目前阻塞型睡眠呼吸中止症在公共衛生上被視為是一個重大的健康問題，因此病症在夜間造成之 間歇性低氧的現象，引起心肌自由基生成量上升及血液中發炎物質增加，導致心肌發炎及纖維化，造 成心臟功能損傷。雖然運動對阻塞型睡眠呼吸中止症具有正面的助益，但鈉氫離子交換蛋白在運動影 響間歇性低氧造成心肌損傷中的角色，目前仍不清楚。從回顧的文獻中得知，運動提升心臟保護功能 降低間歇性低氧造成心肌損傷，其原因可能為運動促進心肌鈉氫離子交換蛋白1 的調節功能，避免間 歇性低氧引起鈉氫離子交換蛋白1 過度活化或功能受損，此結果將提供未來探討阻塞型睡眠呼吸中止 症之預防與治療策略的一個重要的研究方向。

Obstructive sleep apnoea (OSA) has been recognized as a significant health problem in the public health. OSA is recurrent obstruction of the upper airway leading to intermittent hypoxia (IH) during sleep. IH may cause increased levels of oxidative stress, leading to cardiac inflammation and cardiac fibrosis, resulting in cardiac dysfunction. Although exercise provides beneficial effects on adjuvant therapy for OSA, whether the sodium-hydrogen exchanger-1 (NHE-1) plays a role in that exercise prevents IH-induced cardiac fibrosis is unclear. Therefore, the purpose of this study is to investigate the role of NHE-1 and its mechanism in that exercise affects the cardiac fibrosis in patients with OSA by literature review. This study suggests that exercise may provide potent cardioprotective effects by attenuating IH-induced cardiac fibrosis, resulting from that exercise enhances the regulation of NHE-1 preventing IH-induced NHE-1 hyperactivity. These results also provide an important future prospect to investigate the prevention and therapeutic strategies for patients with OSA.