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High-intensity interval training for treating pathological cardiac hypertrophy in spontaneously hypertensive rats: Effects and mechanisms / 中国组织工程研究
Chinese Journal of Tissue Engineering Research ; (53): 3708-3715, 2020.
Article in Chinese | WPRIM | ID: wpr-847447
ABSTRACT

BACKGROUND:

Regular exercise training possesses health promotion effect. Low-to-moderate intensity continuous aerobic exercise has been an important strategy for primary and secondary prevention of chronic diseases such as hypertension; however, the effect of high-intensity interval training is still debated.

OBJECTIVE:

To explore the effects of high-intensity interval training on pathological cardiac hypertrophy and investigate the possible mechanism in spontaneously hypertensive rats.

METHODS:

Thirty male spontaneously hypertensive rats were randomly assigned into a control group and a training group. Fifteen Wistar-Kyoto rats were used as normotensive group. Rats in the normotensive and control group were housed at rest, while those in the training group were subjected to a high-intensity interval training lasting for 8 weeks. After experiment, blood pressure was detected using a non-invasive blood pressure tester, and cardiac structure and function were measured by echocardiogram. Histopathological detection was performed by hematoxylin-eosin and Masson staining to determine myocardial cross-sectional area. mRNA expression of fetal genes including atrial natriuretic peptide and brain natriuretic peptide were detected by RT-PCR. Protein expression of PI3-K, Akt, CnAβ and NFATc3 was detected using western blot assay. RESULTS AND

CONCLUSION:

Compared with the normotensive group, the blood pressure level was significantly elevated (P 0.05) in the control group. Compared with the control group, the blood systolic pressure was lowered (P 0.05). Therefore, the 8-week high-intensity interval training can induce the transfer from pathological hypertrophy to physiological hypertrophy and enhance heart function in spontaneously hypertensive rats via the activation of PI3-K/Akt signal transduction pathway; however, the Cn/NFAT pathway cannot be inhibited.

Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Tissue Engineering Research Year: 2020 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Tissue Engineering Research Year: 2020 Type: Article