The Role of Mitochondria in Obstructive Sleep Apnea: Implications for the Upper Airway Muscles

TL;DR

This review explores how mitochondrial dysfunction in upper airway muscles contributes to obstructive sleep apnea and suggests antioxidant strategies as potential treatments.

Contribution

The paper synthesizes current knowledge on mitochondrial involvement in upper airway muscle dysfunction in obstructive sleep apnea.

Findings

Mitochondrial dysfunction increases reactive oxygen species and oxidative stress in obstructive sleep apnea.

Chronic intermittent hypoxia impairs mitochondrial function, worsening upper airway muscle performance.

Antioxidant strategies may help mitigate the effects of mitochondrial damage in this condition.

Abstract

Obstructive sleep apnea is a common but underdiagnosed sleep-related breathing disorder characterized by recurrent episodes of upper airway obstruction during sleep, leading to intermittent episodes of hypoxia and systemic consequences. Anatomical and ventilatory control factors are well-established contributors, but less is known about how mitochondria influence upper airway muscle function in this condition. As central regulators of muscle performance and cellular adaptation to hypoxia, mitochondria are particularly vulnerable to dysfunction under chronic intermittent hypoxia. Mitochondrial dysfunction increases production of reactive oxygen species, predisposing to oxidative stress, that further impairs mitochondrial function. This review focuses on the mitochondrial involvement in obstructive sleep apnea, specifically synthesizing findings on the impact on upper airway muscles. The role of mitochondrial alterations in muscle dysfunction in this context is not well understood. A better understanding of oxidative damage in these muscles may also contribute to the development of therapeutic approaches, including antioxidant strategies, to mitigate the effects of chronic intermittent hypoxia in the upper airway muscles.

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