Occupational and Environmental Physiology Group, Centre for Physical Activity, Sport, Exercise Sciences, Coventry University, United Kingdom.
Clinical Sciences and Translational Medicine, Centre for Health and Life Sciences, Coventry University, Coventry, United Kingdom.
Appl Physiol Nutr Metab. 2024 Sep 1;49(9):1241-1251. doi: 10.1139/apnm-2024-0094. Epub 2024 May 21.
Heat stress induced damage to the gastrointestinal barrier can induce local and systemic inflammatory reactions implicated in heat-stroke. Gastrointestinal barrier damage has been shown to be greater in older relative to young adults following hyperthermia. However, comparisons between young and older adults have been limited to brief exposures (3 h), which may not reflect the duration of heat stress experienced during heat waves. We therefore evaluated markers of intestinal epithelial damage (log transformed intestinal fatty acid binding protein, IFABP), microbial translocation (soluble cluster of differentiation 14, sCD14), and systemic inflammation (tumour necrosis factor alpha, TNF-α; interleukin 6, IL-6; C-reactive protein, CRP) in 19 young (interquartile range: 21-27 years; 10 females) and 37 older (68-73 years; 10 females) adults before and after 9 h of rest in 40 °C (9% relative humidity). The magnitude of the increase in IFABP was 0.38 log pg/mL (95% CI, 0.10, 0.65 log pg/mL) greater in the older relative to young cohort ( = 0.049) after 9 h heat exposure. At baseline both IL-6 and CRP concentrations were higher in the older (IL-6: 2.67 (1.5) log pg/mL, CRP: 0.28 (1.5) mg/mL) relative to the young (IL-6: 1.59 log pg/mL, SD 1.2; CRP: 0.11 mg/mL, SD 1.7) group (both ≤ 0.001). The change in IL-6 and CRP was similar between groups following 9 h heat exposure (IL-6: = 0.053; CRP: = 0.241). Neither sCD14 and TNF-α were different between groups at baseline nor altered after 9 h heat exposure. Our data indicate that age may modify intestinal epithelial injury following 9 h of passive heat exposure.
热应激对胃肠道屏障的损伤可引起局部和全身炎症反应,与中暑有关。与年轻人相比,老年人在高热后胃肠道屏障损伤更大。然而,年轻人和老年人之间的比较仅限于短暂暴露(3 小时),这可能无法反映热浪期间经历的热应激持续时间。因此,我们评估了肠道上皮损伤标志物(对数转换的肠脂肪酸结合蛋白,IFABP)、微生物易位(可溶性分化簇 14,sCD14)和全身炎症标志物(肿瘤坏死因子-α,TNF-α;白细胞介素 6,IL-6;C 反应蛋白,CRP)在 19 名年轻(四分位距:21-27 岁;10 名女性)和 37 名老年(68-73 岁;10 名女性)成年人中,在 40°C(9%相对湿度)下休息 9 小时前后。与年轻队列相比,老年队列在 9 小时热暴露后 IFABP 的增加幅度高出 0.38 log pg/mL(95%CI,0.10,0.65 log pg/mL)(=0.049)。在基线时,老年组的 IL-6 和 CRP 浓度均高于年轻组(IL-6:2.67(1.5)log pg/mL,CRP:0.28(1.5)mg/mL)(均 ≤0.001)。在 9 小时热暴露后,两组之间的 IL-6 和 CRP 变化相似(IL-6:=0.053;CRP:=0.241)。在基线时,sCD14 和 TNF-α在两组之间无差异,并且在 9 小时热暴露后也没有改变。我们的数据表明,在 9 小时被动热暴露后,年龄可能会改变肠道上皮损伤。