Background Aerobic exercise has been shown to slow tumor progression in rodents and humans, but the mechanisms behind this effect are still unclear. Here we show that aerobic exercise in the form of chronic endurance training suppresses tumor recruitment of FoxP3 + Treg cells thus enhancing antitumor immune efficiency. Methods Adult wild-type and athymic BALB/c female mice were endurance-trained for 8 weeks. Circulating leukocytes as well as muscle and liver mtDNA copy number were compared to aged-matched concurrent sedentary controls to establish systemic effects. 4 T1 murine mammary tumor cells were injected subcutaneously to the 4th mammary pad at the end of the training period. Tumor growth and survival rates were compared, together with antitumor immune response. Results Exercised wild-type had 17% slower growth rate, 24% longer survival, and 2-fold tumor-CD + 8/FoxP3 + ratio than sedentary controls. Exercised athymic BALB/c females showed no difference in tumor growth or survival rates when compared to sedentary controls. Conclusions Cytotoxic T cells are a significant factor in endurance exercise-induced suppression of tumor growth. Endurance exercise enhances antitumor immune efficacy by increasing intratumoral CD8 + /FoxP3 + ratio. Electronic supplementary material The online version of this article (10.1186/s12885-019-5745-7) contains supplementary material, which is available to authorized users.

Chronic endurance exercise is a therapeutic strategy in the treatment of many chronic diseases in humans, including the prevention and treatment of metabolic diseases such as diabetes mellitus. Metabolic, cardiorespiratory and endocrine pathways targeted by chronic endurance exercise have been identified. In the liver however, the cellular and molecular pathways that are modified by exercise and have preventive or therapeutic relevance to metabolic disease remain unresolved. The mouse model used in the current study allows for the quantification of a human-relevant exercise “dosage”. In this study we show hepatic gene expression differences between sedentary female and sedentary male mice, and that chronic exercise modifies the transcription of hepatic genes related to metabolic disease and steatosis in both male and female mice. Chronic exercise induces molecular pathways involved in glucose tolerance, glycolysis and gluconeogenesis while producing a decrease in pathways related to insulin resistance, steatosis, fibrosis, and inflammation. Given these findings, this mouse exercise model has potential to dissect the cellular and molecular hepatic changes following chronic exercise with application to understanding the role that chronic exercise plays in preventing human diseases. Novelty Bullets: • Exercise modifies the hepatic gene expression and hepatic pathways related to metabolic disease in male and female mice. • Gender differences were seen in hepatic gene expression between sedentary and exercised mice. • The mouse exercise model used in this study allows for application and evaluation of exercise effects in human disease

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Introduction: Parkinson’s Disease (PD) is a condition of the brain that consiste of the death of dopaminergic neurons in the substantia nigra, therefore causing dyskinesias and dystonias. Besides the motor symptoms, the neurogastro motility is affected by the disease, since gastrointestinal dysfunction is a frequent and clinically relevant symptom of PD. Objectives: To link the neural pathways and neurotransmitters that involve the neuroenteric system control and the PD’s pathology. Methods: A systematic literature review was performed based on data extraction through the advanced research engine from Pubmed. Publications with the descriptors “dysmotility” OR “gastro motility” AND “Parkinson” were selected. Results: Through clinical and pre-clinical studies on PD, there has been hypothesized a gut-brain axis that is connected through hormones, neurotransmitters and dopamanergic inputs. This hypothesis is supported by evidence in the showing of accumulation of alpha-synuclein in the vagal system and Enteric Nervous System, the use of drugs such as peripheral dopaminergic blockers and serotonin for gastroparesis, the ghrelin effects on the central dopaminergic system through modulation of the mesencephalic dopaminergic signaling tested on rats, the gastrointestinal autonomic neuropathy detected in PD patients and the establishment of gut dysmotility before motor onset symptoms. Therefore, dysmotility isues such as delayed gastric emptying may not only be a symptom of PD, but also contrubute to the pathogenesis itself through impaired signaling. Conclusion: The gut-brain axis can be not only a tool for PD diagnosis but also a treatment target to restrain the advance of the disease. Although many articles are related this subject, there is a lack of designed trials for atypical movement disorders. To explore the dysmotility in PD, there is a need for multi-modality standardized tests to evaluate severity and prevalence.