Introduction <p> Obstructive sleep apnea (OSA) and sarcopenia are highly prevalent in aging adults, both contributing to morbidity and diminished quality of life. Despite plausible biological connections through sleep fragmentation, hormonal dysregulation, and chronic inflammation, their clinical relationship remains poorly understood. </p> Methods <p>This narrative review synthesizes current evidence on pathophysiological links between these conditions.</p> Results <p>Population studies consistently demonstrate increased sarcopenia risk in patients with OSA, with NHANES data showing 12% versus 5.5% prevalence. Recent Mendelian randomization studies provide genetic instrumental variable evidence supporting bidirectional causal relationships. Key mechanisms include sleep fragmentation disrupting growth hormone release, chronic inflammation promoting muscle catabolism, and respiratory muscle dysfunction creating vicious cycles. Population variability, comorbidities such as chronic obstructive pulmonary disease (COPD), and lifestyle factors including smoking further shape this relationship. Limited evidence suggests CPAP therapy may partially reverse these effects.</p> Conclusion <p>Clinical practice should consider routine sarcopenia screening in patients with OSA and sleep assessment in sarcopenic individuals.</p>

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Sleep-disordered breathing as a risk factor for sarcopenia in the elderly: a narrative review

  • Ahmad Jasem Abdulsalam,
  • Mohammad Abdulsalam,
  • Sulaiman Khadadah,
  • Diaa Shehab,
  • Ahmed S. BaHammam

摘要

Introduction

Obstructive sleep apnea (OSA) and sarcopenia are highly prevalent in aging adults, both contributing to morbidity and diminished quality of life. Despite plausible biological connections through sleep fragmentation, hormonal dysregulation, and chronic inflammation, their clinical relationship remains poorly understood.

Methods

This narrative review synthesizes current evidence on pathophysiological links between these conditions.

Results

Population studies consistently demonstrate increased sarcopenia risk in patients with OSA, with NHANES data showing 12% versus 5.5% prevalence. Recent Mendelian randomization studies provide genetic instrumental variable evidence supporting bidirectional causal relationships. Key mechanisms include sleep fragmentation disrupting growth hormone release, chronic inflammation promoting muscle catabolism, and respiratory muscle dysfunction creating vicious cycles. Population variability, comorbidities such as chronic obstructive pulmonary disease (COPD), and lifestyle factors including smoking further shape this relationship. Limited evidence suggests CPAP therapy may partially reverse these effects.

Conclusion

Clinical practice should consider routine sarcopenia screening in patients with OSA and sleep assessment in sarcopenic individuals.