期刊
FASEB JOURNAL
卷 35, 期 10, 页码 -出版社
WILEY
DOI: 10.1096/fj.202100868R
关键词
detraining; lifelong exercise; lipolysis; mitochondrial function; SASP
资金
- National Natural Science Foundation of China [31971099]
- Postgraduate Research & Practice Innovation Program of Jiangsu Province [KYCX21_1313]
The study found that lifelong exercise significantly improved mitochondrial function, SASP-associated inflammation, and lipolysis, inhibiting inflammatory regulation pathways. Detraining, on the other hand, activated the NF-kappa B signaling pathway and elevated serum high-sensitivity C-reactive protein levels.
The primary aims of this study were to determine the effects of lifelong exercise and detraining on age-related alterations in mitochondrial function, inflammation associated with senescence-associated secretory phenotype (SASP), and lipolysis in the perirenal fat and liver of rats. Female Sprague-Dawley rats were randomly assigned to four groups: young control (n = 12), old control (n = 12), detraining (n = 12), and lifelong exercise (n = 12). We then investigated mitochondrial function, SASP-associated inflammation, and lipolysis in the perirenal fat and liver using qRT-PCR and western blotting to assess the expression of AKT, hypoxia-inducible factor 1 alpha (HIF-1 alpha), nuclear factor-kappa B (NF-kappa B), c-jun kinase (JNK), and p38 mitogen-activated protein kinase (p38MAPK). In the tissues of both the perirenal fat and liver, lifelong exercise significantly improved mitochondrial function, SASP-associated inflammation, and lipolysis. Meanwhile, pathways associated with inflammatory regulation were inhibited, predominantly via the activation of phosphorylated-AKT (p-AKT) and suppression of HIF-1 alpha in both tissues, and via JNK in the perirenal fat and p38MAPK in the liver. Furthermore, detraining activated NF-kappa B expression in both tissues and induced the upregulation of serum high-sensitivity C-reactive protein (hsCRP) levels. Collectively, lifelong exercise was found to exert beneficial effects by ameliorating age-related alterations in mitochondrial function, SASP-associated inflammation, and lipolysis in perirenal fat and liver tissues, potentially inhibiting inflammation via the JNK and p38 MAPK pathways, respectively, as well as the HIF-1 alpha and AKT pathways in both tissues. In contrast, detraining induced high levels of circulating hsCRP by activating the NF-kappa B signaling pathway in both tissues.
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