Impacts of Aerobic Exercise on Depression-Like Behaviors in Chronic Unpredictable Mild Stress Mice and Related Factors in the AMPK/PGC-1α Pathway

Abstract

This study was to study the impact of aerobic exercises on the chronic unpredictable mild stress (CUMS) in mice, and to discuss the possible mechanism from the skeletal muscle AMPK/PGC-1α energy metabolism signaling pathway. The healthy male mice were randomly divided into Control Group (CG), Model Group (MG), and Model Exercise Group (ME).Twelve stress methods were adopted for four weeks (28 days) to establish the depression model. ME was subject to aerobic training plan after the model was established. The weight of the mice was recorded weekly. After the experimental intervention, the three groups of mice were subjected to behavioral assessment tests. Western blotting, RT-PCR, and ELISA were performed to test AMPK, p-AMPK, PGC-1α, and ATP in skeletal muscle. There were no significant difference in body weight between the three groups. CUMS leaded to significant decline in behavioral scores. and the p-AMPK and PGC-1α decreased significantly. But boosted ATP content. Aerobic exercise enhanced the expressions of p-AMPK and PGC-1α, increased the ratio of p-AMPK/AMPK, boosted ATP content. And improved behavioral scores significantly. Chronic stress-induced depression-like behavior was improved significantly by Aerobic exercise. The mechanism of aerobic exercise for improving depressive symptoms in mice with chronic stress depression may be related to influence AMPK/PGC-1α pathway.

Acute Interval and Continuous Moderate Intensity Exercise Enhanced Circadian Thermogenic Activity through Browning related Genes in Obese Adolescent Female

“…Importantly, the correlation analysis results in this study indicate a negative relationship between thermogenic gene expression and physiological and oxidative stress (Table 3 and Figure 6). Physiological stress reduces ATP, increases the ATP/AMP ratio, and activates AMPK, thereby inhibiting PGC-1α expression [72]. It also causes metabolic disorders and lowers immunity [73], and is a risk factor for increased disease and a cause for exercise maladaptations [74].…”

Aerobic Exercise Prevents Depression via Alleviating Hippocampus Injury in Chronic Stressed Depression Rats

“…Recent studies have shown that AE improved depression-like behaviors or depressive symptoms in CUMS animal models [ 4 , 11 , 36 ]. Ryan et al [ 37 ] found that an 8-week moderate-intensity aerobic exercise training intervention reduced depressive symptoms among individuals with major depressive disorder.…”

“…Over the last decade, studies have shown favorable effects of exercise on the treatment and rehabilitation of mental and cerebral diseases [ 7 , 8 , 9 ], considering exercise as a nonpharmacological and efficacious approach for the prevention and management of depression [ 4 , 8 , 10 ]. There have been many pieces of research on anti-depression effects of exercise in recent years; however, underlying mechanisms remain obscure [ 7 , 8 , 11 , 12 ]. Previous studies showed that aerobic exercise (AE) could stimulate neuron regeneration, regulate neurotrophin such as brain-derived neurotrophic factor (BDNF) and improve the plasticity of the brain [ 13 , 14 ].…”

“…Previous studies showed that aerobic exercise (AE) could stimulate neuron regeneration, regulate neurotrophin such as brain-derived neurotrophic factor (BDNF) and improve the plasticity of the brain [ 13 , 14 ]. Luo et al [ 11 ] recently reported beneficial effects of AE on depression-like behaviors in chronic unpredictable mild stress (CUMS) mice and enhanced the expressions of p-AMPK and PGC-1alpha, the ratio of p-AMPK/AMPK, and boosted ATP content. Consistently, our recent study also reported the benefits of 8 week AE on improvement of CUMS–induced depressive behavior, neuron injury, and synaptic plasticity [ 15 ].…”

“…Depression development is not only associated with neurotransmitters and their receptors in the brain, but also involves into post-receptor signal transduction systems and gene transcription processes associated with neurotrophic disorders and reduction of neuroplasticity in specific brain regions [ 11 , 16 , 17 , 18 ]. Specifically, glutamatergic abnormalities have recently been implicated in the pathophysiology of depression.…”