Exercise for Cardiovascular Disease Prevention and Treatment From Molecular to Clinical, Part 1

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of the strength and maturity of the collagen – and observed normalized levels in the

non-infarcted area and in the right ventricle of MI rats after ET [ 22 ]. None of the

studies investigated the possible mechanisms associated with ameliorated collagen

deposition in the heart of MI rats.

In front of this lack, inferences can be made by other studies which used similar ET

programs. Rodrigues et al. [ 14 ], showed decreased TNF-α protein content and TNF-α/

IL-10 ratio in the left ventricle of MI rats subjected to 3 months of moderate aerobic ET

[ 14 ]. In addition, a study from Melo et al. [ 36 ], seems to offer a better elucidation trough

microRNA analyses, once the authors report that swimming ET increases MiRNA-29a,

b and c expression on border region and remote myocardial of MI rats. These results

were associated with decreases on collagen expression and content in ~45% [ 36 ].

Once ET showed effectiveness to decrease the percentage of collagen deposition,

as well as normalized the levels of HP in the heart of MI rats, several studies hypoth-

esized that ET could revert and normalize scar formation after MI. Most studies have

been evaluating scar formation through ventricular wall thickness measurement by

echocardiographic analyses. This evaluation has been demonstrating strong correla-

tion with histological data. Results regarding scar formation are uncertain and can be

exercise-dependent, since evidence indicate that after treadmill ET it is possible to

observe an increase in wall thickness [ 13 , 14 , 17 ], whereas 10 weeks of swimming

ET (60 min; 5 days/week) seems not to proportionate the same effect [ 36 ].

A last repercussion elicited by collagen degradation is wall thinning ventricular

dilation, which strongly elevates systolic and diastolic wall stress [ 8 ]. In conjunc-

tion with other cellular signalling mechanisms associated with cytokines, RAAS,

increased sympathetic nerve activity, catecholamines, and fetal genes, this phenom-

enon induces pathological cardiac hypertrophy.

ET has been extensively studied in this context, believed as a stress capable to

counteract the pathological cardiac signalling triggered by MI. Regarding wall thin-

ning ventricular dilation, studies have demonstrated that ET can increase ventricular

dilation [ 13 , 14 , 16 , 17 , 37 , 38 ]. However, different from post-MI pathological

remodelling, the ejection fraction is also increased indicating a physiological

remodelling [ 13 , 14 , 16 , 17 , 37 , 38 ].

When studying the effects of ET on MI-induced cardiac hypertrophy, data have

been demonstrating that ET can attenuate cardiac remodelling. Such as in the con-

text of wall ventricular dilation, cardiac hypertrophy seems to be observed in con-

junction with data from cardiac functional analyses. In the experiment of Bozi et al.

[ 34 ], for example, rats underwent 8 weeks of moderate ET (5 days/week;) previous

to experimental MI. Animals were kept alive for 15 days after MI surgery and, then,

euthanized. Results demonstrated that MI rats showed left ventricular remodelling,

indicated by increased heart weight (HW) and HW-body weight (BW) ratio.

Interestingly, ET rats also showed elevated HW and HW-BW ratio concomitantly

with greater myocyte length and width than sedentary-MI [ 34 ]. However, contrary

to sedentary MI rats, trained MI rats showed elevated cardiac functioning [ 34 ].

Autonomic dysfunction is also an important issue observed after MI, which has

been associated with cardiac inflammation, remodelling and functioning, as well as

strongly associated with several poor outcomes, including more increased mortality

I.C. Moraes-Silva et al.