ABC | Volume 114, Nº1, January 2019

Original Article Brianezi et al. Effects of physical training on the myocardium Arq Bras Cardiol. 2020; 114(1):100-105 Table 2 – Comparison of Cyclooxygenase-2, Volume Density of collagen fibers I and Metalloproteinase type 9, with the groups studied. clinical variables with groups Variables CS COS COT LDL-S LDL-OS LDL-OT p* COX-2 35.0 (23.9; 46.3) 46.5 (44.2; 79.7) 46.1 (31.3; 47.7) 47.7 (45.8; 63.1) 87.8 (42.5; 92.4) 49.4 (49.1; 50.9) 0.232 Vv [fc I] 0.21 (0.21; 0.43) 0.43 (0.21; 0.43) - - 0.21 (0.0; 0.41) A,B,C 0.0 (0.0; 0.21) A,B,C < 0.001 MMP9 44.7 (40.1; 44.8) 40.9 (39.8; 45.6) 53.9 (48.6; 66.2) 53.0 (38.3; 58.1) 42.2 (27.3; 53.7) 64.1 (45.5; 93.9) 0.169 *Kruskal-Wallis. Data expressed as median and 25% and 75% percentiles. COX-2: Cyclooxygenase-2; Vv [fc I]: Volume Density of collagen fibers I; MMP 9: Metalloproteinase type 9; CS: sedentary non-ovariectomized control; COS: sedentary ovariectomized control; COT: trained ovariectomized control; LDL-S: non‑sedentary ovariectomized LDL knockout; LDL-OS: sedentary ovariectomized LDL knockout; LDL-OT: trained ovariectomized LDL knockout. A: statistically significant difference between the studied group and the COS group; B: statistically significant difference between the studied group and the TOC group; C: statistically significant difference between the studied group and the LDL-S group. in relation to the COS group, 76% in relation to the COT group and 70% in relation to the LDL-S group. When training was performed in the dyslipidemic ovariectomized group (LDL‑OT), the data presented a 152% increase in relation to the LDL-OS group and a decrease in relation to the control groups, with 63% for the CS group, 45% for the COS group and 40% for the COT group. For the parameters related to volume density of type III collagen fibers, metalloproteinase type 9 and inflammation (COX2), the values obtained for the control and dyslipidemic groups do not present significant differences in any parameter, table 3. Discussion Physical activity is recognized as an important non‑pharmacological treatment for numerous diseases and conditions, includingdyslipidemiaandmenopause. Studies indicate that collagen fibers are present in the process of myocardial remodeling, which occur due to aging and other factors. 17,18 Our data show that in the myocardium, the expression of type III collagen fibers did not differ between groups and parameters. In relation to type I collagen, ovariectomy and training brought a decrease in the levels presented in relation to the sedentary ovariectomized control group. Results similar to those found in our study verified the same variable in animals after a period of obesity induced by a diet rich in unsaturated fat. 19 Interestingly, the findings reported in this article have similar results only with the proposed physical activity. Another study where acute myocardial infarction was induced in rats, the gradual increase of types I and III collagen Table 3 – Comparison of the variables Metalloproteinase type 2, Anti-8-Hydroxydeoxyguanosine and Volume Density of collagen fibers III (Vv [fc III]), with the groups studied. Variables CS COS COT LDL-S LDL-OS LDL-OT p* MMP 2 28.5 (4.0) 35.3 (9.1) A 49.0 (3.8) A 54.8 (52.0) A 40.5 (9.6) A,B,C,D 46.8 (31.0) A,B,C,E < 0.001 8-OHDg 105.2 (7.6) 70.0 (10.8) A 64.9 (4.7) A 51.7 (0.5) A 15.3 (7.5) A,B,C,D 38.7 (8.4) A,B,C,E < 0.001 Vv[fc III] 0.007 (0.037) 0.003 (0.024) 0.016 (0.067) 0.015 (0.057) 0.013 (0.062) 0.009 (0.043) 0.649 *ANOVA. Data expressed as mean and standard deviation. A: statistically significant difference between the studied group and the CS group; B: statistically significant difference between the studied group and the COS group; C: statistically significant difference between the studied group and the TOC group; D: statistically significant difference between the studied group and the LDL-S group; E: statistically significant difference between the studied group and the LDL-OS group. MMP2: Metalloproteinase type 2; 8OHdG: Anti-8-Hydroxydeoxyguanosine; Vv [fc III]: Volume Density of collagen fibers III; CS: sedentary non-ovariectomized control; COS: sedentary ovariectomized control; COT: trained ovariectomized control; LDL-S: non-sedentary ovariectomized LDLknockout; LDL-OS: sedentary ovariectomized LDL knockout; LDL-OT: trained ovariectomized LDL knockout. was observed at 4 weeks. The kinetics of collagen I/III increase, in combination with the decrease of the elastic fibers in the infarcted area after an MI, provided evidence that impaired cardiac function after an MI was due to healing or infarct scar formation, with increased rigidity and less flexibility of the heart. 20 Our results suggest that the aging period in this study does not appear to interfere with the increase in the expression of collagen fibers presented in other studies. 21,22 However, when evaluating the LDL-OT groups, there is a clear reduction in the volume of type I collagen fibers. This verification was obtained using the proposed training protocol (intensity or duration). 23,24 Metalloproteinase type 2 and type 9 also participate in the remodeling process of cardiac tissue, and are present in several pathologies such as inflammatory and cardiovascular diseases, among other injuries. 24-29 The expression of metalloproteinase type 9 did not differ between groups and parameters. Regarding metalloproteinase type 2, an increase was shown in the control group with ovariectomy and physical training even in the presence of dyslipidemia. This process explains the factor with the collagen indexes when these are not elevated, because the degradation of collagen and the extracellular matrix is peformed by the action of the metalloproteinases. 25,30-32 The elevated presence of MMPs in patients with dyslipidemias found in some studies suggest their participation in the matrix degradation process in atherosclerotic plaques and in the ruptures of these and with exposure of the nucleus 17,33 and are independent predictors for the progression of kidney disease and are independently associated with an increased risk of mortality. 34 103