Genioglossal But Not Palatal Muscle Activity Relates  Closely to Pharyngeal Pressure

Malhotra, Atul; Pillar, Gioru; Fogel, Robert; Beauregard, Josie; Edwards, Jill K.; Slamowitz, David I.; Shea, Steven A.; White, David P.

doi:10.1164/ajrccm.162.3.9912067

Cited by 120 publications

(97 citation statements)

References 22 publications

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“…It can influence both the structure [7] and function [8] of skeletal muscles. However, to the best of the authors9 knowledge, its effects upon the upper airway muscles have not been directly addressed by previous studies in the field [5,[9][10][11]. A retrospective analysis of the current authors9 data [5] suggested that the function of the GG in obese and nonobese patients with OSAS may be different.…”

mentioning

confidence: 74%

Effects of obesity upon genioglossus structure and function in obstructive sleep apnoea

Carrera¹,

Barbé²,

Sauleda³

et al. 2004

Eur Respir J

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Obesity is a common feature of the obstructive sleep apnoea syndrome. It can influence the structure and function of skeletal muscles. However, its effects upon the upper airway muscles have not been explored directly.This study assessed the structure and function of the genioglossus in patients with obstructive sleep apnoea syndrome and in healthy subjects (with and without obesity, defined by a body mass index >30 kg·m−2). Further, to investigate the effects of continuous positive airway pressure (CPAP) treatment, patients with obstructive sleep apnoea syndrome after at least 1 yr under CPAP were also studied.The study found that obese and nonobese patients showed differentin vitrogeniglossus endurance properties. In obese patients, geniglossus endurance was indistinguishable from normal while, nonobese patients, at diagnosis, showed increased genioglossus fatigability; this was not observed in patients treated with CPAP. By contrast, patients with obstructive sleep apnoea syndrome showed at diagnosis a higher percentage of type II fibres than controls and patients under CPAP treatment independently of obesity. This difference is mainly due to a predominance of subtype IIb fibre. This difference was not observed in the group of patients treated with CPAP. Genioglossus twitch force was normal in all patients.These results suggest that different pathogenic mechanisms may underlie the development of obstructive sleep apnoea syndrome in obese and nonobese patients. This observation may have potential clinical implications.

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mentioning

confidence: 74%

Effects of obesity upon genioglossus structure and function in obstructive sleep apnoea

Carrera¹,

Barbé²,

Sauleda³

et al. 2004

Eur Respir J

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“…This defect in neuromuscular control was independent of age, obesity, and sex (86), and may be caused by sleep-related reductions in dilator activity during sleep compared with wakefulness (87,88) or by a loss of compensatory responses during sleep (87)(88)(89)(90)(91)(92)(93)(94)(95)(96)(97)(98)(99). Thus, current evidence indicates that sleep apnea is associated with fundamental disturbances in upper airway mechanical (68,100,101) and neuromuscular control (80,(102)(103)(104)(105)(106)) (see Figure 1, left), and suggests that a combined defect is required to produce sleep apnea (86). Nevertheless, the impact of obesity on upper airway mechanical and neural properties has not been elucidated.…”

Section: Obesity and Upper Airway Neuromechanical Control Modeling Upmentioning

confidence: 95%

Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches

Schwartz

Patil²,

Laffan

et al. 2008

Proceedings of the American Thoracic Society

583

395

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Obstructive sleep apnea is a common disorder whose prevalence is linked to an epidemic of obesity in Western society. Sleep apnea is due to recurrent episodes of upper airway obstruction during sleep that are caused by elevations in upper airway collapsibility during sleep. Collapsibility can be increased by underlying anatomic alterations and/or disturbances in upper airway neuromuscular control, both of which play key roles in the pathogenesis of obstructive sleep apnea. Obesity and particularly central adiposity are potent risk factors for sleep apnea. They can increase pharyngeal collapsibility through mechanical effects on pharyngeal soft tissues and lung volume, and through central nervous system-acting signaling proteins (adipokines) that may affect airway neuromuscular control. Specific molecular signaling pathways encode differences in the distribution and metabolic activity of adipose tissue. These differences can produce alterations in the mechanical and neural control of upper airway collapsibility, which determine sleep apnea susceptibility. Although weight loss reduces upper airway collapsibility during sleep, it is not known whether its effects are mediated primarily by improvement in upper airway mechanical properties or neuromuscular control. A variety of behavioral, pharmacologic, and surgical approaches to weight loss may be of benefit to patients with sleep apnea, through distinct effects on the mass and activity of regional adipose stores. Examining responses to specific weight loss strategies will provide critical insight into mechanisms linking obesity and sleep apnea, and will help to elucidate the humoral and molecular predictors of weight loss responses.

