Intermittent claudication (IC) is the most common symptom of peripheral arterial disease which significantly deteriorates the quality of life of patients. Exercise training is by far the most effective treatment for IC; however, the underlying mechanisms remain elusive. To determine the local mechanisms by which exercise training improves walking performance in claudicants, we developed an implantable device to locally induce ischemic skeletal muscle contraction mimicking exercise via electrical stimulation (ES). Rats were assigned to four groups, Sham, Ischemia (Isch), Isch + exercise and Isch + ES groups. Following both unilateral femoral and iliac artery occlusion, rats showed sustained impairment of walking performance in the treadmill test. Chronic low-frequency ES of ischemic skeletal muscles for 2 weeks significantly recovered the occlusion-induced walking impairment in the rat claudication model. We further analyzed the ischemic skeletal muscles immunohistochemically following ES or exercise training; both ES and exercise training significantly increased capillaries in the ischemic skeletal muscles and shifted the muscle fibers toward oxidative types. These findings demonstrate that ES takes on common features of exercise in the rat claudication model, which may facilitate investigations on the local mechanisms of exercise-induced functional recovery.

中文翻译：

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神经肌肉刺激可改善大鼠跛行模型中缺血引起的行走障碍。


间歇性跛行（IC）是外周动脉疾病最常见的症状，它显着恶化患者的生活质量。运动训练是迄今为止最有效的 IC 治疗方法；然而，根本机制仍然难以捉摸。为了确定运动训练改善跛行者行走能力的局部机制，我们开发了一种可植入装置，通过电刺激（ES）模拟运动，局部诱导缺血性骨骼肌收缩。将大鼠分为四组：假手术组、缺血组(Isch)、Isch+运动组和Isch+ES组。单侧股动脉和髂动脉闭塞后，大鼠在跑步机测试中表现出行走能力持续受损。缺血骨骼肌慢性低频 ES 2 周显着恢复了大鼠跛行模型中咬合引起的行走障碍。我们进一步对 ES 或运动训练后的缺血骨骼肌进行免疫组织化学分析； ES 和运动训练都显着增加了缺血骨骼肌中的毛细血管，并将肌纤维转变为氧化型。这些发现表明，ES 在大鼠跛行模型中具有运动的共同特征，这可能有助于研究运动引起的功能恢复的局部机制。