Effects of 8-Week High-Intensity Interval Training Intervention Regulating the SIRT1/PGC1α Pathway on Hippocampal Neuron Injury and Cognitive Impairment in Obese Rats

Abstract

Background

Obesity can causes changes in cognitive function, leading to cognitive impairment (CI).

Objectives

This study aimed to explore the effects of high-intensity interval training (HIIT) on hippocampal neuronal damage, cognitive function, and the SIRT1/PGC1α pathway in obese rats and provide a theoretical basis for HIIT intervention in improving CI caused by obesity.

Methods

Rats with successful obesity modeling and rats of the same age were randomly divided into a normal quiet group (CSG, n = 10), regular exercise group (CEG, n = 10), high-fat quiet group (HSG, n = 10), and high-fat exercise group (HEG, n = 10). Rats in the exercise group underwent an 8-week (8-wk) HIIT training. Subsequently, behavioral testing and sampling indicator testing were conducted.

Results

Compared with the normal quiet group, the exercise group showed a significant decrease in body weight and Lee index, whereas the obesity group showed a significant increase. The Morris water maze experiment showed that compared with the CSG, the HSG had a longer latency period and a reduced number of platform crossings. The latency period of the CEG was shortened, and the frequency increased. Compared with the HSG, the HEG had a shorter latency period and an increase in frequency. Organizational staining showed that the HSG had reduced neuron number, deepened staining, chaotic arrangement, and Nissl body lysis in the hippocampal CA1 region, whereas HIIT improved these pathological changes. RT-qPCR showed obesity reduces the mRNA level of Sirt1 gene in hippocampal tissue, whereas exercise increases it. Western blot analysis showed exercise and obesity independently regulate the SIRT1/PGC1α pathway: exercise upregulates its expression, whereas obesity downregulates its expression.

Conclusions

An 8-wk HIIT can reduce hippocampal neuronal damage and CI in obese rats, and the specific mechanism may improve neuronal pathological damage and restore cognitive function by activating the SIRT1/PGC1α pathway.