With the rise in physical inactivity and its related diseases, it is necessary to understand the mechanisms involved in physical activity regulation. Biological factors regulating physical activity are studied to establish a possible target for improving the physical activity level. However, little is known about the role metabolism plays in physical activity regulation. Therefore, we studied protein fractional synthesis rate (FSR) of multiple organ tissues of 12-week-old male mice that were previously established as inherently low-active (n = 15, C3H/HeJ strain) and high-active (n = 15, C57L/J strain). Total body water of each mouse was enriched to 5% deuterium oxide (D₂O) via intraperitoneal injection and maintained with D₂O enriched drinking water for about 24 h. Blood samples from the jugular vein and tissues (kidney, heart, lung, muscle, fat, jejunum, ileum, liver, brain, skin, and bone) were collected for enrichment analysis of alanine by LC-MS/MS. Protein FSR was calculated as -ln(1-enrichment). Data are mean±SE as fraction/day (unpaired t-test). Kidney protein FSR in the low-active mice was 7.82% higher than in high-active mice (low-active: 0.1863±0.0018, high-active: 0.1754±0.0028, p = 0.0030). No differences were found in any of the other measured organ tissues. However, all tissues resulted in a generally higher protein FSR in the low-activity mice compared to the high-activity mice (e.g. lung LA: 0.0711±0.0015, HA: 0.0643±0.0020, heart LA: 0.0649± 0.0013 HA: 0.0712±0.0073). Our observations suggest that high-active mice in most organ tissues are no more inherently equipped for metabolic adaptation than low-active mice, but there may be a connection between protein metabolism of kidney tissue and physical activity level. In addition, low-active mice have higher organ-specific baseline protein FSR possibly contributing to the inability to achieve higher physical activity levels.

随着缺乏体育活动及其相关疾病的增加，有必要了解参与体育活动调节的机制。研究调节体育活动的生物因素，以建立提高体育活动水平的可能目标。然而，关于代谢在体育活动调节中所起的作用知之甚少。因此，我们研究了12周龄雄性小鼠多器官组织的蛋白质分数合成速率（FSR），这些小鼠先前被确定为固有的低活性（n = 15，C3H / HeJ株）和高活性（n = 15 ，C57L / J株）。通过腹膜内注射将每只小鼠的体内总水富集至5％氧化氘（D ₂ O），并维持D ₂富含O的饮用水约24小时。收集来自颈静脉和组织（肾脏，心脏，肺，肌肉，脂肪，空肠，回肠，肝脏，脑，皮肤和骨骼）的血样，通过LC-MS / MS进行丙氨酸富集分析。蛋白FSR计算为-ln（1-富集）。数据为平均值±标准误/天（未配对t检验）。低活性小鼠的肾脏蛋白FSR比高活性小鼠高7.82％（低活性：0.1863±0.0018，高活性：0.1754±0.0028，p = 0.0030）。在任何其他测得的器官组织中均未发现差异。但是，与高活性小鼠相比，所有组织在低活性小鼠中产生的蛋白质FSR通常较高（例如，肺LA：0.0711±0.0015，HA：0.0643±0.0020，心脏LA：0.0649±0.0013 HA：0.0712±0.0073 ）。我们的观察结果表明，大多数器官组织中的高活性小鼠没有比低活性小鼠固有地适应代谢的能力，但肾脏组织的蛋白质代谢与身体活动水平之间可能存在联系。此外，低活性小鼠具有更高的器官特异性基线蛋白FSR，可能导致无法实现更高的身体活动水平。