Changes in Lung Volume and Upper Airway Dilator Muscle Activity at Sleep Onset in Obese Male Obstructive Sleep Apnea Patients.

2009 ◽  
Author(s):  
DL Stadler ◽  
PG Catcheside ◽  
D Paul ◽  
J Bradley ◽  
RD McEvoy
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Lung Volume ◽  
Muscle Activity ◽  
Sleep Onset ◽  
Upper Airway ◽  
Dilator Muscle ◽  
Obstructive Sleep ◽  
Obese Male

Changes in lung volume and diaphragm muscle activity at sleep onset in obese obstructive sleep apnea patients vs. healthy-weight controls

2010 ◽  
Vol 109 (4) ◽  
pp. 1027-1036 ◽  
Author(s):  
Daniel L. Stadler ◽  
R. Doug McEvoy ◽  
Jana Bradley ◽  
Denzil Paul ◽  
Peter G. Catcheside
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Lung Volume ◽  
Muscle Activity ◽  
Sleep Onset ◽  
Upper Airway ◽  
Diaphragm Muscle ◽  
Healthy Weight ◽  
Respiratory Events ◽  
Obstructive Sleep

Obese obstructive sleep apnea (OSA) patients potentially defend end-expiratory lung volume (EELV) during wakefulness via increased expiratory diaphragmatic activity (eEMGdia). A reduction in eEMGdia and EELV at sleep onset could, therefore, increase upper airway collapsibility via reduced tracheal traction. The aim of this study was to establish if eEMGdia is greater in obese OSA patients vs. healthy-weight controls during wakefulness, and to compare eEMGdia and EELV changes at sleep onset between groups as a function of stable breathing, hypopnea vs. apnea events developing within the first few breaths after sleep onset. Eight obese men with OSA and eight healthy-weight men without OSA were studied in the supine position while instrumented with an intraesophageal catheter to measure eEMGdia and magnetometer coils to assess changes in EELV. While eEMGdia expressed as %maximal activity was not significantly different between groups during wakefulness, OSA patients experienced a greater fall in eEMGdia following sleep onset (group × breath, P < 0.001) and a greater decrease when respiratory events accompanied sleep onsets (category × breath, P < 0.001). The decrease in EELV by the third postsleep onset breath was small (OSA, 61.4 ± 8.0 ml, P < 0.001; controls, 34.0 ± 4.2 ml, P < 0.001), with the decrease significantly greater in OSA patients over time (group × breath, P = 0.007). There was a greater decrease with more severe events (category × breath, P < 0.001), with EELV decreasing by 89.6 ± 14.2 ml ( P < 0.001) at the onset of apneas in the OSA group. These data support that diaphragm tone and EELV frequently decrease following sleep onset, with greater falls at transitions accompanied by respiratory events. In addition to decrements in upper airway dilator muscle activity, decreasing lung volume potentially contributes to an increased propensity for upper airway collapse in OSA patients at sleep onset.

scholarly journals Airway Dilator Muscle Activity and Lung Volume During Stable Breathing in Obstructive Sleep Apnea

SLEEP ◽  
2009 ◽  
Vol 32 (3) ◽  
pp. 361-368 ◽  
Author(s):  
Amy S. Jordan ◽  
David P. White ◽  
Yu-Lun Lo ◽  
Andrew Wellman ◽  
Danny J. Eckert ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Lung Volume ◽  
Muscle Activity ◽  
Dilator Muscle ◽  
Obstructive Sleep

scholarly journals Abdominal Compression Increases Upper Airway Collapsibility During Sleep in Obese Male Obstructive Sleep Apnea Patients

SLEEP ◽  
2009 ◽  
Vol 32 (12) ◽  
pp. 1579-1587 ◽  
Author(s):  
Daniel L. Stadler ◽  
R. Doug McEvoy ◽  
Kate E. Sprecher ◽  
Kieron J. Thomson ◽  
Melissa K. Ryan ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Upper Airway ◽  
Abdominal Compression ◽  
Obstructive Sleep ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility ◽  
Obese Male

scholarly journals Targeting Endotypic Traits with Medications for the Pharmacological Treatment of Obstructive Sleep Apnea. A Review of the Current Literature

2019 ◽  
Vol 8 (11) ◽  
pp. 1846 ◽  
Author(s):  
Taranto-Montemurro ◽  
Messineo ◽  
Wellman
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Muscle Activity ◽  
Upper Airway ◽  
Loop Gain ◽  
Arousal Threshold ◽  
The Past ◽  
Obstructive Sleep ◽  
Near Future ◽  
Made In

