Thijssen Dick H J, Benda Nathalie M M, Kerstens Thijs P, Seeger Joost P H, van Dijk Arie P J, Hopman Maria T E
Department of Physiology, Radboud University Medical Center, Radboud Institute for Health Sciences, Nijmegen, Netherlands.
Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, United Kingdom.
Front Physiol. 2019 Mar 15;10:264. doi: 10.3389/fphys.2019.00264. eCollection 2019.
Reperfusion is required to salvage ischaemic tissue, but also causes further damage (i.e., ischaemia/reperfusion-injury). Heart failure patients reveal exaggerated ischaemia/reperfusion-injury, whilst traditional ischaemic preconditioning cannot prevent ischaemia/reperfusion-injury. Exercise training may be a more powerful preconditioning stimulus, especially high-intensity interval training given the similarities with ischaemic preconditioning. Therefore, we examined the impact of 12-week continuous training vs. high-intensity interval training on brachial artery endothelial ischaemia/reperfusion-injury in heart failure patients New York Heart Association-class II-III. Twenty heart failure patients (male:female 19:1, 64 ± 8 years, ejection fraction 38 ± 6%) were allocated to 12-weeks of high-intensity interval training (101-min 90% maximal workload - 2.5-min 30% maximal workload) or continuous training (30-min 60-75% maximal workload). Before and after the intervention, we measured brachial artery endothelial function with flow-mediated dilation (FMD) before and after ischaemia/reperfusion (5-min ischemic exercise, 15-min reperfusion). Ischaemia/reperfusion caused a significant decline in FMD (continuous training ( = 10): 5.2 ± 2.5 to 3.4 ± 1.6%, high-intensity interval training ( = 10): 5.3 ± 2.6 to 3.5 ± 1.6%, = 0.01), which was not different between groups ( 0.05). Training improved maximal workload and fitness ( < 0.05), with no differences between groups ( 0.05). Exercise training did not alter FMD ( 0.05), whilst ischaemia/reperfusion did not impair FMD after exercise training (continuous training: 4.8 ± 3.0 to 4.2 ± 2.3%, high-intensity interval training: 4.7 ± 2.5 to 3.8 ± 2.3%, 0.05). No changes were found in FMD before or after ischaemia/reperfusion after 12-weeks in controls ( = 9). We found that 12-week exercise training in heart failure patients mitigated endothelial ischaemia-reperfusion injury, an effect independent of the type of exercise. These changes may contribute to the cardioprotective effects of exercise training, whilst our findings highlight the potency of exercise as a preconditioning stimulus.
再灌注是挽救缺血组织所必需的，但也会造成进一步损伤（即缺血/再灌注损伤）。心力衰竭患者存在过度的缺血/再灌注损伤，而传统的缺血预处理无法预防缺血/再灌注损伤。运动训练可能是一种更强有力的预处理刺激，尤其是高强度间歇训练，因为它与缺血预处理有相似之处。因此，我们研究了12周持续训练与高强度间歇训练对纽约心脏协会II - III级心力衰竭患者肱动脉内皮缺血/再灌注损伤的影响。20名心力衰竭患者（男:女 = 19:1，64±8岁，射血分数38±6%）被分配到12周的高强度间歇训练组（101分钟90%最大工作量 - 2.5分钟30%最大工作量）或持续训练组（30分钟60 - 75%最大工作量）。在干预前后，我们在缺血/再灌注（5分钟缺血运动，15分钟再灌注）前后用血流介导的血管舒张（FMD）测量肱动脉内皮功能。缺血/再灌注导致FMD显著下降（持续训练组（n = 10）：5.2±2.5%降至3.4±1.6%，高强度间歇训练组（n = 10）：5.3±2.6%降至3.5±1.6%，P = 0.01），两组之间无差异（P＞0.05）。训练改善了最大工作量和体能（P＜0.05），两组之间无差异（P＞0.05）。运动训练未改变FMD（P＞0.05），而缺血/再灌注在运动训练后未损害FMD（持续训练组：4.8±3.0%至4.2±2.3%，高强度间歇训练组：4.7±2.5%至3.8±2.3%，P＞0.05）。对照组（n = 9）在12周后缺血/再灌注前后FMD未发现变化。我们发现，心力衰竭患者进行12周运动训练可减轻内皮缺血 - 再灌注损伤，这一效果与运动类型无关。这些变化可能有助于运动训练的心脏保护作用，同时我们的研究结果突出了运动作为预处理刺激的效力。
