![]() The upper airway muscles are composed of a variety of fast and slow muscle fiber types (Table 1) with conventional myosin heavy chain (MHC) isoforms and three primary MHC phenotypes and two subtypes ( in order of prevalence for the adult genioglossus muscle in non-OSA subjects MHCIIA > MHCI-IIX > MHCI > MHCI-IIA > MHCIIX Daugherty et al., 2012). Thus, the reported magnitude of these changes may be an underestimation. Most of these studies did not rule out OSA in the healthy non-OSA/control groups (full polysomnography evaluations are reported in only four studies). Sixteen studies are summarized in Table 2. Broadly, this includes changes in: muscle fiber type, direction of muscle fibers, and anatomical arrangement of nerve fiber terminals. Several histological studies support the presence of upper airway remodeling in patients with OSA (Tables 1 and 2). ![]() Finally, we discuss how upper airway remodeling and neural injury might contribute to upper airway closure during sleep.Īnatomical Structure of Upper Airway Muscles non-OSA subjects is also briefly reviewed. The function of upper airway reflexes and tongue force/fatigue characteristics in OSA vs. ![]() This encompasses evidence from a variety of neurophysiological approaches including histological, electrophysiological, and physiological studies. We review the pathophysiological evidence under three separate headings: (1) anatomical remodeling of the upper airway muscles, (2) efferent changes, and (3) afferent changes (see Figure 1). In this review, some of the more convincing evidence for and against upper airway remodeling in which data have been acquired in both OSA patients and non-OSA controls is highlighted. The extent to which snoring and hypoxia exacerbate the disease and lead to important damage is unresolved. Changes in nerve and muscle properties may result from vibration through snoring, hypoxia, or both. ![]() These changes are loosely termed airway remodeling and may adversely affect upper airway function during sleep. In the upper airway there are changes in sensation, muscle properties, and neural drive in patients with obstructive sleep apnea (OSA). Some unresolved questions including possible treatment targets are noted. This brief review, primarily focused on data in humans, summarizes: (1) the evidence for upper airway sensorimotor injury in OSA and (2) current understanding of how these changes affect upper airway function and their potential to change OSA progression. However, the extent to which the alterations contribute to impairments in upper airway muscle function, and thus OSA disease progression, remains uncertain. Multiple studies have demonstrated altered sensory and motor function in patients with OSA using a variety of neurophysiological and histological approaches. Neural injury affecting the upper airway muscles due to repetitive exposure to intermittent hypoxia and/or mechanical strain resulting from snoring and recurrent upper airway closure have been proposed to contribute to OSA disease progression. The causes of obstructive sleep apnea (OSA) are multifactorial. 2 Faculty of Medicine, University of New South Wales, Sydney, NSW, Australia.1 Neuroscience Research Australia, Sydney, NSW, Australia.
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