Abstract
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.