Islam Hashim, Smith Marysa M W, Scribbans Trisha D, McCrady Emma, Castellani Laura N, Allen Matti D, Wright David C, Simpson Craig A, Gurd Brendon J
School of Kinesiology of Health Studies, Queen's University, Kingston, ONTARIO, CANADA.
Faculty of Kinesiology and Recreation Management, University of Manitoba, Winnipeg, MANITOBA, CANADA.
Int J Exerc Sci. 2020 May 1;13(2):554-566. doi: 10.70252/FQEF4828. eCollection 2020.
Exercise-induced alterations in adipose tissue insulin and/or β-adrenergic signaling may contribute to increases in whole-body fat oxidation following acute exercise. Thus, we examined changes in insulin (Akt, AS160) and β-adrenergic (PKA) signaling proteins in subcutaneous adipose tissue and whole-body fat oxidation in overweight women following acute high-intensity interval exercise (HIIE). Overweight females completed two experimental sessions in a randomized order: 1) control (bed rest) and 2) HIIE (10 × 4 min running intervals at 90% HR, 2-min recovery). Subcutaneous abdominal adipose tissue biopsies were obtained from 10 participants before (pre-), immediately (0hr) after (post-), 2hr post-, and 4hr post-exercise. Plasma glucose and insulin levels were assessed in venous blood samples obtained at each biopsy time-point from a different group of 5 participants (BMI-matched to biopsy group). Fat oxidation rates were estimated using the respiratory exchange ratio (RER) in all participants using indirect calorimetry pre-, 2hr post-, and 4hr post-exercise. RER was decreased ( < 0.05) at 2hr post-exercise after HIIE (0.77 ± 0.04) compared to control (0.84 ± 0.04). Despite higher plasma glucose ( < 0.01) and insulin ( < 0.05) levels at 0hr post-exercise versus control, no significant interaction effects were observed for Akt or AS160 phosphorylation ( > 0.05). Phosphorylation of PKA substrates was unaltered in both conditions ( > 0.05). Collectively, altered β-adrenergic and insulin signaling in subcutaneous adnominal adipose tissue does not appear to explain increased whole-body fat oxidation following acute HIIE.
运动诱导的脂肪组织胰岛素和/或β-肾上腺素能信号变化可能有助于急性运动后全身脂肪氧化增加。因此，我们研究了超重女性在急性高强度间歇运动（HIIE）后皮下脂肪组织中胰岛素（Akt、AS160）和β-肾上腺素能（PKA）信号蛋白的变化以及全身脂肪氧化情况。超重女性按随机顺序完成两个实验阶段：1）对照（卧床休息）和2）HIIE（以90%心率进行10次4分钟跑步间歇，2分钟恢复）。在运动前（预）、运动后即刻（0小时）、运动后2小时和运动后4小时从10名参与者获取皮下腹部脂肪组织活检样本。在每个活检时间点从另一组5名参与者（BMI与活检组匹配）采集的静脉血样本中评估血浆葡萄糖和胰岛素水平。在所有参与者中，使用间接量热法在运动前、运动后2小时和运动后4小时通过呼吸交换率（RER）估计脂肪氧化率。与对照（0.84±0.04）相比，HIIE后运动后2小时RER降低（<0.05）（0.77±0.04）。尽管运动后0小时血浆葡萄糖（<0.01）和胰岛素（<0.05）水平高于对照，但未观察到Akt或AS160磷酸化的显著交互作用（>0.05）。两种情况下PKA底物的磷酸化均未改变（>0.05）。总体而言，皮下腹部脂肪组织中β-肾上腺素能和胰岛素信号的改变似乎无法解释急性HIIE后全身脂肪氧化的增加。
