Sontam Tarun, Deutz Nicolaas E P, Cruthirds Clayton L, Mbilinyi Robert, Ruebush Laura E, Ten Have Gabriella Am, Thaden John J, Engelen Mariёlle P K J
Center for Translational Research in Aging & Longevity, Dept of Kinesiology and Sport Management, Texas A&M University, College Station, TX, USA; Department of Medical Education, Texas A&M School of Medicine, College Station, TX, USA.
Center for Translational Research in Aging & Longevity, Dept of Kinesiology and Sport Management, Texas A&M University, College Station, TX, USA; Department of Primary Care & Rural Medicine, Texas A&M School of Medicine, College Station, TX, USA.
Clin Nutr. 2025 Jun;49:21-32. doi: 10.1016/j.clnu.2025.03.021. Epub 2025 Apr 8.
BACKGROUND & AIMS: Disturbances in arginine (ARG) and protein metabolism, as well as in gut function have been observed in response to an endurance exercise session in patients with Chronic Obstructive Pulmonary Disease (COPD). We studied whether resistance exercise also affects the acute response in arginine (role in nitric oxide synthesis), citrulline (CIT, marker of gut health), and (muscle) protein metabolism differently in COPD as compared to healthy older adults.
Patients with stable moderate to severe COPD (n = 24) and healthy controls (n = 25) completed a high-intensity resistance exercise session in the postabsorptive state. We administered a pulse of multiple stable isotopes of amino acids before, and 1 h and 24 h post-resistance exercise to assess the whole body production (WBP) and intracellular productions by compartmental analysis of ARG and CIT, and of tau-methylhistidine (TauMETHIS), phenylalanine (PHE), tyrosine (TYR), and PHE > TYR conversion as markers of muscle (myofibrillar) protein breakdown and whole body (net) protein breakdown, respectively. Muscle fatigue was determined by assessing the decay in peak leg extension torque post-resistance exercise.
COPD patients overall exhibited lower WBP ARG (p < 0.0001), CIT (p < 0.0001), PHE (p = 0.0001), TYR (p < 0.0001), and tau-METHIS (p = 0.0004) compared to controls. Resistance exercise did not change WBP of PHE, tau-METHIS, or PHE > TYR conversion, despite prolonged muscle fatigue in COPD. WBP CIT was increased at 1- and 24-h post-exercise in both groups (p < 0.003). Plasma CIT concentrations were reduced in both groups (p < 0.006) and remained lower at 24 h post-exercise in COPD only (p < 0.05) despite a third less work performed.
Both COPD and healthy participants exhibited upregulated whole-body citrulline production following resistance exercise. However, in COPD, this increase was insufficient to counteract the sustained reduction in plasma citrulline concentration, despite performing significantly less work during the exercise session. This prolonged disturbance in citrulline metabolism in COPD points to a potential exercise-induced enterocyte dysfunction, highlighting a novel area for understanding the impact of resistance exercise on gut health in this population.
Trial registration ClinicalTrials.gov: NCT02780219.
慢性阻塞性肺疾病（COPD）患者在进行耐力运动后，已观察到精氨酸（ARG）和蛋白质代谢以及肠道功能紊乱。我们研究了与健康老年人相比，抗阻运动是否也会对COPD患者的精氨酸（在一氧化氮合成中的作用）、瓜氨酸（CIT，肠道健康标志物）和（肌肉）蛋白质代谢的急性反应产生不同影响。
稳定的中度至重度COPD患者（n = 24）和健康对照者（n = 25）在空腹状态下完成一次高强度抗阻运动。在抗阻运动前、运动后1小时和24小时给予氨基酸多种稳定同位素脉冲，通过对ARG和CIT以及τ-甲基组氨酸（TauMETHIS）、苯丙氨酸（PHE）、酪氨酸（TYR）的区室分析来评估全身生成（WBP）和细胞内生成，并以PHE > TYR转化分别作为肌肉（肌原纤维）蛋白质分解和全身（净）蛋白质分解的标志物。通过评估抗阻运动后腿部伸展峰值扭矩的衰减来确定肌肉疲劳。
与对照组相比，COPD患者总体上WBP ARG（p < 0.0001）、CIT（p < 0.0001）、PHE（p = 0.0001）、TYR（p < 0.0001）和τ-METHIS（p = 0.0004）较低。尽管COPD患者肌肉疲劳持续时间较长，但抗阻运动并未改变PHE、τ-METHIS的WBP或PHE > TYR转化。两组运动后1小时和24小时WBP CIT均增加（p < 0.003）。两组血浆CIT浓度均降低（p < 0.006），尽管COPD患者运动工作量减少三分之一，但仅在运动后24小时仍较低（p < 0.05）。
COPD患者和健康参与者在抗阻运动后全身瓜氨酸生成均上调。然而，在COPD患者中，尽管运动期间工作量明显较少，但这种增加不足以抵消血浆瓜氨酸浓度的持续降低。COPD患者瓜氨酸代谢的这种长期紊乱表明存在潜在的运动诱导肠细胞功能障碍，突出了一个理解抗阻运动对该人群肠道健康影响的新领域。
试验注册ClinicalTrials.gov：NCT02780219。
