The neurotrophin brain-derived neurotrophic factor (BDNF), which acts as a transducer, is responsible for improving cerebral stroke, neuropathic pain, and depression. Exercise can alter extracellular nucleotide levels and purinergic receptors in central nervous system (CNS) structures. This inevitably activates or inhibits the expression of BDNF via purinergic receptors, particularly the P2X receptor (P2XR), to alleviate pathological progression. In addition, the significant involvement of sensitive P2X4R in mediating increased BDNF and p38-MAPK for intracerebral hemorrhage and pain hypersensitivity has been reported. Moreover, archetypal P2X7R blockade induces mouse antidepressant-like behavior and analgesia by BDNF release. This review summarizes BDNF-mediated neural effects via purinergic receptors, speculates that P2X4R and P2X7R could be priming molecules in exercise-mediated changes in BDNF, and provides strategies for the protective mechanism of exercise in neurogenic disease.

IntroductionThis study was designed to investigate the effect of running exercise on improving bone health in aging mice and explore the role of the SIRT1 in regulating autophagy and osteogenic differentiation of Bone marrow Mesenchymal Stem Cells (BMSCs).MethodsTwelve-month-old male C57BL/6J mice were used in this study as the aging model and were assigned to treadmill running exercise for eight weeks. Non-exercise male C57BL/6J mice of the same old were used as aging control and five-month-old mice were used as young controls. BMSCs were isolated from mice and subjected to mechanical stretching stimulation in vitro.ResultsThe results showed that aging mice had lower bone mass, bone mineral density (BMD), and autophagy than young mice, while running exercise improved BMD and bone mass as well as upregulated autophagy in bone cells. Mechanical loading increased osteogenic differentiation and autophagy in BMSCs, and knockdown of SIRT1 in BMSCs demonstrated that SIRT1-regulated autophagy involved the mechanical loading activation of osteogenic differentiation.ConclusionTaken together, this study revealed that exercise improved bone health during aging by activating bone formation, which can be attributed to osteogenic differentiation of BMSCs through the activation of SIRT1-mediated autophagy. The mechanisms underlying this effect may involve mechanical loading.

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Exercise is considered to be a timing factor (zeitgeber) that can affect rhythm changes in skeletal muscle. The phase of the skeletal muscle clock affects the metabolism of the muscles. However, whether exercise intensity induces phase changes in oscillations of clock genes as well as clock-controlled metabolic genes remains uncertain. We aimed to assess the effects of heavy exercise on skeletal muscle clock genes and phase changes in oscillations of clock-controlled metabolic genes. The expression of clock genes Bmal1 and Clock in the skeletal muscle of rats was analyzed by real-time PCR, and the expression of clock-controlled metabolic proteins NAMPT, NAD+, and SIRT1 was analyzed by ELISA. Sprague Dawley rats were kept under a regular 12/12-h light/dark cycle. Rats in the exercise group were exposed to a downhill run of 90 min at a speed of 16 m/min and an angle of − 16°. Sampling was performed at 6-h intervals. Compared with the control group, the rhythm of Bmal1 mRNA expression in the exercise group disappeared on the first day, and the rhythm recovered on the second day; Clock mRNA expression lost its rhythmicity in 72 h. The expression of NAMPT, NAD+, and SIRT1 was lost on the first day and the second day, but the rhythm recovered on the third day. These data demonstrate that muscle contractions are sufficient to shift the phase of muscle circadian clock and clock-controlled metabolic genes, likely via changes in core clock gene expression.

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Maternal nutrition plays a critical role in fetal growth and lifelong health outcomes. Folate is essential as a methyl donor in the epigenetic programming of offspring. Although it is critical to identify the associations between maternal folate status and child obesity, the results have been controversial. PURPOSE: This study investigates the relationship between maternal folate status and childhood obesity through meta-analysis and to examine the influence of moderating variables. METHODS: Keyword/reference search was performed in EBSCO for Academic Search Complete, Health Source-Nursing Academic Edition, Medline, SPORTDiscus database, and CINAHL. Web of Science database was also used to identify all relevant studies published in English. Meta-analysis was conducted using the CMA program to estimate the pooled effect of maternal folate status on children's obesity (BMI, BMI-Z score, or fat mass) and examine the influence of moderating variables on the overall effect. Among the 8 studies, 3 were randomized controlled trials, and 5 were cohort studies. Standardized mean difference effect size and 95% CI were computed using a random-effects model. The studies were symmetrically distributed in the funnel plot, explained the marginal possibility of publication bias. RESULTS:The better maternal folate intake, the lower the chance that the offspring will become obese: the overall ESs (Hedges' g) was .168 (95% CI = .075, .260, p = .000; small effects; cf., Cohen's criteria). Moderator analysis results revealed that the Q statistic for the age group was statistically significant (Qb = 4.730, df = 1. P = .030; explained the heterogeneity of ESs). In under 7 years, ES was .277 (95% CI =.151, .404), but, over 7 years old of age, ES was .089(95% CI =-.025,.202). However, folate concentration, ingestion volume, measure type, and method did not influence the size of the effect. CONCLUSIONS: The maternal folate status significantly affects child obesity, and the maternal folate status effect appeared to be more effective in the age of the group under 7 years. Future research should focus on the same age group, adopt systematic and field-validated maternal folate concentration or ingestion measures, and elucidate the pathways linking maternal folate status and childhood obesity outcomes.