阻塞型睡眠呼吸中止症常伴隨代謝症候群發生，然而彼此之因果關係尚未釐清口由於睡眠時交替式呼吸中止，會使身體承受異常的間歇性低氧壓力?引發交戚神經系統過度興奮，並增加發炎性細胞激素的釋放，進而造成體內氧化傷害口此一病理過程可能引發異常代謝反應，績而導致心血管疾病的發生口因此，r阻塞型睡眠呼吸中止症」可被視為重要的代謝症候群危險因于口然而，適 當的低氧介入能漸進性增進肺部通氣量，提升循環系統運送氧氣到身體各個組織的程度，改善組織利用氧氣的效率，藉此促進個體有氧適能口並且，間歇性低氧運動訓練亦能提供「前適應」的生理益處T減緩劇烈運動誘發的脂質過氧化或促發炎物質的產生，進而降低後續代謝症候群和心血管\發炎相關疾病的危險口是故，如何設計一套「安全」而「有效」的間歇性低氧運動訓練，以一方面增進個體有氧適能，同時降低阻塞型睡眠呼吸中止症對代謝症候群或心血管疾病的衝擊，將是未來醫療發展的新趨勢。(物理治療2012;37(2):126-135 )

Obstructive sleep apnea syndrome (OSAS) and metabolic syndrome (MS) are comorbìdities, however, the causative relationships are still elusive. Sleep apnea-induced Íntermittent hypoxia (IH) activates sympathetic nerve sensitivity, enhances oxidative stress and promotes proinflammatory cytokines release, finally leads to metabolìc abnormalities and cardiovascular complications. Hence OSAS is suggested to be the diagnostic criteria or risk factor of metabolic syndrome. Adequate IH intervention can progressively improve pulrnonary ventilation, upgrade oxygen delivery and tissue utilization, and eventually conduct better aerobic performance. Additionally,IH-induced “preconditioning"can simultaneously ameliorate lipid peroxidation and pro-inflammatory cytokines production generated by vigorous exercise. We expect to build up a safe and effective strategy to reduce the impact of OSAS on metabolic syndrome by developing suitable IH interventions and/or protocols. (FJPT 2012;37(2):126-135)