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

147

[ 11 , 18 ]. Indeed, in a classical study of La Rovere et al. [ 39 ], impaired baroreflex

sensitivity (BrS) increased the risk of mortality in MI patients. On the other hand,

ET attenuated cardiac mortality in a 10-year follow-up [ 4 ].

Several evidence from animal studies have been demonstrating that ET improves

BrS and normalizes autonomic dysfunction – favouring parasympathetic activity –

in MI animals [ 16 ]. In addition, after MI, it is possible to observe cardiac sympa-

thetic nerve sprouting associated with imbalance of adrenergic receptor (AR) [ 40 ].

The sympathetic activity maintained over time causes downregulation of the β1-AR,

desensitization of β2-AR, and upregulation of β3-AR [ 40 ]. In the experiment of

Chen et al. [ 40 ], ET was capable to normalize autonomic control and AR balance.

Furthermore, in conjunction with ameliorated autonomic functioning, authors

observed improvement of ventricular function, regional blood flow, decrease on

proinflammatory cytokines, and reduced mortality [ 13 , 14 , 16 ].

ET has been shown effective to improve cardiac hemodynamics and functioning

after the ischemic event [ 13 ]. It is important to highlight that studies in animal models

have shown that the earlier the exercise program begins, the greater were the benefits

in ventricular remodelling due ameliorated cardiomyocyte proliferation, angiogene-

sis and reduced apoptosis in cardiomyocytes [ 40 ]. However, the better “window” to

start ET in rodents seems to be after 1 week of MI induction [ 13 , 14 , 16 ] since rats

subjected to ET in the first days after MI showed elevated mortality [ 28 ].

Regarding the protective effects of ET, studies have shown that ET previous to

MI can protect cardiac function after the event. In fact, rats submitted to a swim-

ming protocol and subsequently induced to MI showed preserved left ventricle

function, indicated by left ventricular end-systolic diameter, left ventricular end-

diastolic diameter, and left ventricular shortening fraction [ 37 , 38 ]. Moreover,

results from treadmill ET added data and indicated that previous MI exercise can

also improve echocardiographic parameters, prevent BrS impairment, as well as

autonomic dysfunction [ 17 ]. Results from experiments performed after MI are not

different and showed ameliorated cardiac functioning in MI rats after ET (50–70%

VO2max, for 1 h a day, 5 days per week) [ 13 , 14 , 16 , 17 ].

Lastly, results have demonstrated to be controversial in relation to the effects of

ET on MI area. In summary, MI area is an evaluation that quantifies cardiomyocyte

akinetic and kinetic area. Several studies have been demonstrating the effectiveness

of ET to cause significant decrease on MI area, evaluated by echocardiographic

(i.e., MI akinetic area) and histologic (i.e., fibrosis score) analyses [ 13 , 14 , 16 , 19 ].

However, this phenomenon is not observed after swimming ET [ 36 ].

During the period of cardiac rehabilitation, some events can make the patient

stop the practice of ET avoiding the ideal adherence to the rehabilitation program,

such as vacation, travels, economical issues, or even the desire to “take a break”,

although it is not advisable. In this sense, Barboza et al. [ 13 ] and Rodrigues et al.

[ 17 ] investigated whether 1 month of detraining could reverse the beneficial effects

of moderate ET after MI.  Results showed that the reduction in MI area, fibrosis

score, cardiac morphology and functioning, BrS, proinflammatory state and sur-

vival observed after ET did not vanish after 1  month of detraining in rats [ 17 ].

However, longer breaks were not studied.

9 Myocardial Infarction and Exercise Training: Evidence from Basic Science