Cheng Baishuo, Du Jinchan, Tian Shuai, Zhang Zixiong, Chen Wei, Liu Yang
Physical Education College, Hebei Normal University, Shijiazhuang, China.
Provincial Key Lab of Measurement and Evaluation in Human Movement and Bio-Information, Hebei Normal University, No. 20, South Second Ring Road East, Shijiazhuang, Hebei, China.
Lipids Health Dis. 2024 Dec 18;23(1):405. doi: 10.1186/s12944-024-02397-2.
High-intensity interval training (HIT) does not burn fat during exercise. However, it significantly reduces visceral adipose after long-term training. The underlying mechanism may be related to the elevation of fat consumption during the post-exercise recovery period, which is regulated by the hypothalamus-adipose axis. Lactate is a hallmark metabolite of high-intensity exercise, which could mediate significant neuroplasticity through the brain-derived neurotrophic factor (BDNF) pathway. However, whether HIT could enhance hypothalamus activity and adipose catabolism in the recovery period remains to be elucidated. Also, it is worth exploring whether adding lactate administration to prolonged, continuous submaximal aerobic training (AT) could simulate HIT-induced neuroplastic effects and fat loss.
First, we compared the influence of 4-week HIT and aerobic training (AT) on the electrophysiology of the ventromedial hypothalamus (VMH), which is deeply involved in the regulation of lipolysis, as well as the 24-hour excess post-exercise oxygen consumption (EPOC), the fat oxidation rate and lipolysis. To further confirm whether excess lactate during AT could reproduce the effect of HIT, we also observed the effects of lactate infusion during AT (AT + Lac) on neuroplasticity and metabolism.
Four-week HIT induced higher BDNF expression and a higher neuronal spike firing rate in VMH than AT, accompanied by elevated EPOC, fat oxidation and visceral fat lipolysis. AT + Lac and HITT could induce similar hypothalamic and metabolic changes. However, power spectral density analysis of local field potentials (LFPs) showed that the AT + Lac group was affected in fewer frequency bands than the HIT group.
HIT-induced reduction of visceral fat was accompanied by increased VMH activity. Adding lactate administration to AT could partially reproduce hypothalamic plasticity and the metabolic effects of HIT. However, different band changes of LFPs implied that the neuronal subpopulations or pathways influenced by these two methods were not entirely consistent.
高强度间歇训练（HIT）在运动过程中并不燃烧脂肪。然而，长期训练后它能显著减少内脏脂肪。其潜在机制可能与运动后恢复期脂肪消耗的增加有关，这一过程受下丘脑 - 脂肪轴调控。乳酸是高强度运动的标志性代谢产物，它可通过脑源性神经营养因子（BDNF）途径介导显著的神经可塑性。然而，HIT是否能在恢复期增强下丘脑活性和脂肪分解代谢仍有待阐明。此外，在长时间、持续的次最大强度有氧运动（AT）中添加乳酸给药是否能模拟HIT诱导的神经可塑性效应和脂肪减少也值得探索。
首先，我们比较了4周的HIT和有氧运动（AT）对腹内侧下丘脑（VMH）电生理的影响，VMH深度参与脂肪分解的调节，同时比较了24小时运动后过量耗氧量（EPOC）、脂肪氧化率和脂肪分解情况。为进一步确认AT期间过量乳酸是否能重现HIT的效果，我们还观察了AT期间乳酸输注（AT + Lac）对神经可塑性和代谢的影响。
4周的HIT比AT诱导VMH中更高的BDNF表达和更高的神经元放电频率，同时伴有EPOC升高、脂肪氧化和内脏脂肪分解增加。AT + Lac和HITT可诱导相似的下丘脑和代谢变化。然而，局部场电位（LFP）的功率谱密度分析表明，AT + Lac组受影响的频段比HIT组少。
HIT诱导的内脏脂肪减少伴随着VMH活性增加。在AT中添加乳酸给药可部分重现下丘脑可塑性和HIT的代谢效应。然而，LFP不同频段的变化表明这两种方法影响的神经元亚群或途径并不完全一致。
