Abstract：
BACKGROUND: Mitochondria represent key organelles influencing cellular homeostasis and have been implicated in the signalling events regulating protein synthesis.
METHODS: We examined whether mitochondrial bioenergetics (oxidative phosphorylation and reactive oxygen species (H2O2) emission, ROS) measured in vitro in permeabilized muscle fibres represent regulatory factors for integrated daily muscle protein synthesis rates and skeletal muscle mass changes across the spectrum of physical activity, including free-living and bed-rest conditions: n = 19 healthy, young men (26 ± 4 years, 23.4 ± 3.3 kg/m2) and following 12 weeks of resistance-type exercise training: n = 10 healthy older men (70 ± 3 years, 25.2 ± 2.1 kg/m2). Additionally, we evaluated the direct relationship between attenuated mitochondrial ROS emission and integrated daily myofibrillar and sarcoplasmic protein synthesis rates in genetically modified mice (mitochondrial-targeted catalase, MCAT).
RESULTS: Neither oxidative phosphorylation nor H2O2 emission were associated with muscle protein synthesis rates in healthy young men under free-living conditions or following 1 week of bed rest (both P > 0.05). Greater increases in GSSG concentration were associated with greater skeletal muscle mass loss following bed rest (r = -0.49, P < 0.05). In older men, only submaximal mitochondrial oxidative phosphorylation (corrected for mitochondrial content) was positively associated with myofibrillar protein synthesis rates during exercise training (r = 0.72, P < 0.05). However, changes in oxidative phosphorylation and H2O2 emission were not associated with changes in skeletal muscle mass following training (both P > 0.05). Additionally, MCAT mice displayed no differences in myofibrillar (2.62 ± 0.22 vs. 2.75 ± 0.15%/day) and sarcoplasmic (3.68 ± 0.35 vs. 3.54 ± 0.35%/day) protein synthesis rates when compared with wild-type mice (both P > 0.05).
CONCLUSIONS: Mitochondrial oxidative phosphorylation and reactive oxygen emission do not seem to represent key factors regulating muscle protein synthesis or muscle mass regulation across the spectrum of physical activity.
METHODS: We examined whether mitochondrial bioenergetics (oxidative phosphorylation and reactive oxygen species (H2O2) emission, ROS) measured in vitro in permeabilized muscle fibres represent regulatory factors for integrated daily muscle protein synthesis rates and skeletal muscle mass changes across the spectrum of physical activity, including free-living and bed-rest conditions: n = 19 healthy, young men (26 ± 4 years, 23.4 ± 3.3 kg/m2) and following 12 weeks of resistance-type exercise training: n = 10 healthy older men (70 ± 3 years, 25.2 ± 2.1 kg/m2). Additionally, we evaluated the direct relationship between attenuated mitochondrial ROS emission and integrated daily myofibrillar and sarcoplasmic protein synthesis rates in genetically modified mice (mitochondrial-targeted catalase, MCAT).
RESULTS: Neither oxidative phosphorylation nor H2O2 emission were associated with muscle protein synthesis rates in healthy young men under free-living conditions or following 1 week of bed rest (both P > 0.05). Greater increases in GSSG concentration were associated with greater skeletal muscle mass loss following bed rest (r = -0.49, P < 0.05). In older men, only submaximal mitochondrial oxidative phosphorylation (corrected for mitochondrial content) was positively associated with myofibrillar protein synthesis rates during exercise training (r = 0.72, P < 0.05). However, changes in oxidative phosphorylation and H2O2 emission were not associated with changes in skeletal muscle mass following training (both P > 0.05). Additionally, MCAT mice displayed no differences in myofibrillar (2.62 ± 0.22 vs. 2.75 ± 0.15%/day) and sarcoplasmic (3.68 ± 0.35 vs. 3.54 ± 0.35%/day) protein synthesis rates when compared with wild-type mice (both P > 0.05).
CONCLUSIONS: Mitochondrial oxidative phosphorylation and reactive oxygen emission do not seem to represent key factors regulating muscle protein synthesis or muscle mass regulation across the spectrum of physical activity.
摘要：
背景：线粒体代表了影响细胞稳态的关键细胞器，并且与调节蛋白质合成的信号事件有关。
方法：我们检查了线粒体生物能学（氧化磷酸化和活性氧（H2O2）排放，ROS）在透化肌纤维中体外测量，代表了整个身体活动范围内综合每日肌肉蛋白质合成速率和骨骼肌质量变化的调节因素，包括自由生活和卧床休息条件：n=19健康，年轻男子(26±4岁，23.4±3.3kg/m2），并在12周的阻力型运动训练后：n=10名健康的老年男性（70±3岁，25.2±2.1kg/m2)。此外,我们评估了在转基因小鼠中减弱的线粒体ROS发射与整合的每日肌原纤维和肌浆蛋白合成速率之间的直接关系（线粒体靶向过氧化氢酶，MCAT）。
结果：在自由生活条件下或卧床休息1周后，健康年轻男性的氧化磷酸化和H2O2释放均与肌肉蛋白合成率无关（均P>0.05）。卧床休息后，GSSG浓度增加与骨骼肌质量损失增加相关（r=-0.49，P<0.05）。在年长的男人中，在运动训练过程中,只有次最大线粒体氧化磷酸化(校正线粒体含量)与肌原纤维蛋白合成率呈正相关(r=0.72,P<0.05)。然而,氧化磷酸化和H2O2排放的变化与训练后骨骼肌质量的变化无关(均P>0.05).此外,MCAT小鼠的肌原纤维无差异（2.62±0.22vs.2.75±0.15%/天）和肌浆（3.68±0.35vs.3.54±0.35%/天)蛋白质合成率与野生型小鼠相比(均P>0.05)。
结论：线粒体氧化磷酸化和活性氧释放似乎并不代表在整个身体活动范围内调节肌肉蛋白质合成或肌肉质量调节的关键因素。
方法：我们检查了线粒体生物能学（氧化磷酸化和活性氧（H2O2）排放，ROS）在透化肌纤维中体外测量，代表了整个身体活动范围内综合每日肌肉蛋白质合成速率和骨骼肌质量变化的调节因素，包括自由生活和卧床休息条件：n=19健康，年轻男子(26±4岁，23.4±3.3kg/m2），并在12周的阻力型运动训练后：n=10名健康的老年男性（70±3岁，25.2±2.1kg/m2)。此外,我们评估了在转基因小鼠中减弱的线粒体ROS发射与整合的每日肌原纤维和肌浆蛋白合成速率之间的直接关系（线粒体靶向过氧化氢酶，MCAT）。
结果：在自由生活条件下或卧床休息1周后，健康年轻男性的氧化磷酸化和H2O2释放均与肌肉蛋白合成率无关（均P>0.05）。卧床休息后，GSSG浓度增加与骨骼肌质量损失增加相关（r=-0.49，P<0.05）。在年长的男人中，在运动训练过程中,只有次最大线粒体氧化磷酸化(校正线粒体含量)与肌原纤维蛋白合成率呈正相关(r=0.72,P<0.05)。然而,氧化磷酸化和H2O2排放的变化与训练后骨骼肌质量的变化无关(均P>0.05).此外,MCAT小鼠的肌原纤维无差异（2.62±0.22vs.2.75±0.15%/天）和肌浆（3.68±0.35vs.3.54±0.35%/天)蛋白质合成率与野生型小鼠相比(均P>0.05)。
结论：线粒体氧化磷酸化和活性氧释放似乎并不代表在整个身体活动范围内调节肌肉蛋白质合成或肌肉质量调节的关键因素。
