High-Fat and Fat-Enriched Diets Impair the Benefits of Moderate Physical Training in the Aorta and the Heart in Rats

Abstract

Aim: 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).

Methods: 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.

Results: 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.

Conclusion: Our findings reveal that an increased intake of fat undermines the potential benefits of physical exercise on the heart and the aorta.

Keywords: biochemistry; blood vessels; heart; obesity; swimming.

Figure 1

A high-fat diet (HFD) damages the aorta aside from protective effects of physical training. (A) Representative pictures illustrate reactions with an anti-nitrotyrosine antibody for each experimental group in aorta samples. A black arrow shows a positively stained cell with that anti-nitrotyrosine antibody. Sedentary rats were given a regular chow [standard diet (STD)-SED]; exercised rats were fed a regular chow (STD-E60); sedentary rats were given an HFD (HFD-SED); and, exercised were rats fed an HFD (HFD-E60). (B) A histopathological analysis determined nitrotyrosine values (%) by optical density. (C) A microscopic analysis determined atrial thickness (micrometers) in aortic slices stained with hematoxylin and eosin. (D) Representative pictures illustrate picrosirius red staining for each experimental group in aorta samples. A black arrow shows red-stained collagen fibers. A blue arrow shows yellow stained elastic fibers. (D,E) A histopathological analysis determined the density of elastic (E) and collagen fibers (F). (G) Representative pictures illustrate reactions with an anti-α-actin antibody for each experimental group in aorta samples. A black arrow shows a positively stained cell with that anti-α-actin antibody. (H) A microscopic analysis determined the number of positive α-actin cells per area (millimeter; index). Statistical Analysis I: ^¢p < 0.05 vs. HFD-SED. Statistical Analysis II: *p < 0.05 and ***p < 0.001. Data analysis: two-way ANOVA test (Bonferroni’s post hoc test). Reported values are the mean ± SD.

Figure 2

A high-fat diet (HFD) promotes inflammation in the aortic tissue. Antibodies against matrix metalloproteinase 2 [MMP2; (A)], the cluster of differentiation 68 [CD68; (B)], and cyclooxygenase 2 [COX-2; (C)] stained aortic samples for histopathological analysis. The index was determined to be the number of positive cells per area (square millimeter). Statistical Analysis I: ^¢p < 0.05 vs. STD-SED or HFD-SED. Statistical Analysis II: *p < 0.05 and **p < 0.01. Data analysis: two-way ANOVA test (Bonferroni’s post hoc test). Reported values are the mean ± SD.

Figure 3

Physical exercises do not protect the heart from side effects of a fat-enriched diet (FED). Computerized tomography analyzed the heart area (A), and the cardiac fat tissue density (B). A histopathological analysis determined the thickness (micrometer) of the left ventricle [LVT; (C)], the right ventricle [RVT; (D)], and the septum [ST; (E)]. Staining heart samples with anti-nitrotyrosine antibody determined damage in this tissue (F). Statistical Analysis I: ^¢p < 0.05 vs STD-SED of FED-SED; ^§p < 0.05 vs STD-SED. Statistical Analysis II: *p < 0.05. Data analysis: two-way ANOVA test (Bonferroni’s post hoc test). Reported values are the mean ± SD.

Figure 4

A fat-enriched diet promotes inflammation in the heart. (A) Representative pictures illustrate reactions with an anti-cyclooxygenase-2 (COX-2) antibody for each experimental group in heart samples. A black arrow shows a positively stained cell with that anti-COX-2 antibody. Sedentary rats were given a regular chow [standard diet (STD)-SED]; exercised rats were fed a regular chow (STD-E60); sedentary rats were given an HFD (HFD-SED); and exercised rats were fed an HFD (HFD-E60). (B) The COX-2 index was determined to be the number of positive cells per area (square millimeter). Statistical Analysis I: ^¢p < 0.05 vs. FED-SED. Statistical Analysis II: *p < 0.05. Data analysis: two-way ANOVA test (Bonferroni’s post hoc test). Reported values are the mean ± SD.

Figure 5

A fat-enriched diet and physical training alter serum biochemical markers. Standard biochemical analyses determined serum levels of cholesterol (A), triglycerides [TG; (B)], glucose (C), aspartate aminotransferase [AST; (D)], and alanine aminotransferase [ALT; (E)]. Statistical Analysis I: ^¢p < 0.05 vs standard diet (STD)-SED or FED-SED; ^§p < 0.05 vs STD-SED or FED-SED. Statistical Analysis II: *p < 0.05, **p < 0.01, ***p < 0.001. Data analysis: two-way ANOVA test (Bonferroni’s post hoc test). Reported values are the mean ± SD.

Figure 6

A physical training does not recover the hepatic tissue damage induced by a fat-enriched diet. Computerized tomography analyzed the fat tissue density in visceral (A) and liver areas (B). Standard biochemical analyses determined malondialdehyde [MDA; (C)] and reduced glutathione [GSH; (D)] levels in liver samples. Statistical Analysis I: ^¢p < 0.05 vs standard diet (STD)-SED or FED-SED; ^§p < 0.05 vs STD-SED or FED-SED. Statistical Analysis II: ***p < 0.001. Data analysis: two-way ANOVA test (Bonferroni’s post hoc test). Reported values are the mean ± SD.