Department of Health and Sport Sciences, TUM School of Medicine and Health, Technical University of Munich, Munich, Germany.
Department of Sport, Exercise and Health, Division Sports and Exercise Medicine, University of Basel, Basel, Switzerland.
Atherosclerosis. 2024 Dec;399:118631. doi: 10.1016/j.atherosclerosis.2024.118631. Epub 2024 Oct 16.
Endothelial dysfunction predicts elevated cardiovascular (CV) risk in healthy individuals. Aerobic exercise reduces endothelial dysfunction in part by improving CV risk factors. Yet, this explains less than 50 % of the effect and a direct influence of exercise training on the endothelium is discussed as possible contributor. The VascuFit study applied non-linear periodized aerobic exercise (NLPE) training to assess its multilevel effects on endothelial function including potential epigenetic endothelial modifications by circulating micro-ribonucleic acids (endomiRs).
Sedentary adults with elevated CV risk between 40 and 60 years were randomized 2:1 and engaged in an eight-week ergometer-based NLPE training (n = 30) or received standard exercise recommendations (n = 14). Macro-, microvascular, cellular and molecular adaptations were assessed via brachial-arterial flow-mediated dilation (baFMD), static retinal vessel analysis (SVA), flow cytometry, and endomiRs regulating key pathways of endothelial function. Statistics included ANCOVA, Principal Component Analysis (PCA), and regression analyses.
baFMD improved by 2.38 % (CI:0.70-4.06, p = 0.007) independent of CV risk, whereas SVA parameters and circulating endothelial (progenitor) cells did not significantly change in the NLPE group. The mean distance between baseline and follow-up PCA loadings of the endomiR dataset explaining 44.2 % of dataset variability was higher in the NLPE-group compared to the control group (2.71 ± 2.02 vs. 1.65 ± 0.93). However, regression analyses showed no evidence of endomiRs explaining the improvement of baFMD.
The improvement of macrovascular endothelial function by aerobic exercise training was independent from CV risk factors. Increased heterogeneity among endomiRs did not explain this effect, but suggests an adaptive response to the exercise stimulus on the epigenetic level.
血管内皮功能障碍可预测健康个体心血管(CV)风险升高。有氧运动可改善 CV 危险因素,从而部分减轻血管内皮功能障碍。然而,这仅能解释不到 50%的效果,因此有人认为运动训练对内皮的直接影响可能是一个促成因素。VascuFit 研究采用非线性周期性有氧运动(NLPE)训练来评估其对内皮功能的多层次影响,包括循环微小核糖核酸(endomiR)对潜在的表观遗传内皮修饰的影响。
40 至 60 岁之间心血管风险升高的久坐成年人按 2:1 随机分组,并进行为期 8 周的基于测功计的 NLPE 训练(n=30)或接受标准运动建议(n=14)。通过肱动脉血流介导的舒张(baFMD)、静态视网膜血管分析(SVA)、流式细胞术和调节内皮功能关键途径的 endomiR 评估宏观、微观血管、细胞和分子适应性。统计分析包括协方差分析、主成分分析(PCA)和回归分析。
baFMD 改善了 2.38%(CI:0.70-4.06,p=0.007),与 CV 风险无关,而 NLPE 组的 SVA 参数和循环内皮(祖)细胞没有明显变化。解释数据集变异性 44.2%的 endomiR 数据集的基线和随访 PCA 加载之间的平均距离在 NLPE 组中高于对照组(2.71±2.02 vs. 1.65±0.93)。然而,回归分析显示,endomiR 没有证据可以解释 baFMD 的改善。
有氧运动训练对大血管内皮功能的改善与 CV 危险因素无关。endomiR 的异质性增加并不能解释这种效应,但表明在表观遗传水平上对运动刺激有适应性反应。