Gungor-Orhan Irem, Akin Senay, Powers Scott K, Olgaz-Bingol Seda, Demirel Haydar A
Department of Exercise and Sport Sciences, Exercise and Sport Physiology Division, Faculty of Sport Sciences, Hacettepe University, Ankara, Türkiye.
Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida, USA.
Exp Physiol. 2025 Jun;110(6):857-865. doi: 10.1113/EP092331. Epub 2025 Jan 29.
Abundant evidence indicates that skeletal muscle plays a key role in regulating metabolic homeostasis. Therefore, maintaining healthy skeletal muscles is essential to good health. While prolonged muscle inactivity is known to cause oxidative stress and muscle loss, it remains unclear whether a shift from an active to a sedentary lifestyle induces similar effects. This study tested the hypothesis that transitioning to a sedentary lifestyle rapidly leads to oxidative stress and muscle loss in the load-bearing soleus muscle. Adult Wistar rats were randomly divided into control (CON; n = 8) and sedentary (SED; n = 8) groups. During a 7-day experimental period, CON rats were housed in standard cages allowing free movement, while SED rats were confined to smaller cages promoting sedentary behaviour. Soleus muscles were analysed for antioxidant enzyme activities (superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX)), as well as two oxidative stress biomarkers (advanced protein oxidation products (AOPPs) and 4-hydroxynonenal (4-HNE)). Sedentary behaviour caused a 17.2% reduction in the soleus-to-body weight ratio (P < 0.001). Moreover, the activities of SOD, CAT and GPX were significantly lower in the soleus muscle of SED animals (P < 0.05), while AOPPs and 4-HNE levels were higher (P < 0.001 and P < 0.05) compared to CON animals. These findings provide the first evidence that transitioning from an active to a sedentary lifestyle leads to the rapid onset of oxidative stress and atrophy in the soleus muscle. Importantly, the results suggest that impaired antioxidant defences contribute to sedentary behaviour-induced oxidative stress in load-bearing muscles.
大量证据表明，骨骼肌在调节代谢稳态中起关键作用。因此，保持健康的骨骼肌对良好的健康状况至关重要。虽然已知长时间的肌肉不活动会导致氧化应激和肌肉流失，但从活跃生活方式转变为久坐生活方式是否会产生类似影响仍不清楚。本研究检验了这样一个假设，即转变为久坐生活方式会迅速导致承重比目鱼肌出现氧化应激和肌肉流失。成年Wistar大鼠被随机分为对照组（CON；n = 8）和久坐组（SED；n = 8）。在为期7天的实验期内，CON组大鼠饲养在标准笼中，可自由活动，而SED组大鼠被限制在较小的笼子里，以促进久坐行为。分析了比目鱼肌的抗氧化酶活性（超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶（GPX）），以及两种氧化应激生物标志物（晚期蛋白质氧化产物（AOPPs）和4-羟基壬烯醛（4-HNE））。久坐行为导致比目鱼肌与体重之比降低了17.2%（P < 0.001）。此外，与CON组动物相比，SED组动物比目鱼肌中SOD、CAT和GPX的活性显著降低（P < 0.05），而AOPPs和4-HNE水平则更高（P < 0.001和P < 0.05）。这些发现首次证明，从活跃生活方式转变为久坐生活方式会导致比目鱼肌迅速出现氧化应激和萎缩。重要的是，结果表明抗氧化防御受损是久坐行为导致承重肌肉氧化应激的原因。