Obstructive sleep apnea (OSA) is a highly prevalent condition with few therapeutic options. To date there is no approved pharmacotherapy for this disorder, but several attempts have been made in the past and are currently ongoing to find one. The recent identification of multiple endotypes underlying this disorder has oriented the pharmacological research towards tailored therapies targeting specific pathophysiological traits that contribute differently to cause OSA in each patient. In this review we retrospectively analyze the literature on OSA pharmacotherapy dividing the medications tested on the basis of the four main endotypes: anatomy, upper airway muscle activity, arousal threshold and ventilatory instability (loop gain). We show how recently introduced drugs for weight loss that modify upper airway anatomy may play an important role in the management of OSA in the near future, and promising results have been obtained with drugs that increase upper airway muscle activity during sleep and reduce loop gain. The lack of a medication that can effectively increase the arousal threshold makes this strategy less encouraging, although recent studies have shown that the use of certain sedatives do not worsen OSA severity and could actually improve patients’ sleep quality.

scholarly journals Obstructive Sleep Apnea: Emerging Treatments Targeting the Genioglossus Muscle

2019 ◽  
Vol 8 (10) ◽  
pp. 1754 ◽  
Author(s):  
Olga Mediano ◽  
Sofia Romero-Peralta ◽  
Pilar Resano ◽  
Irene Cano-Pumarega ◽  
Manuel Sánchez-de-la-Torre ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Muscle Tone ◽  
Treatment Strategies ◽  
Upper Airway ◽  
Apnea Hypopnea Index ◽  
Compensatory Response ◽  
Dilator Muscle ◽  
Obstructive Sleep ◽  
Osa Treatment

Obstructive sleep apnea (OSA) is characterized by repetitive episodes of upper airway obstruction caused by a loss of upper airway dilator muscle tone during sleep and an inadequate compensatory response by these muscles in the context of an anatomically compromised airway. The genioglossus (GG) is the main upper airway dilator muscle. Currently, continuous positive airway pressure is the first-line treatment for OSA. Nevertheless, problems related to poor adherence have been described in some groups of patients. In recent years, new OSA treatment strategies have been developed to improve GG function. (A) Hypoglossal nerve electrical stimulation leads to significant improvements in objective (apnea-hypopnea index, or AHI) and subjective measurements of OSA severity, but its invasive nature limits its application. (B) A recently introduced combination of drugs administered orally before bedtime reduces AHI and improves the responsiveness of the GG. (C) Finally, myofunctional therapy also decreases AHI, and it might be considered in combination with other treatments. Our objective is to review these therapies in order to advance current understanding of the prospects for alternative OSA treatments.

scholarly journals Obstructive Sleep Apnea Syndrome

2021 ◽  
pp. 1577-1589
Author(s):  
Suresh Menon
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Sleep Apnea Syndrome ◽  
Upper Airway ◽  
Causative Factor ◽  
Treatment Modalities ◽  
Muscle Physiology ◽  
Dilator Muscle ◽  
Obstructive Sleep ◽  
Apnea Syndrome

AbstractObstructive sleep apnea (OSA) is a condition that occurs due to aberrations in the oropharyngeal anatomy and the upper airway dilator muscle physiology with neurocognitive and cardiovascular sequelae. The mandibular-maxillary complex as the causative factor entails the maxillofacial surgeon to diagnose and treat the case when present, using the different treatment modalities available in the armamentarium.

Asynchrony of lingual muscle recruitment during sleep in obstructive sleep apnea

2015 ◽  
Vol 118 (12) ◽  
pp. 1516-1524 ◽  
Author(s):  
Yaniv Dotan ◽  
Giora Pillar ◽  
Alan R. Schwartz ◽  
Arie Oliven
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Upper Airway ◽  
Esophageal Pressure ◽  
Emg Activity ◽  
Muscle Coordination ◽  
Flow Limitation ◽  
Tongue Muscle ◽  
Dilator Muscle ◽  
Obstructive Sleep

Pharyngeal collapsibility during sleep increases primarily due to decline in dilator muscle activity. However, genioglossus EMG is known to increase during apneas and hypopneas, usually without reversing upper airway obstruction or inspiratory flow limitation. The present study was undertaken to test the hypothesis that intense activation of the genioglossus fails to prevent pharyngeal obstruction during sleep, and to evaluate if sleep-induced changes in tongue muscle coordination may be responsible for this phenomenon. We compared genioglossus and tongue retractors EMG activity in 13 obstructive sleep apnea (OSA) patients during wakefulness, while breathing through inspiratory resistors, to the activity observed at the end of apneas and hypopneas after 25 mg of brotizolam, before arousal, at equal esophageal pressure. During wakefulness, resistive breathing triggered increases in both genioglossus and retractor EMG. Activation of agonist tongue muscles differed considerably from that of the arm, as both genioglossus and retractors were activated similarly during all tongue movements. During sleep, flow limitation triggered increases in genioglossal EMG that could reach more than twofold the level observed while awake. In contrast, EMGs of the retractors reached less than half the wakefulness level. In sleeping OSA patients, genioglossal activity may increase during obstructed breathing to levels that exceed substantially those required to prevent pharyngeal collapse during wakefulness. In contrast, coactivation of retractors is deficient during sleep. These findings suggest that sleep-induced alteration in tongue muscle coordination may be responsible for the failure of high genioglossal EMG activity to alleviate flow limitation.

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