Institute of Neuroscience, Université catholique de Louvain, Louvain-la-Neuve, Belgium.
Departement of Diabetology and Nutrition, Institut de Recherche Expérimentale et Clinique, Université catholique de Louvain, Brussels, Belgium.
Am J Physiol Endocrinol Metab. 2021 Jan 1;320(1):E43-E54. doi: 10.1152/ajpendo.00263.2020. Epub 2020 Oct 26.
This study aimed to investigate the mechanisms known to regulate glucose homeostasis in human skeletal muscle of healthy and prediabetic subjects exercising in normobaric hypoxia. Seventeen healthy (H; 28.8 ± 2.4 yr; maximal oxygen consumption (V̇O): 45.1 ± 1.8 mL·kg·min) and 15 prediabetic (P; 44.6 ± 3.9 yr; V̇O: 30.8 ± 2.5 mL·kg·min) men were randomly assigned to two groups performing an acute exercise bout (heart rate corresponding to 55% V̇O) either in normoxic (NE) or in hypoxic (HE; fraction of inspired oxygen [Formula: see text] 14.0%) conditions. An oral glucose tolerance test (OGTT) was performed in a basal state and after an acute exercise bout. Muscle biopsies from m. vastus lateralis were taken before and after exercise. Venous blood samples were taken at regular intervals before, during, and after exercise. The two groups exercising in hypoxia had a larger area under the curve of blood glucose levels during the OGTT after exercise compared with baseline (H: +11%; P: +4%). Compared with pre-exercise, an increase in p-TBC1D1 Ser237 and in p-AMPK Thr172 was observed postexercise in P NE (+95%; +55%, respectively) and H HE (+91%; +43%, respectively). An increase in p-ACC Ser212 was measured after exercise in all groups (H NE: +228%; P NE: +252%; H HE: +252%; P HE: +208%). Our results show that an acute bout of exercise in hypoxia reduces glucose tolerance in healthy and prediabetic subjects. At a molecular level, some adaptations regulating glucose transport in muscle were found in all groups without associations with glucose tolerance after exercise. The results suggest that hypoxia negatively affects glucose tolerance postexercise through unidentified mechanisms. The molecular mechanisms involved in glucose tolerance after acute exercise in hypoxia have not yet been elucidated in human. Due to the reversible character of their status, prediabetic individuals are of particular interest for preventing the development of type 2 diabetes. The present study is the first to investigate muscle molecular mechanisms during exercise and glucose metabolism after exercise in prediabetic and healthy subjects exercising in normoxia and normobaric hypoxia.
本研究旨在探讨健康人和前驱糖尿病患者在常氧和常压低氧条件下运动时调节葡萄糖稳态的已知机制。17 名健康人(H;28.8±2.4 岁;最大摄氧量(V̇O):45.1±1.8 mL·kg·min)和 15 名前驱糖尿病患者(P;44.6±3.9 岁;V̇O:30.8±2.5 mL·kg·min)被随机分配到两组,分别在常氧(NE)或低氧(HE;吸入氧分数[Formula: see text]14.0%)条件下进行急性运动。在基础状态和急性运动后进行口服葡萄糖耐量试验(OGTT)。在运动前后从股外侧肌采集肌肉活检。在运动前、运动中和运动后定期采集静脉血样。与基线相比,在低氧条件下运动的两组在 OGTT 中运动后的血糖水平曲线下面积更大(H:+11%;P:+4%)。与运动前相比,P NE 组(+95%;+55%)和 H HE 组(+91%;+43%)运动后 p-TBC1D1 Ser237 和 p-AMPK Thr172 增加。所有组在运动后均测量到 p-ACC Ser212 增加(H NE:+228%;P NE:+252%;H HE:+252%;P HE:+208%)。我们的结果表明,低氧条件下的急性运动降低了健康人和前驱糖尿病患者的葡萄糖耐量。在分子水平上,所有组都发现了一些调节肌肉葡萄糖转运的适应,但与运动后葡萄糖耐量无关。结果表明,缺氧通过未知机制对运动后葡萄糖耐量产生负面影响。在人类中,关于低氧急性运动后葡萄糖耐量的分子机制尚未阐明。由于前驱糖尿病患者状态可逆,因此对于预防 2 型糖尿病的发生,前驱糖尿病患者特别感兴趣。本研究首次在常氧和常压低氧条件下运动时以及运动后对健康人和前驱糖尿病患者的肌肉分子机制和葡萄糖代谢进行了研究。