Clearly, UA myopathy is not a major contributing factor to OSA pathogenesis for most patients. 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 myopathy per se is important in OSA. Furthermore, most OSA patients 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 myopathy were fundamentally important in OSA pathogenesis. Furthermore, disease progression appears to be modest at best and is largely explained by increased weight gain. Nonetheless, it is acknowledged that subtle changes in UAM output due to factors such as repeated UA vibration, trauma, inflammation, and hypoxia 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 patients 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 patients, if any, are susceptible to these potentially detrimental effects.