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
{"title":"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","authors":"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","doi":"10.1113/EP092849","DOIUrl":null,"url":null,"abstract":"<p><p>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<sup>-2</sup> h<sup>-1</sup>, P = 0.011) despite greater thermoregulatory strain (e.g., terminal T<sub>rec</sub>: 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.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8000,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Faecal microbiome, gastrointestinal integrity, inflammation and thermoregulation in recent exertional heat illness patients and matched controls.\",\"authors\":\"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\",\"doi\":\"10.1113/EP092849\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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<sup>-2</sup> h<sup>-1</sup>, P = 0.011) despite greater thermoregulatory strain (e.g., terminal T<sub>rec</sub>: 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.</p>\",\"PeriodicalId\":12092,\"journal\":{\"name\":\"Experimental Physiology\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":2.8000,\"publicationDate\":\"2025-06-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Experimental Physiology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1113/EP092849\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"PHYSIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Experimental Physiology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1113/EP092849","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"PHYSIOLOGY","Score":null,"Total":0}
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.
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.