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Background <p>Visceral adipose tissue (VAT) is strongly associated with metabolic diseases. Both high-intensity interval training (HIT) and moderate-intensity training (MIT) reduce VAT effectively; however, HIT might mediate greater VAT loss in females. The estrogen receptor α (ERα) pathway may play a key role. The aim of the present study was to confirm the role of adipose/hypothalamic ERα in HIT/MIT-mediated VAT loss, as well as the associated hypothalamic electrophysiology and body catabolism changes in pre- and post-menopausal animal models.</p> Methods <p>Ovariectomy (OVX) or sham surgeries were conducted to establish pre/postmenopausal female rat models. After distance-matched long-term HIT and MIT interventions, ERα expression in hypothalamic/VAT, as well as food intake, spontaneous physical activity (SPA), VAT mass and morphology, local field potential (LFPs) in paraventricular nuclei (PVN) and excessive post-exercise oxygen consumption (EPOC), were observed. A target chemical block during the post-exercise recovery period was executed to further verify the role of the hypothalamic ERα pathway.</p> Results <p>HIT enhanced the expression of ERα in the hypothalamus rather than VAT in the pre-, but not the postmenopausal group, which was accompanied by elevated LFP power density in α and β bands, enhanced EPOC and larger VAT loss than MIT. Chemical blockade of ERα suppressed EPOC and VAT catabolism mediated by HIT.</p> Conclusion <p>During the post-exercise recovery period, the hypothalamic ERα pathway involved in HIT induced EPOC elevation and VAT reduction in premenopausal female rats.</p>

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The hypothalamic estrogen receptor α pathway is involved in high-intensity interval training-induced visceral fat loss in premenopausal rats

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年3月27日

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  • Juanjuan Wang,
  • Shuai Tian,
  • Jinchan Du,
  • Sihao Du,
  • Wei Chen,
  • Yang Liu

摘要

Background

Visceral adipose tissue (VAT) is strongly associated with metabolic diseases. Both high-intensity interval training (HIT) and moderate-intensity training (MIT) reduce VAT effectively; however, HIT might mediate greater VAT loss in females. The estrogen receptor α (ERα) pathway may play a key role. The aim of the present study was to confirm the role of adipose/hypothalamic ERα in HIT/MIT-mediated VAT loss, as well as the associated hypothalamic electrophysiology and body catabolism changes in pre- and post-menopausal animal models.

Methods

Ovariectomy (OVX) or sham surgeries were conducted to establish pre/postmenopausal female rat models. After distance-matched long-term HIT and MIT interventions, ERα expression in hypothalamic/VAT, as well as food intake, spontaneous physical activity (SPA), VAT mass and morphology, local field potential (LFPs) in paraventricular nuclei (PVN) and excessive post-exercise oxygen consumption (EPOC), were observed. A target chemical block during the post-exercise recovery period was executed to further verify the role of the hypothalamic ERα pathway.

Results

HIT enhanced the expression of ERα in the hypothalamus rather than VAT in the pre-, but not the postmenopausal group, which was accompanied by elevated LFP power density in α and β bands, enhanced EPOC and larger VAT loss than MIT. Chemical blockade of ERα suppressed EPOC and VAT catabolism mediated by HIT.

Conclusion

During the post-exercise recovery period, the hypothalamic ERα pathway involved in HIT induced EPOC elevation and VAT reduction in premenopausal female rats.