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“…During sleep, the phasic activation increases slowly when upper airway pressure becomes more negative due to a substantial reduction but not complete loss of reflex mechanisms. 27 Using our sleeping upper airway model, we assessed pharyngeal collapsibility (ie, Pcrit) during normal sleep and following three anatomic manipulations: mandibular advancement, uvulopalatopharyngoplasty (UPPP), and palatal stiffening. In our model, we simulated mandibular advancement by stretching the muscle to reach a 1-cm anterior mandibular displacement.…”

Section: Methodsmentioning

confidence: 99%

The Impact of Anatomic Manipulations on Pharyngeal Collapse

Huang

White

Malhotra

2005

Chest

Self Cite

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Obstructive sleep apnea (OSA) is a common disease with important neurocognitive and cardiovascular sequelae. Existing therapies are unsatisfactory, leading investigators to seek alternative forms of anatomic manipulation to influence pharyngeal mechanics. We have developed a two-dimensional computational model of the normal human upper airway based on signal averaging of MRI. Using the finite element method, we can perform various anatomic perturbations on the structure in order to assess the impact of these manipulations on pharyngeal mechanics and collapse. By design, the normal sleeping upper airway model collapses at −13 cm H 2 O. This closing pressure becomes more negative (ie, less collapsible) when we perform mandibular advancement (−21 cm H 2 O), palatal resection (−18 cm H 2 O), or palatal stiffening (−17 cm H 2 O). Where clinical data are available in the literature, the results of our model correspond reasonably well. Furthermore, our model provides information regarding the site of obstruction and provides hypotheses for clinical studies that can be undertaken in the future (eg, combination therapies). We believe that, in the future, finite element modeling will provide a useful tool to help advance our understanding of OSA and its response to various therapies. Keywords breathing; computational model; lung; MRI; obstructive sleep apnea; pharyngeal collapse Obstructive sleep apnea (OSA) is an important disorder due to both its high prevalence and its well-established sequelae. 1,2 Although effective therapies exist for sleep apnea, [3][4][5][6] investigators continue to seek alternative methods to manipulate pharyngeal mechanics/ anatomy with the ultimate goal of improving currently available therapeutic modalities. [3][4][5][6][7][8] Various different methods of manipulating pharyngeal mechanics have been used to treat snoring in individuals with largely normal upper airway anatomy and to treat sleep apnea in those with a compromised pharyngeal lumen. These methods include weight loss, oral appliances, and upper airway surgery. 9-11 However, these techniques have also been problematic due to variable efficacy and minimal ability to predict therapeutic response. A number of investigators have attempted to determine which patients are most likely to respond to treatment, but without great success. [12][13][14][15][16] We believe that improvements in our Our group has been involved in the development of a computational model to better understand the behavior of the human upper airway. 17 We have used finite element analysis, which is a mathematical technique to quantitatively analyze the behavior of a given mechanical structure. We have previously published our two-dimensional model that uses anatomically correct structure from MRI of normal human subjects. 17 With this model, we have used the critical closing pressure (Pcrit) as our outcome measure to assess the collapsibility of the upper airway. 18 Using finite element analysis, we sought to determine the impact of mandibular advancement, pa...

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Genioglossal But Not Palatal Muscle Activity Relates Closely to Pharyngeal Pressure

Cited by 120 publications

References 22 publications

Effects of obesity upon genioglossus structure and function in obstructive sleep apnoea

Effects of obesity upon genioglossus structure and function in obstructive sleep apnoea

Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches

The Impact of Anatomic Manipulations on Pharyngeal Collapse

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