Grenoble Alpes University, HP2 laboratory, Grenoble, F-38042, France.
INSERM, U1042, Grenoble, F-38042, France.
Sci Rep. 2017 Mar 3;7:43663. doi: 10.1038/srep43663.
Chronic intermittent hypoxia (IH) associated with obstructive sleep apnea (OSA) is a major risk factor for cardiovascular and metabolic diseases (insulin resistance: IR). Autophagy is involved in the pathophysiology of IR and high intensity training (HIT) has recently emerged as a potential therapy. We aimed to confirm IH-induced IR in a tissue-dependent way and to explore the preventive effect of HIT on IR-induced by IH. Thirty Swiss 129 male mice were randomly assigned to Normoxia (N), Intermittent Hypoxia (IH: 21-5% FiO, 30 s cycle, 8 h/day) or IH associated with high intensity training (IH HIT). After 8 days of HIT (2*24 min, 50 to 90% of Maximal Aerobic Speed or MAS on a treadmill) mice underwent 14 days IH or N. We found that IH induced IR, characterized by a greater glycemia, an impaired insulin sensitivity and lower AKT phosphorylation in adipose tissue and liver. Nevertheless, MAS and AKT phosphorylation were greater in muscle after IH. IH associated with HIT induced better systemic insulin sensitivity and AKT phosphorylation in liver. Autophagy markers were not altered in both conditions. These findings suggest that HIT could represent a preventive strategy to limit IH-induced IR without change of basal autophagy.
慢性间歇性低氧（IH）与阻塞性睡眠呼吸暂停（OSA）相关，是心血管和代谢疾病（胰岛素抵抗：IR）的主要危险因素。自噬参与 IR 的病理生理学，高强度训练（HIT）最近已成为一种潜在的治疗方法。我们旨在以组织依赖性的方式确认 IH 诱导的 IR，并探讨 HIT 对 IH 诱导的 IR 的预防作用。30 只瑞士 129 只雄性小鼠被随机分配到常氧（N）、间歇性低氧（IH：21-5% FiO，30s 周期，8h/天）或与高强度训练（IH HIT）相关的 IH。在进行 8 天的 HIT（2*24min，在跑步机上达到最大有氧速度或 MAS 的 50-90%）后，小鼠接受 14 天 IH 或 N。我们发现 IH 诱导了 IR，表现为血糖升高、胰岛素敏感性降低和脂肪组织和肝脏中 AKT 磷酸化降低。然而，在 IH 后肌肉中的 MAS 和 AKT 磷酸化更高。与 IH 相关的 HIT 诱导了更好的全身胰岛素敏感性和肝脏中的 AKT 磷酸化。在这两种情况下，自噬标志物都没有改变。这些发现表明，HIT 可能是一种预防策略，可以在不改变基础自噬的情况下限制 IH 诱导的 IR。
