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.

Keywords: High-intensity interval training; LFPs; Lactate; VMH; Visceral fat.

Fig. 1

Main experimental procedures (figure generated by Figdraw2.0)

Fig. 2

Body weight, food intake, VAT and lactate during and after Exp. 1. A Body weight changes during the 4-week training; B Periuterine fat mass (representing visceral fat); C Changes in food intake during the 4-week training; D Total food intake; E OFT trajectory and horizontal moving distance; F Lactate levels immediately after training. +: Time×Group, P<0.05; *: HIT vs Control, P<0.05; **: HIT vs control, P<0.01; #: HIT vs AT, P<0.05; ##: HIT vs AT, P<0.01; &&: AT vs Control group, P<0.01

Fig. 3

1–24-Hour EPOC and HSL-ser660 phosphorylation in Exp. 1. A Changes in oxygen uptake within 24 hours post-exercise; B, C and D Total oxygen uptake during 1–12, 12–24 and 1–24 hours post-exercise; E Changes in fat oxidation rate within 24 hours post-exercise; F, G and H Total fat oxidation during 1–12, 12–24 and 1–24 hours post-exercise; I Respiratory quotient (RQ) within 24 hours post-exercise; J Serum glycerol concentration; K Glycerol concentration of periuterine fat; L HSL-ser660 phosphorylated expression. +: Time×Group, P<0.05; *: HIT vs Control, P<0.05; **: HIT vs Control, P<0.01; #: HIT vs AT, P<0.05; ##: HIT vs AT, P<0.01; &: AT vs control, P<0.05

Fig. 4

LFPs, spike firing rate, and BDNF expression of VMH in Exp. 1. A Spike firing point for 150 s; B Spike firing counts; C LFPs spectrogram of the VMH for 3 min; D-E Power spectral density distribution and integration of δ-γ bands; F IHC images of BDNF in the VMH (red: BDNF, blue: DAPI); G Number of BDNF positive cells; H Optical density of BDNF. *: HIT vs Control, P<0.05. **: HIT vs Control, P<0.01; #: HIT vs AT, P<0.05; ##: HIT vs AT, P<0.01; &: AT vs Control, P<0.05; &&: AT vs Control, P<0.01

Fig. 5

Body weight and food intake during and after Exp. 2. A Body weight changes during the 4-week training; B Periuterine fat mass (representing visceral fat); C Changes in food intake during the 4-week training; D Total food intake. +: Time×Group, P<0.05; *: AT+Lac vs Control, P<0.05; #: AT+Lac vs AT+saline, P<0.05; ##: AT+Lac vs AT+saline, P<0.01

Fig. 6

1–24-Hour EPOC and HSL-ser660 phosphorylation in Exp. 2. A Changes in oxygen uptake within 24 hours post-exercise; B, C and D Total oxygen uptake during 1–12, 12–24 and 1–24 hours post-exercise; E Changes in fat oxidation rate within 24 hours post-exercise; F, G and H Total fat oxidation during 1–12, 12–24 and 1–24 hours post-exercise; I Respiratory quotient (RQ) within 24 hours post-exercise; J Serum glycerol concentration; K Glycerol concentration of periuterine fat; L HSL-ser660 phosphorylated expression. +: Time×Group, P<0.05; *: AT+Lac vs Control, P<0.05; **: AT+Lac vs Control, P<0.01; #: AT+Lac vs AT+Saline, P<0.05; ##: AT+Lac vs AT+Saline, P<0.01

Fig. 7

LFPs, spike firing rate and BDNF expression of VMH in Exp. 2. A Spike firing point for 150 seconds; B Spike firing counts; C LFP spectrogram of the VMH for 3 minutes; D-E Power spectral density distribution and integration of δ-γ bands; F IHC images of BDNF in the VMH (red: BDNF, blue: DAPI); G Number of BDNF positive cells; H Optical density of BDNF. *: AT+Lac vs Control, P<0.05; #: AT+Lac vs AT-saline, P<0.05; &: AT+Saline vs Control, P<0.05