阻塞型睡眠呼吸中止症(obstructive sleep apnea, OSA)常常合併心血管疾病，其原因與心肌氧化壓力有關。OSA患者夜間之血氧飽和度反覆的變化類似慢性間歇性低氧(chronic intermittent hypoxia)之生理現象，造成心肌氧化壓力增加，導致抗氧化酵素含量下降，而降低細胞之抗氧化能力，進而使心肌細胞受損而影響心臟功能。此外，研究也顯示長期規律運動訓練具有提升心肌細胞抗氧化傷害的保護能力，可能具有清除OSA患者夜間因上呼吸道發生類似間歇性低氧所造成之氧化壓力，減少心肌細胞損傷或死亡，進而達到保護心臟功能的效果，但目前對於其引發的機制仍未清楚，故運動訓練對臨床長期OSA患者心肌細胞氧化傷害之分子細胞層級的機轉，值得進一步加以研究。

Patients with obstructive sleep apneas (OSA) have greater risk developing cardiovascular diseases secondary to greater oxidative damage in cardiac muscle. OSA is characterized by recurrent episodes of partial or complete obstruction of the upper airway during sleep. Periodic obstruction of the upper airway in patients with OSA leads to a significant decreased arterial oxygen saturation, which rapidly returns to normal after ventilation resumes during sleep. This condition resembles a chronic intermittent hypoxia resulting in increased oxidative stress and decreased antioxidant capacity. This in turn contributes to the cardiac muscle injury and subsequently leading to cardiac dysfunctions. Moreover, several studies have demonstrated that regular exercise training is able to increase antioxidant capacity. This will help to eliminate the oxidative stress caused by chronic intermittent hypoxia and results in cardioprotection by reducing the cardiac muscle injury and cell death. So far, the underlying mechanisms involving this cardioprotective function of exercise is not completely clear. Thus, the aim of this report is to review that the current knowledge regarding the protective effects of exercise and related molecular mechanisms for cardiac muscle oxidative injury in patients with OSA.