IJCS | Volume 31, Nº6, November / December 2018

614 Table 2 - Cross-sectional area, glycogen content and wet weight of the soleus and EDL muscles corrected for tibial length after 8 weeks of either sedentary status or exercise training Skeletal muscle Cross sectional area (µm²) Glycogen (ug/mg) Wet weight (mg/cm) Groups EDL CTR 82.0 ± 4.9 324.0 ± 23.8 74.8 ± 1.5 DMC 50.9 ± 6.2 105 ± 14 a 26.1 ± 1.7 a DMS 70.3 ± 5.3 638.5 ± 57.8 ab 29.8 ± 1.2 a DMT 189.8 ± 17.0 c 500.6 ± 43.5 ab 27.5 ± 1.2 a Soleus CTR 103.9 ± 39.3 90.4 ± 11.2 60.1 ± 2.8 DMC 69.0 ± 1.9 46.1 ± 3.3 35.3 ± 1.5 a DMS 111.1 ± 7.8 162.7 ± 20.2 ab 38.7 ± 1.0 a DMT 318.4 ± 36.0 c 139.3 ± 8.9 b 36.1 ± 1.4 a CTR (n = 10), DMC (n = 11), DMS (n = 12), and DMT (n = 9). a ≠ CTR, b ≠ DMC, c ≠ DMS, DMC and CTR (p < 0.05). Results are presented as mean ± standard derivation of the mean; One-way ANOVA with post-hoc Bonferroni test. Table 3 - Cross-sectional diameter, collagen volume fraction and wet weight of left ventricle corrected for tibial length after 8 weeks of either sedentary status or exercise training Left ventricle Cross-sectional diameter of cardiomyocytes (µm) Collagen (%) Wet weight (mg/cm) Groups CTR 18.8 ± 1.0 5.78 ± 0.45 225.8 ± 685 DMC 17.8 ± 1.4 6.34 ± 1.03 162.2 ± 585 a DMS 34.6 ± 6.8 ab 8.15 ± 0.68 175.8 ± 449 a DMT 25.7 ± 1.0 abc 7.55 ± 0.69 161.3 ± 298 a CTR (n = 10), DMC (n = 11), DMS (n = 12), and DMT (n = 9). a ≠ CTR, b ≠ DMC, c ≠ DMS (p < 0.05). Results are presented as mean ± standard derivation of the mean; One-way ANOVA with post-hoc Bonferroni test. Moura et al. Diabetic rats and aerobic training Int J Cardiovasc Sci. 2018;31(6)610-618 Original Article exercise training protocols were not able to change this variable (Table 4). Discussion Some studies show that aerobic ET aids in controlling blood glucose, whereas other studies showed no significant improvement regarding this control. 14,20 What is known and is widely discussed in the literature is that, physiologically, ET increases the expression of GLUT4 transporters, optimizing glucose uptake in muscle cells and accordingly, it is argued that this has a significant impact on the control of serumglucose, whilemaintaining hepatic glucose production stable. 21 However, this glucose control was not verified in our study. Neither ET protocol was able to reestablish the body weight of the diabetic groups. Body weight maintenance is one of the variables affected by the clinical condition of DM1. 22 With the diminishing supply of glucose into cells, physiological mechanisms degrade other substrates that are available as energy sources, such as proteins and lipids, resulting in the loss of muscle mass, fat reserves, and consequently, loss of body weight. If a person has good glycemic control, these mechanisms