Faculty of Pharmacy, Meijo University, Nagoya, Aichi, Japan.
Research and Development, Matsutani Chemical Industry Co., Ltd, Itami, Hyogo, Japan.
Physiol Rep. 2022 May;10(9):e15297. doi: 10.14814/phy2.15297.
This study investigated the combined effects of exercise training and D-allulose intake on endurance capacity in mice. Male C57BL/6J mice were fed either a control diet (Con) or a 3% D-allulose diet (Allu) and further divided into the sedentary (Sed) or exercise training (Ex) groups (Con-Sed, Con-Ex, Allu-Sed, Allu-Ex, respectively; n = 6-7/group). The mice in the Ex groups were trained on a motor-driven treadmill 5 days/week for 4 weeks (15-18 m/min, 60 min). After the exercise training period, all mice underwent an exhaustive running test to assess their endurance capacity. At 48 h after the running test, the mice in the Ex groups were subjected to run at 18 m/min for 60 min again. Then the gastrocnemius muscle and liver were sampled immediately after the exercise bout. The running time until exhaustion tended to be higher in the Allu-Ex than in the Con-Ex group (p = 0.08). The muscle glycogen content was significantly lower in the Con-Ex than in the Con-Sed group and was significantly higher in the Allu-Ex than in the Con-Ex group (p < 0.05). Moreover, exercise training increased the phosphorylation levels of adenosine monophosphate-activated protein kinase (AMPK) in the muscle and liver. The phosphorylation levels of acetyl coenzyme A carboxylase (ACC), a downstream of AMPK, in the muscle and liver were significantly higher in the Allu-Ex than in the Con-Sed group (p < 0.05), suggesting that the combination of exercise training and D-allulose might have activated the AMPK-ACC signaling pathway, which is associated with fatty acid oxidation in the muscle and liver. Taken together, our data suggested the combination of exercise training and D-allulose intake as an effective strategy to upregulate endurance capacity in mice. This may be associated with sparing glycogen content and enhancing activation of AMPK-ACC signaling in the skeletal muscle.
本研究旨在探讨运动训练和 D-阿洛酮糖摄入对小鼠耐力的综合影响。雄性 C57BL/6J 小鼠分别喂食对照饮食(Con)或 3% D-阿洛酮糖饮食(Allu),并进一步分为久坐不动(Sed)或运动训练(Ex)组(Con-Sed、Con-Ex、Allu-Sed、Allu-Ex,每组 n = 6-7)。Ex 组小鼠每周 5 天在电动跑步机上训练 4 周(15-18 m/min,60 min)。运动训练期结束后,所有小鼠进行力竭性跑步测试以评估其耐力。在跑步测试后 48 小时,Ex 组小鼠再次以 18 m/min 的速度运动 60 min。然后,在运动后立即采集比目鱼肌和肝脏样本。与 Con-Ex 组相比,Allu-Ex 组的小鼠力竭时间有增加的趋势(p = 0.08)。与 Con-Sed 组相比,Con-Ex 组的肌肉糖原含量显著降低,而 Allu-Ex 组的肌肉糖原含量显著升高(p < 0.05)。此外,运动训练增加了肌肉和肝脏中 AMPK 的磷酸化水平。肌肉和肝脏中 ACC(AMPK 的下游)的磷酸化水平在 Allu-Ex 组显著高于 Con-Sed 组(p < 0.05),提示运动训练和 D-阿洛酮糖的结合可能激活了肌肉和肝脏中的 AMPK-ACC 信号通路,与脂肪酸氧化有关。综上所述,我们的数据表明,运动训练和 D-阿洛酮糖摄入的结合是提高小鼠耐力的有效策略。这可能与肌肉糖原含量的节省和 AMPK-ACC 信号通路的激活有关。