Introduction SHANK3 is an important excitatory postsynaptic scaffold protein, and its mutations lead to genetic cause of neurodevelopmental diseases including autism spectrum disorders (ASD), Philan McDermid syndrome (PMS), and intellectual disability (ID). Early prevention and treatment are important for Shank3 gene mutation disease. Swimming has been proven to have a positive effect on neurodegenerative diseases. Methods Shank3 gene exon 11–21 knockout rats were intervened by a 40 min/day, 5 day/week for 8‐week protocol. After the intervention, the rats were tested to behavioral measures such as learning and memory, and the volume and H‐spectrum of the brain were measured using MRI; hippocampal dendritic spines were measured using Golgi staining and laser confocal. Results The results showed that Shank3‐deficient rats had significant deficits in social memory, object recognition, and water maze learning decreased hippocampal volume and number of neurons, and lower levels of related scaffold proteins and receptor proteins were found in Shank3‐deficient rats. Conclusion It is suggested that early swimming exercise has a positive effect on Shank3 gene‐deficient rats, which provides a new therapeutic strategy for the prevention and recovery of neurodevelopmental disorders.

Background Autism spectrum disorder (ASD) is a developmental disorder characterized by social behavior deficits and stereotyped behaviors in childhood that lacks satisfactory medical intervention. Early swimming intervention is a noninvasive method combining enriched environment and exercise, which has been proven to improve brain development in young children and to treat neurodevelopmental diseases. Methods In this study, we tested the autism-like behavior of rats with deletions in exons 11–21 of the Shank3 gene and evaluated the effect of early swimming intervention (from postnatal day 8 to 60) on the behavior of this animal model of autism. In addition, the transcriptomes of the striatal tissues of wild-type, Shank3 knockout and Shank3 knockout swimming groups rats were analyzed. Results Shank3 knockout rats exhibit core symptoms of autism, and early swimming improved the social and stereotyped behaviors in this autism rat model. Transcriptomics results revealed that compared to the wild-type group, 291 differentially expressed genes (DEGs) were identified in the striatum of the Shank3 knockout group. Compared to Shank3 knockout group, 534 DEGs were identified in the striatum of Shank3 knockout swimming group. The DEGs annotated by Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway shows that the impacts of Shank3 deletion were primarily reflected in synaptic structure, development, morphology, receptor function and signaling, and swimming primarily changed the terms related to the synapses in the striatum of Shank3 knockout rats, including the morphology, structure, composition, development and regulation of synapses. Conclusion Early swimming intervention can ameliorate behavioral abnormalities caused by Shank3 knockout, by a mechanism that may involve the process of striatal synaptic development and should be further investigated.

Purpose Urine can sensitively reflect early pathophysiological changes in the body. The purpose of this study was to explore the changes of urine proteome in rats with regular swimming exercise. Methods In this study, experimental rats were subjected to daily moderate-intensity swimming exercise for 7 weeks. Urine samples were collected at weeks 2, 5, and 7 and were analyzed by using liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS). Results Unsupervised clustering analysis of all urinary proteins identified at week 2 showed that the swimming group was distinctively different from the control group. Compared to the control group, a total of 112, 61 and 44 differential proteins were identified in the swimming group at weeks 2, 5 and 7, respectively. Randomized grouping statistical analysis showed that more than 85% of the differential proteins identified in this study were caused by swimming exercise rather than random allocation. According to the Human Protein Atlas, the differential proteins that have human orthologs were strongly expressed in the liver, kidney and intestine. Functional annotation analysis revealed that these differential proteins were involved in glucose metabolism and immunity-related pathways. Conclusion Our results revealed that the urinary proteome could reflect significant changes after regular swimming exercise. These findings may provide an approach to monitor the effects of exercise of the body.

Aim: To explore associations between sleep duration and physical fitness (PF) of children aged 3–6 years. Methods: This study investigated the sleep duration and PF data of children aged 3–6 years by stratified random sampling. The restricted cubic spline model and binary logistic regression analysis were mainly used for the empirical analysis of the correlation effect between sleep duration and PF. The final data had a total of 21,857 children, of which 11,245 (51.45%) were boys and 10,612 (48.55%) were girls. Results: The PF level of the children in this study showed a relatively positive level (pass rate = 93.6%), and 19.7% of them had abnormal sleep duration; the results of the restricted cubic spline showed an inverted U-shaped association between the level of PF and the risk of abnormal sleep duration (X2 = 28.13, p < 0.0001). The results of logistic regression analysis showed that children with abnormal sleep duration were more likely to have a low PF, body morphology and motor ability levels at an OR (95% CI) of 1.077 (1.023–1.133), 1.077 (1.016–1.142) and 1.035 (1.08–1.062), respectively. The results of the bias correlation analysis showed varying degrees of correlation between sleep duration and various components of children’s PF. Conclusion: Insufficient or excessive amounts of sleep were significantly associated with PF in children, with abnormal sleep duration leading to reduced levels of PF and its components.

The effect of exercise interventions on autism spectrum disorder (ASD) has been demonstrated in many studies. Then, the discovery of a bidirectional relationship between the gut microbiome (GM) and the central nervous system (CNS) led to the concept of the microbial gut-brain axis (MGBA) and linked the abnormal GM to a variety of neuropsychiatric disorders, autism being one of them. Research on improving the GM through exercise is also starting to come into focus. However, there are currently few studies on exercise intervention in the GM of autism. The purpose of this review was to find evidence to explore the possible potential effects of exercise to improve the behavior of individuals with autism in the MGBA in this treatment, as well as the potential of GM as an exercise treatment for autism. We will explore (1) changes in GM components of ASD and their relationship to the pathophysiology of ASD; (2) the relationship between exercise and changes in GM components (3) the effect of exercise on GM in CNS disorders. Ultimately, we conclude to find that Streptococcus, Bifidobacterium, Clostridium, Bacteroides, and Blautia may be potential effectors through the MGBA network during exercise to ameliorate ASD targeting microbiotas. They deserve high attention in the follow-up studies.