Upper airway XXXX is not important in the pathophysiology of obstructive sleep apnea.

@entity1 @entity32 @entity519 @entity1017 @entity121 @entity130
Clearly, UA @entity121 is not a major contributing factor to OSA pathogenesis for most @entity1 . Rather, state-dependent reductions in neural drive to UAMs would appear to be a more critical pathogenic mechanism. While there are subtle changes in UA structure and function, there is little evidence to suggest that @entity121 per se is important in OSA. Furthermore, most OSA @entity1 are indeed capable of achieving stable periods of breathing at least part of the night, an effect believed to be importantly mediated via compensation of UA dilator muscles. It is extremely difficult to conceptualize how this may occur if @entity121 were fundamentally important in OSA pathogenesis. Furthermore, disease progression appears to be modest at best and is largely explained by increased @entity1017 . Nonetheless, it is acknowledged that subtle changes in UAM output due to factors such as repeated UA vibration, @entity130 , @entity32 , and @entity519 may contribute to this effect. However, the current evidence would suggest that, if present, most of these changes would appear to be neurogenic rather than truly myopathic in origin. Adaptive processes to preserve UAM function in OSA in spite of these changes also appear to occur. In addition, these apparent changes may be an epiphenomenon rather than functionally important. Finally, some @entity1 may be more vulnerable to UAM weakness with greater consequential functional effects than others, although this remains scarcely studied. Thus, future studies should carefully explore the functional consequences of UAM abnormalities and define which @entity1 , if any, are susceptible to these potentially detrimental effects.
