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factors are widely elucidated in clinical trials, experimental studies and observa-

tional studies (i.e., cross-sectional). For now, ET should compose the rehabilitation

programs of cardiac patients, since its practice has been demonstrated to improve

exercise tolerance, quality of life, functional capacities and job-related physical

tasks, as well as decrease cardiovascular risk factors and cardiac mortality [ 26 ].

4 Physical Activity and Myocardial Infarction

In animal studies, PA can be mimicked by the voluntary run performed by the ani-

mals in a running wheel during a determined period. In the context of MI, authors

have studied the posterior and previous plus posterior effects of PA on cardiac

remodelling and functioning in infarcted mice. However, just few evidence have

been published in this issue and more experiments are necessary.

In this sense, Bito et al. [ 27 ] studied the effects of PA posterior to MI on cardiac

remodelling of infarcted mice. Thus, after MI, animals had free access to the run-

ning wheel during 8 weeks. To investigate cardiac remodelling, myocytes from the

non-infarcted left ventricle were isolated and investigated regarding morphological

and functional aspects. After several analyses, authors observed that sedentary mice

showed a cardiac remodelling phenotype, characterized by increased heart weight-

body weight ratio and cell width. PA was not effective to inhibit such morphological

alterations and both groups presented similar results. In turn, cell shortening elicited

by electrical stimulation, which was decreased in infarcted sedentary mice, was

restored in the cardiomyocyte of infarcted mice which had access to the running

wheel [ 27 ]. Further analyses showed that calcium transient was increased in ani-

mals from the PA group due to an elevated capacity of Ca2+ removal by Na+-Ca2+

exchanger (NCX) [ 27 ].

In turn, Puhl et al. [ 28 ] not only studied the posterior effects of PA on MI, but

also the previous effects. Firstly, mice could voluntary run in a running wheel for

6 weeks mimicking a PA context. After this period, mice underwent experimental

MI and, 5 days after the surgery, were allowed to use the running wheel for more

4  weeks. Similar to Bito et  al. [ 27 ], results indicated that PA did not modulate

MI-induced cardiac hypertrophy, since increased organ weight and cardiomyocyte

diameter were equally observed in both PA and sedentary groups. However, histo-

logical and magnetic resonance imaging analyses indicated that PA decreased

collagen content and scar formation of the whole left ventricle and in the scar region

after MI, as well as partially inhibited the formation of apical aneurysms associated

with left ventricle dilation. Authors also observed decreased MMP activity and

mRNA expression of proinflammatory citokynes (i.e., TNF-α, IL-6 and IL-1β).

These alterations on inflammatory state seem to have impacted cardiac morphology,

as the mRNA expression of TNF-α was positively correlated with infarct size and

collagen mRNA expression in sedentary mice, whereas this phenomenon was

blunted and not showed in the exercised group.

9 Myocardial Infarction and Exercise Training: Evidence from Basic Science