Abstract
Unstable ventilatory chemoreflex control, quantified as loop gain, is recognized as one of four key pathophysiological traits that contribute to cause obstructive sleep apnea (OSA). Novel treatments aimed at reducing loop gain are being investigated, with the intention that future OSA treatment may be tailored to the individual's specific cause of apnea. However, few studies have evaluated loop gain in OSA and non-OSA controls and those that have provide little evidence to support an inherent abnormality in either overall chemical loop gain in OSA patients vs. non-OSA controls, or its components (controller and plant gain). However, intermittent hypoxia may induce high controller gain through neuroplastic changes to chemoreflex control, and may also decrease plant gain via oxidative stress induced inflammation and reduced lung function. The inherent difficulties and limitations with loop gain measurements are discussed and areas where further research are required are highlighted, as only by understanding the mechanisms underlying OSA are new therapeutic approaches likely to emerge in OSA.
Highlights
Obstructive sleep apnea (OSA) is a condition in which the upper airway either partially or completely obstructs during sleep
As several factors of upper airway anatomy and neuromuscular control interact to promote airway collapse, even a low/normal loop gain may be associated with pharyngeal airway collapse in participants with highly susceptible airways [38]
The lack of strong evidence for inherently high loop gain in OSA patients does not imply that loop gain does not contribute to OSA pathogenesis
Summary
Obstructive sleep apnea (OSA) is a condition in which the upper airway either partially or completely obstructs during sleep. In recent years it has been recognized that four quantifiable traits of upper airway anatomy and neuromuscular control contribute to variable degrees in each patient to cause OSA [3]. There is growing interest in treatments that may alter ventilatory chemoreflex control as a potential treatment for OSA [5, 6]. It is currently uncertain whether ventilatory chemoreflex control, and loop gain, is consistently abnormal in OSA patients.
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