High-intensity interval training or lactate administration combined with aerobic training enhances visceral fat loss while promoting VMH neuroplasticity in female rats.

Abstract

Background: 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.

Methods: 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.

Results: 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.

Conclusion: 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.