Abstract：
Resistance exercise provides significant benefits to skeletal muscle, including hypertrophy and metabolic enhancements, supporting overall health and disease management. However, skeletal muscle responsiveness to resistance exercise is significantly reduced in conditions such as aging and diabetes. Recent reports suggest that glycation stress contributes to muscle atrophy and impaired exercise-induced muscle adaptation; however, its role in the muscle response to resistance exercise remains unclear. Therefore, in this study, we investigated whether methylglyoxal (MGO), a key factor in glycation stress, affects the acute responsiveness of skeletal muscles to resistance exercise, focusing on protein synthesis and the key signaling molecules. This study included 12 8-week-old male Sprague-Dawley rats divided into two groups: one received 0.5% MGO-supplemented drinking water (MGO group) and the other received regular water (control group). After 10 weeks, the left tibialis anterior muscle of each rat was subjected to electrical stimulation (ES) to mimic resistance exercise, with the right muscle serving as a non-stimulated control. Muscle protein-synthesis rates were evaluated with SUnSET, and phosphorylation levels of key signaling molecules (p70S6K and S6rp) were quantified using western blotting. In the control group, stimulated muscles exhibited significantly increased muscle protein synthesis and phosphorylation levels of p70S6K and S6rp. In the MGO group, these increases were attenuated, indicating that MGO treatment suppresses the adaptive response to resistance exercise. MGO diminishes the skeletal muscle\'s adaptive response to ES-simulated resistance exercise, affecting both muscle protein synthesis and key signaling molecules. The potential influence of glycation stress on the effectiveness of resistance exercise or ES emphasizes the need for individualized interventions in conditions of elevated glycation stress, such as diabetes and aging.
摘要：
抗阻运动对骨骼肌有显著的好处，包括肥大和代谢增强，支持全面的健康和疾病管理。然而,在衰老和糖尿病等情况下，骨骼肌对阻力运动的反应性显著降低。最近的报道表明，糖化应激有助于肌肉萎缩和运动诱导的肌肉适应受损；然而，其在抗阻运动的肌肉反应中的作用尚不清楚。因此,在这项研究中，我们调查了甲基乙二醛(MGO)，糖化应激的一个关键因素，影响骨骼肌对抗阻运动的急性反应，专注于蛋白质合成和关键信号分子。这项研究包括12只8周龄雄性Sprague-Dawley大鼠，分为两组：一组接受0.5％MGO补充的饮用水（MGO组），另一组接受常规水（对照组）。10周后,对每只大鼠的左胫骨前肌进行电刺激（ES）以模拟阻力运动，右肌肉作为非刺激控制。用SUnSET评估肌肉蛋白质合成率，关键信号分子(p70S6K和S6rp)的磷酸化水平使用蛋白质印迹进行定量。在对照组中，受刺激的肌肉显示肌肉蛋白质合成和p70S6K和S6rp的磷酸化水平显着增加。在MGO组中，这些增加减弱了，表明MGO治疗抑制了对抵抗运动的适应性反应。MGO降低了骨骼肌对ES模拟阻力运动的适应性反应，影响肌肉蛋白质合成和关键信号分子。糖化应激对抗阻运动或ES有效性的潜在影响强调在糖化应激升高的情况下需要个体化干预措施，比如糖尿病和衰老。
