Prolonged periods of sedentary behaviour, for instance, engendered by home confinement in Shenzhen city, has led to negative mental health consequences, especially in adolescents. Previous research suggests, in general, that sedentary behavior can increase negative emotions. However, the specific mechanism driving the relationship between sedentary behavior and negative emotions is still relatively unclear. Social support and sleep quality might partly explain the effect of sedentary behavior on negative emotions. Thus, the current study aimed to examine the associations between sedentary behavior and negative emotions, and to investigate if social support and sleep quality mediate such a relationship. During home confinement due to the COVID-19 Omicron variant outbreak, 1179 middle and high school students in Shenzhen were invited to voluntarily complete an e-questionnaire, including the 21-item Depression Anxiety Stress Scale (DASS-21), the short form of the International Physical Activity Questionnaire (IPAQ-SF), the Social Support Rating Scale (SSRS) and the Pittsburgh Sleep Quality Index (PSQI). Data from 1065 participants were included in the analysis. We observed significant sex-related and demografic-related differences in emotional (e.g., anxiety, stress and social support) and other outcome variables (e.g., sitting duration and PSQI score). Furthermore, sedentary behavior, social support, and sleep quality were associated with negative emotions (p < .01), even after controlling for sex, age, only-child case, body mass index, and metabolic equivalent level. In addition, social support and sleep quality partially mediated the association between sedentary behavior and negative emotions. The findings of the current study suggest that social support and sleep quality partially mediate the relationship between sedentary behavior and negative emotions in middle and high school students during home confinement in Shenzhen city.

Neuropsychiatric disorders shorten human life spans through multiple ways and become major threats to human health. Exercise can regulate the estrogen signaling, which may be involved in depression, Alzheimer's disease (AD) and Parkinson's disease (PD), and other neuropsychiatric disorders as well in their sex differences. In nervous system, estrogen is an important regulator of cell development, synaptic development, and brain connectivity. Therefore, this review aimed to investigate the potential of estrogen system in the exercise intervention of neuropsychiatric disorders to better understand the exercise in neuropsychiatric disorders and its sex specific. Exercise can exert a protective effect in neuropsychiatric disorders through regulating the expression of estrogen and estrogen receptors, which are involved in neuroprotection, neurodevelopment, and neuronal glucose homeostasis. These processes are mediated by the downstream factors of estrogen signaling, including N-myc downstream regulatory gene 2 (Ndrg2), serotonin (5-HT), delta like canonical Notch ligand 1 (DLL1), NOD-like receptor thermal protein domain associated protein 3 (NLRP3), etc. In addition, exercise can act on the estrogen response element (ERE) fragment in the genes of estrogenic downstream factors like β-amyloid precursor protein cleavase 1 (BACE1). However, there are few studies on the relationship between exercise, the estrogen signaling pathway, and neuropsychiatric disorders. Hence, we review how the estrogen signaling mediates the mechanism of exercise intervention in neuropsychiatric disorders. We aim to provide a theoretical perspective for neuropsychiatric disorders affecting female health and provide theoretical support for the design of exercise prescriptions.

Disruption of cerebral energy metabolism is increasingly recognized as a key factor in the pathophysiology of mood disorders. Lactate, beyond its role as a metabolic byproduct, is now understood to be a critical player in brain energy homeostasis and a modulator of neuronal function. Recent advances in understanding lactate shuttling between astrocytes and neurons have opened new avenues for exploring its multifaceted roles in mood regulation. Exercise, known to modulate brain lactate levels, further underscores the potential of lactate as a therapeutic target in mood disorders. This review delves into the alterations in cerebral lactate associated with mood disorders, emphasizing their implications for brain energy dynamics and signaling pathways. Additionally, we discuss the therapeutic potential of lactate in mood disorders, particularly through its capacity to remodel cerebral function. We conclude by assessing the promise of exercise-induced lactate production as a novel strategy for mood disorder treatment. Alterations in brain lactate may contribute to the pathogenesis of mood disorders. In several studies, lactate is not only a substrate for brain energy metabolism, but also a molecule that triggers signaling cascades. Specifically, lactate is involved in the regulation of neurogenesis, neuroplasticity, endothelial cell function, and microglia lysosomal acidification, therefore improving mood disorders. Meanwhile, exercise as a low-risk intervention strategy can improve mood disorders through lactate regulation. Thus, the evidence from this review supports that lactate could be a potential therapeutic target for mood disorder, contributing to a deeper understanding of mood disorder pathogenesis and intervention.

Physical exercise is known to reduce depression, but the underlying brain mechanisms remain unclear. Based on a chronic restraint stress model in mice, we showed that 4-wk treadmill exercise profoundly maintained normal neural activity in the nucleus accumbens (NAc), in association with the prevention of depressive-like behaviors. Microarray analysis conducted in the NAc revealed that the oxytocin (OT) receptor displayed the most significant differential expression, implying a crucial involvement of OT signaling in exercise-induced antidepressant effects. In vivo fiber photometry revealed disrupted OT release in the NAc and altered activity of OT neurons in the paraventricular nucleus (PVN) and their projections to the NAc in stressed mice, which were restored by exercise. Moreover, we found that stress-induced depressive-like behaviors were prevented by activation of the PVN–NAc OT circuit. Additional inhibition of the PVN–NAc OT circuit blocked the antidepressant effects of exercise in stressed mice. In summary, our findings reveal a critical role of the PVN–NAc OT circuit in regulating depressive-like behaviors, which is required for the antidepressant effects of exercise. This neural circuit mechanism provides an explanation for brain network adaptations upon exercise and also suggests a promising therapeutic target for depression.

Targeting viperin improves diet-induced glucose intolerance but not adipose tissue inflammation Targeting viperin improves diet-induced glucose intolerance but not adipose tissue inflammation