Abdominal compression increases upper airway collapsibility during sleep in obese male obstructive sleep apnea patients.

STUDY OBJECTIVES: Abdominal obesity, particularly common in centrally obese males, may have a negative impact on upper airway (UA) function during sleep. For example, cranial displacement of the diaphragm with raised intra-abdominal pressure may reduce axial tension exerted on the UA by intrathoracic structures and increase UA collapsibility during sleep. DESIGN: This study aimed to examine the effect of abdominal compression on UA function during sleep in obese male obstructive sleep apnea patients. SETTING: Participants slept in a sound-insulated room with physiologic measurements controlled from an adjacent room. PARTICIPANTS: Fifteen obese (body mass index: 34.5 +/- 1.1 kg/m2) male obstructive sleep apnea patients (apnea-hypopnea index: 58.1 +/- 6.8 events/h) aged 50 +/- 2.6 years participated. INTERVENTIONS: Gastric (PGA) and transdiaphragmatic pressures (P(DI)), UA closing pressure (UACP), UA airflow resistance (R(UA)), and changes in end-expiratory lung volume (EELV) were determined during stable stage 2 sleep with and without abdominal compression, achieved via inflation of a pneumatic cuff placed around the abdomen. UACP was assessed during brief mask occlusions. MEASUREMENTS AND RESULTS: Abdominal compression significantly decreased EELV by 0.53 +/- 0.24 L (P=0.045) and increased PGA (16.2 +/- 0.8 versus 10.8 +/- 0.7 cm H2O, P < 0.001), P(DI) (11.7 +/- 0.9 versus 7.6 +/- 1.2 cm H2O, P < 0.001) and UACP (1.4 +/- 0.8 versus 0.9 +/- 0.9 cm H2O, P = 0.039) but not R(UA)(6.5 +/- 1.4 versus 6.9 +/- 1.4 cm H2O x L/s, P=0.585). CONCLUSIONS: Abdominal compression negatively impacts on UA collapsibility during sleep and this effect may help explain strong associations between central obesity and obstructive sleep apnea.

Effects of hypoxia on genioglossus and scalene reflex responses to brief pulses of negative upper-airway pressure during wakefulness and sleep in healthy men.

Hypoxia can depress ventilation, respiratory load sensation, and the cough reflex, and potentially other protective respiratory reflexes such as respiratory muscle responses to increased respiratory load. In sleep-disordered breathing, increased respiratory load and hypoxia frequently coexist. This study aimed to examine the effects of hypoxia on the reflex responses of 1) the genioglossus (the largest upper airway dilator muscle) and 2) the scalene muscle (an obligatory inspiratory muscle) to negative-pressure pulse stimuli during wakefulness and sleep. We hypothesized that hypoxia would impair these reflex responses. Fourteen healthy men, 19-42 yr old, were studied on two separate occasions, approximately 1 wk apart. Bipolar fine-wire electrodes were inserted orally into the genioglossus muscle, and surface electrodes were placed overlying the left scalene muscle to record EMG activity. In random order, participants were exposed to mild overnight hypoxia (arterial oxygen saturation approximately 85%) or medical air. Respiratory muscle reflex responses were elicited via negative-pressure pulse stimuli (approximately -10 cmH(2)O at the mask, 250-ms duration) delivered in early inspiration during wakefulness and sleep. Negative-pressure pulse stimuli resulted in a short-latency activation followed by a suppression of the genioglossus EMG that did not alter with hypoxia. Conversely, the predominant response of the scalene EMG to negative-pressure pulse stimuli was suppression followed by activation with more pronounced suppression during hypoxia compared with normoxia (mean +/- SE suppression duration 64 +/- 6 vs. 38 +/- 6 ms, P = 0.006). These results indicate differential sensitivity to the depressive effects of hypoxia in the reflex responsiveness to sudden respiratory loads to breathing between these two respiratory muscles.

Genioglossus reflex inhibition to upper-airway negative-pressure stimuli during wakefulness and sleep in healthy males.

During wakefulness, obstructive sleep apnoea patients appear to compensate for an anatomically narrow upper airway by increasing upper airway dilator muscle activity, e.g. genioglossus, at least partly via a negative-pressure reflex that may be diminished in sleep. Previous studies have assessed the negative-pressure reflex using multi-unit, rectified, moving-time-average EMG recordings during brief pulses of negative upper-airway pressure. However, moving-time averaging probably obscures the true time-related reflex morphology, potentially masking transient excitatory and inhibitory components. This study aimed to re-examine the genioglossus negative-pressure reflex in detail, without moving-time averaging. Bipolar fine-wire electrodes were inserted per orally into the genioglossus muscle in 17 healthy subjects. Two upper airway pressure catheters were inserted per nasally. Genioglossus EMG reflex responses were generated via negative-pressure stimuli (approximately -10 cmH2O at the choanae, 250 ms duration) delivered during wakefulness and sleep. Ensemble-averaged, rectified, genioglossus EMG recordings demonstrated reflex activation (onset latency 26+/-1 ms; peak amplitude 231+/-29% of baseline) followed by a previously unreported suppression (peak latency 71+/-4 ms; 67+/-8% of baseline). Single-motor-unit activity, clearly identifiable in approximately 10% of trials in six subjects, showed a concomitant increase in the interspike interval from baseline (26+/-9 ms, P=0.01). Genioglossus negative-pressure reflex morphology and amplitude of the initial peak were maintained in non-rapid eye movement (NREM) sleep but suppression amplitude was more pronounced during NREM and declined further during REM sleep compared to wakefulness. These data indicate there are both excitatory and inhibitory components to the genioglossus negative-pressure reflex which are differentially affected by state.