Data_Sheet_1_Response of Resistance Exercise-Induced Muscle Protein Synthesis and Skeletal Muscle Hypertrophy Are Not Enhanced After Disuse Muscle Atrophy in Rat.docx

Skeletal muscle disuse rapidly decreases muscle mass. Resistance training (RT) is believed as the most effective way to gain muscle mass via an increase in mTORC1 activity and muscle protein synthesis (MPS). However, it remains unclear whether muscle atrophy by disuse alters the mTORC1 activation and MPS response to an acute resistance exercise (RE) and chronic RT–mediated skeletal muscle hypertrophy. This study investigated the influence of disuse muscle atrophy on the response of mTORC1 activation and MPS to an acute RE. We also evaluated whether disuse muscle atrophy affects the response of RT-induced muscle mass gain. Thirty male Sprague-Dawley rats were randomly divided into control (CON) or hindlimb suspension (HS) groups. A 14-day HS via the tail was used as the model for gastrocnemius muscle disuse in the HS group. Unilateral lower limb muscle contraction using by percutaneous electrical stimulation was used to mimic the stimuli of RE. Ten bouts of RE were performed in 3-week as chronic RT. Our results showed that MPS and mTORC1 activity was unchanged after HS at basal state. However, the ribosomal RNA (rRNA) level was reduced in HS rats compared to that in CON rats at basal state. MPS and rRNA increased in both HS and CON rats in response to acute RE to the same extent. However, the level of mTORC1 activation in response to an acute RE was significantly higher in HS than that in the CON group at 12 h after exercise, even though no difference was observed at 3 h after exercise. The 10-bout RT significantly increased gastrocnemius muscle mass in both CON and HS rats. The response of muscle hypertrophy did not differ between the groups. Therefore, MPS in response to acute RE and muscle hypertrophy in response to chronic RT were unaltered after disuse muscle atrophy.

骨骼肌废用会快速降低肌肉质量。阻力训练（Resistance Training, RT）被认为是通过提升哺乳动物雷帕霉素靶蛋白复合物1（mTORC1）活性与肌肉蛋白质合成（Muscle Protein Synthesis, MPS）水平来增加肌肉质量的最有效手段。然而，废用性肌肉萎缩是否会改变mTORC1激活与MPS对单次急性阻力运动（Acute Resistance Exercise, RE）以及慢性阻力训练介导的骨骼肌肌肥大的响应，目前仍不明确。本研究探讨了废用性肌肉萎缩对mTORC1激活与MPS响应单次急性阻力运动的影响，同时评估了废用性肌肉萎缩是否会影响阻力训练诱导的肌肉质量增加响应。30只雄性Sprague-Dawley大鼠被随机分为对照组（Control, CON）与后肢悬吊组（Hindlimb Suspension, HS）。后肢悬吊组采用为期14天的尾部悬吊法构建腓肠肌废用模型。本研究采用经皮电刺激诱导单侧下肢肌肉收缩，以模拟阻力运动的刺激效应。本研究在3周内完成10次急性阻力运动，以此作为慢性阻力训练干预方案。结果显示，后肢悬吊处理后，基础状态下的MPS与mTORC1活性无明显变化。但基础状态下，后肢悬吊组大鼠的核糖体RNA（Ribosomal RNA, rRNA）水平较对照组显著降低。急性阻力运动刺激后，两组大鼠的MPS与rRNA水平均出现同等程度的升高。然而，运动后12小时，后肢悬吊组大鼠响应急性阻力运动的mTORC1激活水平显著高于对照组，尽管运动后3小时两组间未观察到显著差异。10次慢性阻力训练干预后，两组大鼠的腓肠肌质量均显著提升，且两组的肌肥大响应无显著差异。综上，废用性肌肉萎缩并未改变机体响应急性阻力运动的MPS水平，以及响应慢性阻力训练的骨骼肌肌肥大程度。