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

Baishuo Cheng; Jinchan Du; Shuai Tian; Zixiong Zhang; Wei Chen; Yang Liu

doi:10.1186/s12944-024-02397-2

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

Lipids Health Dis. 2024 Dec 18;23(1):405. doi: 10.1186/s12944-024-02397-2.

Authors

Baishuo Cheng^#¹, Jinchan Du^#¹, Shuai Tian¹, Zixiong Zhang¹, Wei Chen^{1

2}, Yang Liu^{3

4}

Affiliations

¹ Physical Education College, Hebei Normal University, Shijiazhuang, China.
² 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.
³ Physical Education College, Hebei Normal University, Shijiazhuang, China. liuyang1982@hebtu.edu.cn.
⁴ 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. liuyang1982@hebtu.edu.cn.

^# Contributed equally.

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.

MeSH terms

Animals
Brain-Derived Neurotrophic Factor* / metabolism
Female
High-Intensity Interval Training* / methods
Intra-Abdominal Fat* / metabolism
Lactic Acid*
Lipolysis / drug effects
Neuronal Plasticity* / drug effects
Neuronal Plasticity* / physiology
Oxygen Consumption / drug effects
Physical Conditioning, Animal*
Rats
Rats, Sprague-Dawley
Ventromedial Hypothalamic Nucleus / drug effects
Ventromedial Hypothalamic Nucleus / metabolism

Substances

Lactic Acid
Brain-Derived Neurotrophic Factor