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已发表论文
有氧运动对睡眠剥夺小鼠心肌损伤的影响
Authors Zhao J, Zhang D, Li X, Zhu A
Received 12 August 2025
Accepted for publication 21 November 2025
Published 23 December 2025 Volume 2025:17 Pages 3181—3191
DOI https://doi.org/10.2147/NSS.S559465
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Marco Veneruso
Jiayi Zhao,1,2 Dongshan Zhang,3 Xiaozhou Li,3 Aiqun Zhu1,3
1Clinical Nursing Teaching and Research Section, The Second Xiangya Hospital of Central South University, Changsha, Hunan, People’s Republic of China; 2Xiangya Nursing School of Central South University, Changsha, Hunan, People’s Republic of China; 3Emergency Department, The Second Xiangya Hospital of Central South University, Changsha, People’s Republic of China
Correspondence: Aiqun Zhu, Clinical Nursing Teaching and Research Section, The Second Xiangya Hospital of Central South University, Changsha, Hunan, People’s Republic of China, Tel +86 731 85292120, Fax +86 731 82233525, Email zhuaiqun74@csu.edu.cn
Purpose: To investigate the effect of aerobic exercise on myocardial injury in sleep deprived mice, and explore the possible causative role.
Methods: Forty male C57BL/6J mice were randomly assigned to five groups (n=8/group): control (Ctrl), sleep deprivation for 7 or 28 days (SD7, SD28), and sleep deprivation with daily 7% weight-bearing exhaustion swimming for 7 or 28 days (SD+ES7, SD+ES28). Mental behavior was observed, cardiac markers were analyzed through blood biochemistry, and myocardial structures were examined using H&E staining.
Results: Compared to the Ctrl group, mice in each experimental group showed reduced body weight (p < 0.001). The levels of alpha-hydroxybutyrate dehydrogenase were significantly higher in the SD7 group (p < 0.01) and lower in the SD+ES7 group. Regarding creatine kinase expression, it was elevated in the SD7, SD28 and SD+ES28 groups (p < 0.05), but lower in the SD+ES7. Creatine kinase-MB was notably higher in the SD7 group (p < 0.01), and significantly reduced in the SD+ES7, SD28, and SD+ES28 groups (p < 0.01). High-sensitivity troponin T level was significantly higher only in the SD7 group (p < 0.01). Histological examination by H&E staining revealed varying degrees of cardiomyocyte swelling, morphological changes, widened intercellular spaces, disordered arrangement of myocardial fibers and infiltration of inflammatory cells in all experimental groups. Importantly, compared to the SD group at the corresponding time point, the SD+ES group showed attenuated pathological changes, with reduced myocardial edema. However, the SD+ES28 group still exhibited some inflammatory cell infiltration and perinuclear blank areas.
Conclusion: Sleep deprivation can cause myocardial ischemic injury and structural changes in cardiomyocytes, which is most prominent biochemically in the initial week. Daily exhaustion swimming, as an aerobic exercise, may have a short-term protective effect on the myocardium. With prolonged sleep deprivation, the compensatory mechanism of aerobic exercise may be exhausted.
Keywords: sleep deprivation, exhaustion swimming, myocardial injury
1Clinical Nursing Teaching and Research Section, The Second Xiangya Hospital of Central South University, Changsha, Hunan, People’s Republic of China; 2Xiangya Nursing School of Central South University, Changsha, Hunan, People’s Republic of China; 3Emergency Department, The Second Xiangya Hospital of Central South University, Changsha, People’s Republic of China
Correspondence: Aiqun Zhu, Clinical Nursing Teaching and Research Section, The Second Xiangya Hospital of Central South University, Changsha, Hunan, People’s Republic of China, Tel +86 731 85292120, Fax +86 731 82233525, Email zhuaiqun74@csu.edu.cn
Purpose: To investigate the effect of aerobic exercise on myocardial injury in sleep deprived mice, and explore the possible causative role.
Methods: Forty male C57BL/6J mice were randomly assigned to five groups (n=8/group): control (Ctrl), sleep deprivation for 7 or 28 days (SD7, SD28), and sleep deprivation with daily 7% weight-bearing exhaustion swimming for 7 or 28 days (SD+ES7, SD+ES28). Mental behavior was observed, cardiac markers were analyzed through blood biochemistry, and myocardial structures were examined using H&E staining.
Results: Compared to the Ctrl group, mice in each experimental group showed reduced body weight (p < 0.001). The levels of alpha-hydroxybutyrate dehydrogenase were significantly higher in the SD7 group (p < 0.01) and lower in the SD+ES7 group. Regarding creatine kinase expression, it was elevated in the SD7, SD28 and SD+ES28 groups (p < 0.05), but lower in the SD+ES7. Creatine kinase-MB was notably higher in the SD7 group (p < 0.01), and significantly reduced in the SD+ES7, SD28, and SD+ES28 groups (p < 0.01). High-sensitivity troponin T level was significantly higher only in the SD7 group (p < 0.01). Histological examination by H&E staining revealed varying degrees of cardiomyocyte swelling, morphological changes, widened intercellular spaces, disordered arrangement of myocardial fibers and infiltration of inflammatory cells in all experimental groups. Importantly, compared to the SD group at the corresponding time point, the SD+ES group showed attenuated pathological changes, with reduced myocardial edema. However, the SD+ES28 group still exhibited some inflammatory cell infiltration and perinuclear blank areas.
Conclusion: Sleep deprivation can cause myocardial ischemic injury and structural changes in cardiomyocytes, which is most prominent biochemically in the initial week. Daily exhaustion swimming, as an aerobic exercise, may have a short-term protective effect on the myocardium. With prolonged sleep deprivation, the compensatory mechanism of aerobic exercise may be exhausted.
Keywords: sleep deprivation, exhaustion swimming, myocardial injury