Decreased pancreatic amylase activity after acute high-intensity exercise and its effects on post-exercise muscle glycogen recovery

Decreased pancreatic amylase activity after acute high-intensity exercise and its effects on post-exercise muscle glycogen recovery
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DOI:
10.1139/apnm-2023-0265
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发表时间:
2024-05-30
影响因子:
3.4
通讯作者:
Terada,Shin
Terada,Shin
中科院分区:
医学3区
文献类型:
--
作者:
Kondo,Saki;Karasawa,Takuya;Terada,Shin

文献摘要

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我们之前的结果表明,持续 6 小时而非 1 小时的急性耐力运动会降低胰腺淀粉酶活性,这表明急性耐力运动可能以运动持续时间依赖性的方式影响碳水化合物的消化能力。在这里,我们研究了不同强度的急性耐力运动对小鼠胰淀粉酶活性的影响。雄性 C57BL/6J 小鼠以 10(Ex-Low 组)或 20 m/min(Ex-High 组)的速度进行 60 分钟的低强度或高强度跑步运动。对照组包括久坐的小鼠。急性运动后,与对照组相比,Ex-High组的胰淀粉酶活性立即显着降低,而Ex-Low组则没有显着降低。为了确定高强度运动引起的淀粉酶活性降低是否影响运动后肌糖原的恢复,我们研究了运动后立即给予口服葡萄糖或淀粉溶液(2.0 mg/g 体重)的 Ex-High 组小鼠的肌糖原再合成率。与葡萄糖喂养的小鼠相比,淀粉喂养的小鼠在 2 小时恢复期内表现出明显较低的运动后糖原积累率。在久坐(不运动)对照组中,淀粉和葡萄糖喂养的小鼠不存在糖原积累率的差异。此外,在运动后早期恢复期间(0-60 分钟),淀粉喂养的小鼠的血浆葡萄糖 AUC 显着低于葡萄糖喂养的小鼠。因此,我们的研究结果表明,急性耐力运动会以取决于运动强度的方式降低胰腺的碳水化合物消化能力,而多糖会导致运动后肌糖原恢复延迟。
Our prior results showed that an acute bout of endurance exercise for 6 h, but not 1 h, decreased pancreatic amylase activity, indicating that acute endurance exercise may affect carbohydrate digestive capacity in an exercise duration-dependent manner. Here, we investigated the effects of acute endurance exercise of different intensities on mouse pancreatic amylase activity. Male C57BL/6J mice performed low- or high-intensity running exercise for 60 min at either 10 (Ex-Low group) or 20 m/min (Ex-High group). The control group comprised sedentary mice. Immediately after acute exercise, pancreatic amylase activity was significantly decreased in the Ex-High group and not the Ex-Low group in comparison with the control group. To determine whether the decreased amylase activity induced by high-intensity exercise influenced muscle glycogen recovery after exercise, we investigated the rates of muscle glycogen resynthesis in Ex-High group mice administered either oral glucose or starch solution (2.0 mg/g body weight) immediately after exercise. The starch-fed mice exhibited significantly lower post-exercise glycogen accumulation rates in the 2-h recovery period compared with the glucose-fed mice. This difference in the glycogen accumulation rate was absent for starch- and glucose-fed mice in the sedentary (no exercise) control group. Furthermore, the plasma glucose AUC during early post-exercise recovery (0–60 min) was significantly lower in the starch-fed mice than in the glucose-fed mice. Thus, our findings suggest that acute endurance exercise diminishes the carbohydrate digestive capacity of the pancreas in a manner dependent on exercise intensity, with polysaccharides leading to delayed muscle glycogen recovery after exercise.