肠道通透性
磁导率
渗透(HVAC)
医学
内科学
炎症
小肠
肠粘膜
体育锻炼
内分泌学
适度运动
化学
中性粒细胞
肠缺血
血管通透性
拉顿
肠动力
作者
Saki Kondo,Takahiro Nagatake,Koji Hosomi,Yoko Tojima,Kei Ishida,Azusa Saika,Jun Kunisawa
标识
DOI:10.1249/mss.0000000000003858
摘要
INTRODUCTION: Although the health benefits of exercise are well-documented, intense exercise can induce gastrointestinal symptoms, potentially due to disruption of the intestinal barrier. This disruption allows foreign substances to enter the intestine and circulation, triggering immune system activation and inflammation. In this study, we investigated the effects of a single bout of running exercise at different intensities on intestinal permeability and systemic immune cell responses. METHODS: Male C57BL/6J mice were assigned to a control group, a low-intensity exercise group (10 m/min, Ex-low), and a high-intensity exercise group (20 m/min, Ex-high). The exercise lasted 60 min, while the control group remained sedentary. Immediately after exercise, intestinal permeability was assessed using FITC-Dextran. Immune cells were isolated from the lungs, blood, small intestinal lamina propria (siLP), and large intestinal lamina propria (liLP), while neutrophils, macrophages, eosinophils, B cells, and T cells were quantified by flow cytometry. RESULTS: The Ex-high group exhibited significantly increased intestinal permeability and neutrophil infiltration in the siLP compared with both the control and Ex-low groups. No significant differences in other immune cell types were observed between the groups. Furthermore, the Ex-high group demonstrated elevated neutrophil counts in the liLP, lungs, and blood. The expression of inflammatory cytokines ( Il-1β and Il-6 ) and chemokines ( Cxcl1 and Cxcl2 ) was also significantly higher in the small intestines of the Ex-high group. CONCLUSIONS: A single bout of high-intensity exercise increases intestinal permeability and neutrophil infiltration in both the intestines and systemic tissues, highlighting a potential mechanism by which intense exercise induces intestinal and systemic inflammation.
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