IJCS | Volume 31, Nº5, September / October 2018

510 Figure 4 - Lung water content in control (C), infarcted sedentary (S), continuous exercise (CE) and accumulated exercise (AE) groups. Values expressed as mean ± SEM. *p < 0.05 vs. C; †p < 0.05 vs. S; §p < 0.05 vs. AE. Feriani et al. Accumulated exercise in infarcted old rats Int J Cardiovasc Sci. 2018;31(5)505-512 Original Article atrophy) and function (e.g., impairedmetabolism), which may collaborate with the development of the myopathy observed during heart failure. 18,21,22,23 Regarding the preserved capacity demonstrated by both trained groups, our data are in line with evidence that have demonstrated that adult rats underwent to exercise training programs previous to MI showed increased cardiorespiratory fitness in comparison with sedentary groups. 8 However, as aforementioned, the CE group demonstrated a phenomenon that was not described before in the literature, indicating that older rats submitted to surgical induction of MI might show decreased aerobic capacity associated with pulmonary congestion. These controversial results are probably a product of the animal used in the current study. In fact, most studies have studied adult animals and, for the first time, the protective effect of exercise training was investigated in older animals. The plausibility behind this theory is based on the decreased capacity of the old organic system to cope with stressful agents (e.g., physical, chemical), as postulated by Fransceschi et al. 24 in the inflammaging metatheory. This possibility has been confirmed by several experiments, including the recent data from El Assar et al. 25 that indicated that frail older adults present a low expression of genes involved in the cellular response to stress (i.e., oxidative stress and cellular hypoxia). 25 In congruence, a phenomenon denominated as myocardial injury - which is characterized by a transient myocardial injury in the right ventricle (RV) - might be observed in response to aerobic exercise due to the greater hemodynamic load and wall stress. 26-28 In fact, animal and human studies have demonstrated impaired RV function, decreased cardiac handling, and increased cardiac biomarkers (i.e., creatine kinase and N-terminal pro-brain natriuretic peptide), during and immediately after the end of the aerobic exercise. 26-28 Therefore, it is possible to infer that very-old adult rats present an impaired capacity to cope with the stressful environment developed in response to continuous aerobic exercise, leading to significant pulmonary congestion; thus, fractioned aerobic exercise seems to be a more beneficial recommendation for older adults, especially those with increased risk to develop cardiovascular diseases and frailty, since after an ischemic event they can present a better prognosis. Although some limitations of the present study should be considered (e.g., the absence of echocardiographic evaluations to evaluate left ventricle dimensions and function) our observations suggest that the improvements observed after accumulated aerobic training may have occurred due to beneficial cardiac remodeling induced by the exercise training, as shown by the increased LV relative weight observed in AE. These data are supported by several evidences, which indicate a beneficial cardiac remodeling after exercise training due to increased LV cavity and dilation, inducing significant functional changes in cardiac contractility and, consequently, improving cardiac output. 29,30 Additionally, MI area was not evaluated and this is a limitation of the present study.