EMGdi, an index of neural drive, to VT could detect histamine induced changes in lower airway resistance given the assumption that respiratory resistance (except for the lower airway resistance) is unaffected by histamine. Conventional histamine challenge tests were undertaken in 44 asthma patients (age 47±14 years; FEV1% 76±14) diagnosed by a history of repeated attack of asthma and positive bronchial challenge test and 51 healthy subjects (age 36 ± 13 years; FEV1% 96 ± 11). Diaphragm EMG was recorded from chest wall surface electrodes (EMGdi) under the fixed breathing frequency (18 times/min.) and an additional inspiratory load to improve a signal–noise ratio. Airflow was recorded with a digital output flowmeter. ΔFEV1 correlated with ΔEMGdi /VT (r=0.63). Corresponding to ≥20% fall in FEV1 during histamine challenge test, change in EMGdi/VT in patients with asthma was significantly higher than that in healthy subjects who received maximal dose (7.8 µmol) of histamine (90.5% ± 75.5% vs 2.4% ± 21.7%, p

Inspiratory capacity (IC) is widely used to assess dynamic hyperinflation in patients with chronic obstructive pulmonary disease (COPD) based on the assumption that this maneuver maximally activates inspiratory muscle and thus reliably achieves total lung capacity (TLC). However, inspiration during inflation is partially or wholly controlled by involuntary drive from brainstem and whereas the IC is derived from voluntary drive from the motor cortex. We hypothesized that voluntary IC maneuvers initiated from the motor cortex may be increased if there is additional chemical stimulation to the brainstem by hypercapnia. Nineteen healthy subjects (Age 43±15 years, 13 men/6 women) were studied. Diaphragm EMG (EMGdi) from multipair esophageal electrode and ventilation were recorded during inhalation 8%CO 2 (8%CO 2 +92%O 2 ) and room air. The order of inhalation of gases was random and was blind to subjects. Forced inspiratory vital capacity (FIVC) from residual volume and IC were performed. The EMGdi and FIVC elicited by a FIVC maneuver breathing 8%CO 2 were 169±61 µV and 4.92±1.00 l and were significantly greater than those breathing room air (143±47 µV, 4.3±0.89 l, p 2 were 172±55 µV and 3.28±0.66 L and were significantly greater than those during breathing room air (148±42 µV, 2.83±0.72 l, p This study was supported by NSFC (no.81120108001).

Rationale Dynamic hyperinflation in patients with COPD is usually assessed by inspiratory capacity (IC) manoeuvres with the assumption that maximal activation of the respiratory muscles can be reliably achieved. Objectives We hypothesized that the neural output to the respiratory muscles during an IC manoeuvre will increase under the condition of exercise or hypercapnia, since these are known to increase neural output from the brainstem to the respiratory muscles. Methods Nineteen patients with COPD (mean FEV 1 =29.7±12.5%) and 31 normal subjects were studied. Diaphragm electromyogram (EMGdi) and IC were measured during exhaustive exercise and during inhalation of 8%CO 2 with or without hypoxia. Measurements and Main Results IC changed from 1.78 ± 0.50 L and 1.41 ± 0.40 L at rest to 2.18 ± 0.58 L and 1.29 ± 0.46 L at the end of exercise for normal subjects and COPD patients, respectively. The mean EMGdi during an IC manoeuver increased during exercise from 0.158 ± 0.036 mV and 0.172 ± 0.048mV at rest to 0.203 ± 0.041 mV and 0.220 ± 0.056mV at the end of exercise for normal subjects and patients with COPD, respectively. Both the IC and EMGdi observed during an IC manoeuver during inhalation of 8%CO 2 in normal subjects was significantly larger than those breathing room air (2.10±0.80L vs 1.87±0.60L for IC and 0.183±0.038 mV vs 0.154±0.040 mV for EMGdi, p Conclusions We conclude that the neural drive generated by an IC manoeuvre increases during exercise and hypercapnia, leading to potential underestimation of dynamic hyperinflation assessed by IC manoeuvres.

The mechanisms underlying sleep related hypoventilation in patients with coexisting COPD and OSA, an overlap syndrome, are incompletely understood. We compared neural drive expressed as diaphragm EMG (EMGdi) and ventilation during sleep in patients with COPD alone and patients with overlap syndrome. EMGdi and airflow via pneumotachography were recorded during overnight full polysomnography in fourteen normal subjects and 39 consecutive patients with COPD. The ratio of tidal volume to EMGdi was measured to indirectly assess upper airway resistance. 35 patients and 12 normal subjects completed the study. Of 35 patients with COPD, 19 had COPD alone [FEV138.5%±16.3%, apnea-hypopnea index (AHI), 1.9±1.6 events/h] whereas 16 had an overlap syndrome (FEV1 47.5±16.2%, AHI 20.5±14.1 events/h). Ventilation(VE) was lower during NREM sleep than wakefulness in both patients with COPD alone (8.6±2.0 L/min to 6.5±1.5 L/min, p 0.05) or normal subjects (12.6±3.7%to 12.2±3.3%p>0.05). The ratio of tidal volume to EMGdi was unchanged from wakefulness to sleep in both patients with COPD alone and normal subjects but was significantly reduced in patients with overlap syndrome (p

Inspiratory capacity (IC) is widely used to assess dynamic hyperinflation in patients with chronic obstructive pulmonary disease (COPD) based on the assumption that this maneuver maximally activates inspiratory muscle and thus reliably achieves total lung capacity (TLC). However, inspiration during inflation is partially or wholly controlled by involuntary drive from brainstem and whereas the IC is derived from voluntary drive from the motor cortex. We hypothesized that voluntary IC maneuvers initiated from the motor cortex may be increased if there is additional chemical stimulation to the brainstem by hypercapnia. Nineteen healthy subjects (Age 43±15 years, 13 men/6 women) were studied. Diaphragm EMG (EMGdi) from multipair esophageal electrode and ventilation were recorded during inhalation 8%CO 2 (8%CO 2 +92%O 2 ) and room air. The order of inhalation of gases was random and was blind to subjects. Forced inspiratory vital capacity (FIVC) from residual volume and IC were performed. The EMGdi and FIVC elicited by a FIVC maneuver breathing 8%CO 2 were 169±61 µV and 4.92±1.00 l and were significantly greater than those breathing room air (143±47 µV, 4.3±0.89 l, p 2 were 172±55 µV and 3.28±0.66 L and were significantly greater than those during breathing room air (148±42 µV, 2.83±0.72 l, p We concluded that IC and diaphragm EMG generated by IC maneuver is submaximal at normacapnia. Therefore dynamic hyperinflation assessed by IC maneuver could have been underestimated in patients with COPD if they became hypercapnic. This study was supported by NSFC (No.81120108001).