近期运动性热病患者和对照组的粪便微生物群、胃肠道完整性、炎症和体温调节

IF 2.8 4区 医学 Q2 PHYSIOLOGY
Alex A M Gould, Neil P Walsh, Michael J Tipton, Michael J Zurawlew, Omar Tayari, Carol House, Simon K Delves, Samuel C Robson, Janis J Shute, Joy E M Watts, Andrew J Roberts, Alex J Rawcliffe, Megan R Robinson, Jo Corbett
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引用次数: 0

摘要

假设胃肠道(GI)微生物群和胃肠道屏障完整性有助于运动性热病(EHI)病因学。我们比较了29名最近(4个月)EHI患者(EHI风险升高组)和29名没有EHI病史的对照组的粪便微生物群、胃肠道屏障完整性、炎症和体温调节,匹配了影响体温调节和胃肠道微生物群的变量。参与者完成了运动耐热性评估(HTA),通过粪便样本的16S rRNA基因扩增子测序评估粪便微生物组,并在HTA前后测量GI屏障完整性和炎症的血液生物标志物。除Simpson指数(患者= 0.97±0.01 vs.对照组= 0.98±0.00,P = 0.030)外,各组间粪便微生物组组成(α-多样性、β-多样性、相对丰度、差异丰度)、胃肠道屏障完整性、炎症和终末体温调节指标均无差异。根据HTA将个体分为耐热型(n = 46)和不耐热型(n = 12)。热不耐受个体表现出较低的sudomotor反应(不耐受= 0.53 (0.17)vs.耐受= 0.62 (0.20)L m-2 h-1, P = 0.011),尽管有较大的热调节菌株(例如,Trec末端:不耐受= 39.20±0.31 vs.耐受= 38.80±0.31°C, P
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Faecal microbiome, gastrointestinal integrity, inflammation and thermoregulation in recent exertional heat illness patients and matched controls.

The gastrointestinal (GI) microbiota and GI barrier integrity are hypothesised to contribute to exertional heat illness (EHI) aetiology. We compared the faecal microbiome, GI barrier integrity, inflammation and thermoregulation of 29 recent (∼4 months) EHI patients (a group with elevated EHI risk) and 29 control individuals without prior EHI history, matched for variables influencing thermoregulation and GI microbiota. Participants completed an exercise heat tolerance assessment (HTA), with faecal microbiome assessed by 16S rRNA gene amplicon sequencing of stool samples and blood biomarkers of GI barrier integrity and inflammation measured pre- and post-HTA. With the exception of the Simpson index (patient = 0.97 ± 0.01 vs. control = 0.98 ± 0.00, P = 0.030), there were no between-groups differences in faecal microbiome composition (α-diversity, β-diversity, relative abundance, differential abundance), GI barrier integrity, inflammation or terminal thermoregulatory indices. Individuals were subsequently classified as heat tolerant (n = 46) or intolerant (n = 12) on the basis of the HTA. Heat intolerant individuals demonstrated lower sudomotor response (intolerant = 0.53 (0.17) vs. tolerant = 0.62 (0.20) L m-2 h-1, P = 0.011) despite greater thermoregulatory strain (e.g., terminal Trec: intolerant = 39.20 ± 0.31 vs. tolerant = 38.80 ± 0.31°C, P < 0.001), lower Firmicutes:Bacteroidota ratio (intolerant = 3.7 (0.6) vs. tolerant = 4.5 (2.0), P = 0.019) and higher plasma [sCD14] (P = 0.014), but other aspects of faecal microbiome, GI integrity or inflammation did not differ from heat tolerant individuals. In conclusion, the faecal microbiome composition and the GI barrier integrity and inflammatory responses to exercise heat-stress showed limited differences between recent EHI patients and matched controls, or between individuals classified as heat intolerant or heat tolerant and are unlikely to explain elevated EHI risk in recent EHI patients, or heat intolerance.

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来源期刊
Experimental Physiology
Experimental Physiology 医学-生理学
CiteScore
5.10
自引率
3.70%
发文量
262
审稿时长
1 months
期刊介绍: Experimental Physiology publishes research papers that report novel insights into homeostatic and adaptive responses in health, as well as those that further our understanding of pathophysiological mechanisms in disease. We encourage papers that embrace the journal’s orientation of translation and integration, including studies of the adaptive responses to exercise, acute and chronic environmental stressors, growth and aging, and diseases where integrative homeostatic mechanisms play a key role in the response to and evolution of the disease process. Examples of such diseases include hypertension, heart failure, hypoxic lung disease, endocrine and neurological disorders. We are also keen to publish research that has a translational aspect or clinical application. Comparative physiology work that can be applied to aid the understanding human physiology is also encouraged. Manuscripts that report the use of bioinformatic, genomic, molecular, proteomic and cellular techniques to provide novel insights into integrative physiological and pathophysiological mechanisms are welcomed.
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