Fernandes Cleverson Rodrigues, Kannen Vinicius, Mata Karina Magalhães, Frajacomo Fernando Tadeu, Jordão Junior Alceu Afonso, Gasparotto Bianca, Sakita Juliana Yumi, Elias Junior Jorge, Leonardi Daphne Santoro, Mauad Fernando Marum, Ramos Simone Gusmão, Uyemura Sergio Akira, Garcia Sergio Britto
Department of Pathology, University of Sao Paulo, Ribeirao Preto, Brazil.
Department of Toxicology, Bromatology, and Clinical Analysis, University of Sao Paulo, Ribeirao Preto, Brazil.
Front Nutr. 2017 May 18;4:21. doi: 10.3389/fnut.2017.00021. eCollection 2017.
Millions of people die each year due to cardiovascular disease (CVD). A Western lifestyle not only fuses a significant intake of fat with physical inactivity and obesity but also promotes CVD. Recent evidence suggests that dietary fat intake impairs the benefits of physical training. We investigated whether aerobic training could reverse the adverse effects of a high-fat diet (HFD) on the aorta. Then, we explored whether this type of exercise could reverse the damage to the heart that is imposed by fat-enriched diet (FED).
Rats were randomly assigned to two experiments, which lasted 8 weeks each. First, rats swam for 60 min and were fed either a regular diet [standard diet (STD)] or an HFD. After aortic samples had been collected, the rats underwent a histopathological analysis for different biomarkers. Another experiment subjected rats that were fed either an STD or an FED to swimming for 20 or 90 min.
The first experiment revealed that rats that were subjected to an HFD-endured increased oxidative damage in the aorta that exercises could not counteract. Together with increased cyclooxygenase 2 expression, an HFD in combination with physical training increased the number of macrophages. A reduction in collagen fibers with an increased number of positive α-actin cells and expression of matrix metalloproteinase-2 occurred concomitantly. Upon analyzing the second experiment, we found that physically training rats that were given an FED for 90 min/day decreased the cardiac adipose tissue density, although it did not protect the heart from fat-induced oxidative damage. Even though the physical training lowered cholesterol levels that were promoted by the FED, the levels were still higher than those in the animals that were given an STD. Feeding rats an FED impaired the swimming protocol's effects on lowering triglyceride concentration. Additionally, exercise was unable to reverse the fat-induced deregulation in hepatic antioxidant and lipid peroxidation activities.
Our findings reveal that an increased intake of fat undermines the potential benefits of physical exercise on the heart and the aorta.
每年有数百万人死于心血管疾病(CVD)。西方生活方式不仅使大量脂肪摄入与缺乏身体活动和肥胖相结合,还会促进心血管疾病的发生。最近的证据表明,膳食脂肪摄入会削弱体育锻炼的益处。我们研究了有氧训练是否可以逆转高脂饮食(HFD)对主动脉的不利影响。然后,我们探讨了这种类型的运动是否可以逆转富含脂肪的饮食(FED)对心脏造成的损害。
将大鼠随机分为两个实验,每个实验持续8周。首先,大鼠游泳60分钟,并分别给予常规饮食[标准饮食(STD)]或高脂饮食。在收集主动脉样本后,对大鼠进行不同生物标志物的组织病理学分析。另一个实验让分别喂食标准饮食或富含脂肪饮食的大鼠游泳20或90分钟。
第一个实验表明,接受高脂饮食的大鼠主动脉氧化损伤增加,运动无法抵消这种损伤。高脂饮食与体育锻炼相结合,除了增加环氧化酶2的表达外,还增加了巨噬细胞的数量。同时,胶原纤维减少,α-肌动蛋白阳性细胞数量增加,基质金属蛋白酶-2的表达也增加。在分析第二个实验时,我们发现每天给予富含脂肪饮食的大鼠进行90分钟的体育锻炼可降低心脏脂肪组织密度,尽管它不能保护心脏免受脂肪诱导的氧化损伤。尽管体育锻炼降低了富含脂肪饮食所促进的胆固醇水平,但该水平仍高于给予标准饮食的动物。给大鼠喂食富含脂肪的饮食会削弱游泳方案对降低甘油三酯浓度的作用。此外,运动无法逆转脂肪诱导的肝脏抗氧化和脂质过氧化活性失调。
我们的研究结果表明,脂肪摄入量增加会削弱体育锻炼对心脏和主动脉的潜在益处。