Department of Physical Therapy, Faculty of Health Sciences, Okayama Healthcare Professional University, 3-2-18 Daiku, Kita-ku, Okayama-shi, Okayama, 700-0913, Japan.
Department of Physical Therapy, Faculty of Human Sciences, Osaka University of Human Sciences, 1-4-1 Shojaku, Settsu-shi, Osaka, 566-8501, Japan.
J Muscle Res Cell Motil. 2024 Dec;45(4):263-273. doi: 10.1007/s10974-024-09680-w. Epub 2024 Jul 31.
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.
抗阻运动对骨骼肌有显著的益处，包括促进肌肉肥大和代谢增强，从而支持整体健康和疾病管理。然而，在衰老和糖尿病等情况下，骨骼肌对抗阻运动的反应性显著降低。最近的报告表明，糖基化应激导致肌肉萎缩和运动引起的肌肉适应性受损；然而，其在肌肉对抗阻运动反应中的作用尚不清楚。因此，在这项研究中，我们研究了甲基乙二醛（MGO），糖基化应激的关键因素，是否会影响骨骼肌对抗阻运动的急性反应性，重点关注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：一组给予 0.5% MGO 补充饮用水（MGO 组），另一组给予常规饮用水（对照组）。10 周后，每只大鼠的左侧比目鱼肌接受电刺激（ES）模拟抗阻运动，右侧肌肉作为非刺激对照。使用 SUnSET 评估肌肉蛋白质合成率，并使用 Western blot 定量测定关键信号分子（p70S6K 和 S6rp）的磷酸化水平。在对照组中，刺激肌肉的肌肉蛋白质合成和 p70S6K 和 S6rp 的磷酸化水平显著增加。在 MGO 组中，这些增加被减弱，表明 MGO 处理抑制了对抗阻运动的适应性反应。MGO 减弱了 ES 模拟抗阻运动对骨骼肌的适应性反应，影响肌肉蛋白质合成和关键信号分子。糖基化应激对抗阻运动或 ES 效果的潜在影响强调了在高糖基化应激情况下，如糖尿病和衰老，需要进行个体化干预。
