Genioglossal activation in patients with obstructive sleep apnea versus control subjects. Mechanisms of muscle control.

Pharyngeal dilator muscle activation (GGEMG) during wakefulness is greater in patients with obstructive sleep apnea (OSA) than in healthy control subjects, representing a neuromuscular compensatory mechanism for a more collapsible airway. As previous work from our laboratory has demonstrated a close relationship between GGEMG and epiglottic pressure, we examined the relationship between genioglossal activity and epiglottic pressure in patients with apnea and in control subjects across a wide range of epiglottic pressures during basal breathing, negative-pressure (iron-lung) ventilation, heliox breathing, and inspiratory resistive loading. GGEMG was greater in the patients with apnea under all conditions (p < 0.05 for all comparisons), including tonic, phasic, and peak phasic GGEMG. In addition, patients with apnea generated a greater peak epiglottic pressure on a breath-by-breath basis. Although the relationship between GGEMG and epiglottic negative pressure was tight across all conditions in both groups (all R values > = 0.69), there were no significant differences in the slope of this relationship between the two groups (all p values > 0.30) under any condition. Thus, the increased GGEMG seen in the patient with apnea during wakefulness appears to be a product of an increased tonic activation of the muscle, combined with increased negative-pressure generation during inspiration.

[1]  D. Fuller,et al.  Invited review: Intermittent hypoxia and respiratory plasticity. , 2001, Journal of applied physiology.

[2]  S A Shea,et al.  Genioglossal but not palatal muscle activity relates closely to pharyngeal pressure. , 2000, American journal of respiratory and critical care medicine.

[3]  T. Young,et al.  Prospective study of the association between sleep-disordered breathing and hypertension. , 2000, The New England journal of medicine.

[4]  Peretz Lavie,et al.  Obstructive sleep apnoea syndrome as a risk factor for hypertension: population study , 2000, BMJ : British Medical Journal.

[5]  J. Terán-Santos,et al.  The Association between Sleep Apnea and the Risk of Traffic Accidents , 1999 .

[6]  P. Lavie,et al.  Impaired respiratory response to resistive loading during sleep in healthy offspring of patients with obstructive sleep apnea. , 1997, American journal of respiratory and critical care medicine.

[7]  D. White,et al.  Influence of sleep onset on upper-airway muscle activity in apnea patients versus normal controls. , 1996, American journal of respiratory and critical care medicine.

[8]  V. Somers,et al.  Investigating the relationship between stroke and obstructive sleep apnea. , 1996, Stroke.

[9]  A I Pack,et al.  Upper airway and soft tissue anatomy in normal subjects and patients with sleep-disordered breathing. Significance of the lateral pharyngeal walls. , 1995, American journal of respiratory and critical care medicine.

[10]  D. White,et al.  Influence of gender on waking genioglossal electromyogram and upper airway resistance. , 1995, American journal of respiratory and critical care medicine.

[11]  E. Phillipson,et al.  Effects of sleep on the tonic drive to respiratory muscle and the threshold for rhythm generation in the dog. , 1994, The Journal of physiology.

[12]  A I Pack,et al.  Dynamic upper airway imaging during awake respiration in normal subjects and patients with sleep disordered breathing. , 1993, The American review of respiratory disease.

[13]  T. Young,et al.  The occurrence of sleep-disordered breathing among middle-aged adults. , 1993, The New England journal of medicine.

[14]  D. White,et al.  Waking genioglossal electromyogram in sleep apnea patients versus normal controls (a neuromuscular compensatory mechanism). , 1992, The Journal of clinical investigation.

[15]  A. Guz,et al.  Afferent pathway(s) for pharyngeal dilator reflex to negative pressure in man: a study using upper airway anaesthesia. , 1991, The Journal of physiology.

[16]  K. Murphy,et al.  Evidence for reflex upper airway dilator muscle activation by sudden negative airway pressure in man. , 1991, The Journal of physiology.

[17]  D. Hillman,et al.  Association of sleep apnoea with myocardial infarction in men , 1990, The Lancet.

[18]  S A Shea,et al.  Pharyngeal size and shape during wakefulness and sleep in patients with obstructive sleep apnoea. , 1989, The Quarterly journal of medicine.

[19]  A. Rothberg,et al.  Effects of temperature and composition on the viscosity of respiratory gases. , 1989, Journal of applied physiology.

[20]  S. Kuna,et al.  Interaction of hypercapnia and phasic volume feedback on motor control of the upper airway. , 1987, Journal of applied physiology.

[21]  E. vanLunteren,et al.  The muscles of the upper airways. , 1986, Clinics in chest medicine.

[22]  S. Kuna.  Inhibition of inspiratory upper airway motoneuron activity by phasic volume feedback. , 1986, Journal of applied physiology.

[23]  T. Dick,et al.  Activity of respiratory neurons during NREM sleep. , 1985, Journal of Neurophysiology.

[24]  D. White,et al.  Pharyngeal resistance in normal humans: influence of gender, age, and obesity. , 1985, Journal of applied physiology.

[25]  O. Mathew.  Upper airway negative-pressure effects on respiratory activity of upper airway muscles. , 1984, Journal of applied physiology: respiratory, environmental and exercise physiology.

[26]  P. L. Smith,et al.  Computerized tomography in obstructive sleep apnea. Correlation of airway size with physiology during sleep and wakefulness. , 1983, The American review of respiratory disease.

[27]  Phillipson Ea,et al.  Control of breathing during sleep. , 1978 .

[28]  Remmers Je,et al.  Pathogenesis of upper airway occlusion during sleep , 1978 .