Mitochondrial dysfunction in muscle cells induced by snoring vibrations

Area of Science:

• Muscle physiology
• Mitochondrial biology
• Sleep medicine

Background:

• Snoring vibrations are implicated in upper airway muscle dysfunction in obstructive sleep apnea (OSA).
• Understanding the cellular mechanisms linking snoring to muscle weakness is crucial for OSA management.

Purpose of the Study:

• To investigate the effects of snoring-induced vibrations on mitochondrial homeostasis in muscle cells.
• To compare in vitro findings with mitochondrial alterations in upper airway muscles of snorers and OSA patients.

Main Methods:

• In vitro vibration model using L6 muscle cells.
• Proteomic and transcriptomic analysis of muscle cells and patient samples.
• Mitochondrial respiration and glycolysis assays (Seahorse).

Main Results:

• Vibration induced significant mitochondrial proteome remodeling, affecting oxidative phosphorylation and RNA processing.
• Impaired RNA processing and protein synthesis were observed, leading to transcript-protein uncoupling.
• Mitochondrial respiration collapsed, and glycolytic reserve was impaired, with persistent deficits in patients.

Conclusions:

• Snoring vibrations act as a stressor disrupting mitochondrial homeostasis and leading to muscle dysfunction.
• Impaired RNA processing, protein synthesis, and mechanotransduction contribute to muscle weakness in OSA.
• Findings highlight a novel mechanism linking snoring to OSA-related muscle pathology.