| ORIGINAL ARTICLE |
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| Year : 2022 | Volume
: 65
| Issue : 6 | Page : 290-300 |
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Optimization of exercise preconditioning duration in protecting from exhausted exercise-induced cardiac injury in rats
Zheng Ping, Jinyu Li, Yawei Sun, Xiaoli Zhang, Ziwen Wang, Xuebin Cao
Department of Cardiology and Nephrology, The 82nd Group Army Hospital of PLA (252 Hospital of PLA), Baoding, Hebei, China
Correspondence Address:
Prof. Xuebin Cao
Department of Cardiology and Nephrology, the 82nd Group Army Hospital of PLA, No. 991 Baihua East Road, Lianchi District, Baoding, Hebei
China
Dr. Ziwen Wang
Department of Cardiology and Nephrology, the 82nd Group Army Hospital of PLA, No. 991 Baihua East Road, Lianchi District, Baoding, Hebei
China
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/0304-4920.365457
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The effect of different duration of exercise preconditioning (EP) on protecting from exhaustive exercise-induced cardiac injury (EECI) has been optimized in rats. Male Sprague-Dawley rats were divided into six groups: the control group, exhaustive exercise (EE) group, EP 20-min + EE group, EP 40-min + EE group, EP 60-min + EE group and EP 80-min + EE group. The EP groups were subjected to treadmill running at the intensity of 74.0% V̇O2 max. Changes of exercise capacity, cardiac pathology, myocardial enzymology, electrocardiogram (ECG), cardiac function, and mitochondrial respiratory function were compared. Compared to the C group, the EE group has shown significant decrease of exercise capacity, elevation of serum N-terminal pro B-type natriuretic peptide (NT-proBNP) and cardiac troponin-I (cTn-I) levels, cardiac morphology change, ECG disturbance, cardiac dysfunction and reduction of myocardial mitochondrial respiration function. Compared to the EE group, the EP groups have shown significant elevation of exercise capacity, decrease of serum NT-proBNP and cTn-I, improvement of cardiac function and myocardial mitochondrial electron transfer pathway complex I, II and IV activity. The correlation analyses showed protection of EP was proportional to EP duration from 20-min to 60-min. EE caused cardiac injury. EP could protect from EECI by alleviating myocardial damage, improving cardiac function and mitochondrial ETP complex I, II and IV activity. EP protection was positively correlated to EP duration from 20-min to 60-min with EP intensity fixed at 74.0% V̇O2 max.
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