IJCS | Volume 31, Nº5, September / October 2018

509 Figure 3 - Body weight in control (C), infarcted sedentary (S), continuous exercise (CE) and accumulated exercise (AE) groups. Values expressed as mean ± SEM. #p < 0.05 vs. Baseline. Table 1 - Organ and muscles relative weight in control (C), infarcted sedentary (S), continuous exercise (CE) and accumulated exercise (AE) groups C S CE AE LV (g/100 g l.w.) 0.206 ± 0.002 0.253 ± 0.009 0.257 ± 0.010 0.276 ± 0.017* RV (g/100 g l.w.) 0.064 ± 0.012 0.056 ± 0.001 0.056 ± 0.001 0.061 ± 0.006 Soleus (g/100 g l.w.) 0.028 ± 0.003 0.035 ± 0.003 0.032 ± 0.002 0.035 ± 0.001 Gastrocnemius (g/100 g l.w.) 0.338 ± 0.03 0.362 ± 0.059 0.371 ± 0.029 0.388 ± 0.039 Values expressed as mean ± SEM. LV: left ventricle; RV: right ventricle. *p < 0.05 vs. C. Feriani et al. Accumulated exercise in infarcted old rats Int J Cardiovasc Sci. 2018;31(5)505-512 Original Article function of the differences in the design of exercise programand sample types. Indeed, whenMartinez et al. 17 underwent Wistar rats to a moderate-intensity aerobic exercise protocol similar with the ET that was used in the current study, the researchers observed a similar magnitude of improvements among the groups. Interestingly, after MI, both groups demonstrated a two-fold increase on physical capacity in relation to the S group. However, this evaluation was significantly decreased in CE when it was compared with the time before MI, whereas no significant alterations were observed in CE. Furthermore, CE demonstrated a higher index of pulmonary congestion - lung water content - in comparison with all other experimental groups. These data suggest that elderly rats trained through continuous aerobic trainingmight present decreased capacity to cope with MI injury in relation to elderly rats trained through aerobic fractioned exercise. Decreased physical capacity in S is widely described in the literature. Indeed, after MI, cardiorespiratory fitness is commonly decreased due to a central mechanism - characterized by decreased cardiac output, which is the product of cardiomyocyte death and, consequently, impaired cardiac function and unwanted cardiac remodeling - and a peripheral mechanism - caused by marked alterations on skeletal muscle architecture (i.e.,