Abstract
AimsWe assessed the effects of a short-term exercise training on cardiac function, oxidative stress markers, and type 3 iodothyronine deiodinase (D3) activity in cardiac tissue of spontaneously hypertensive rats (SHR) following experimental myocardial infarction (MI).MethodsTwenty-four SHR (aged 3 months) were allocated to 4 groups: sham+sedentary, sham+trained, MI+sedentary and MI+trained. MI was performed by permanent ligation of the coronary artery. Exercise training (treadmill) started 96 hours after MI and lasted for 4 weeks (~60% maximum effort, 4x/week and 40 min/day). Cardiac function (echocardiography), thioredoxin reductase (TRx), total carbonyl levels, among other oxidative stress markers and D3 activity were measured. A Generalized Estimating Equation was used, followed by Bonferroni’s test (p<0.05).ResultsMI resulted in an increase in left ventricular mass (p = 0.002) with decreased cardiac output (~22.0%, p = 0.047) and decreased ejection fraction (~41%, p = 0.008) as well as an increase in the carbonyl levels (p = 0.001) and D3 activity (~33%, p<0.001). Exercise training resulted in a decrease in left ventricular mass, restored cardiac output (~34%, p = 0.048) and ejection fraction (~20%, p = 0.040), increased TRx (~85%, p = 0.007) and reduced carbonyl levels (p<0.001) and D3 activity (p<0.001).ConclusionsOur short-term exercise training helped reverse the effects of MI on cardiac function. These benefits seem to derive from a more efficient antioxidant response and lower D3 activity in cardiac tissue.
Highlights
Myocardial infarction (MI) leads to changes in the oxidative metabolism of cardiomyocytes in response to ischemic injury, which arises from an imbalance between reactive oxygen species (ROS) production and antioxidant agents [1]
MI resulted in an increase in left ventricular mass (p = 0.002) with decreased cardiac output (~22.0%, p = 0.047) and decreased ejection fraction (~41%, p = 0.008) as well as an increase in the carbonyl levels (p = 0.001) and D3 activity (~33%, p
We evaluated the expression of hypoxia-inducible factor 1 (HIF-1) and vascular endothelial growth factor (VEGF) considering that HIF-1 is primarily involved in promoting angiogenesis [13], and that reduced HIF-1 levels in the myocardium may be associated with increased ROS [14]
Summary
Myocardial infarction (MI) leads to changes in the oxidative metabolism of cardiomyocytes in response to ischemic injury, which arises from an imbalance between reactive oxygen species (ROS) production and antioxidant agents [1]. Increased D3 activity may lead to lower intracellular T3 levels and impaired cellular metabolism. We have found increased D3 activity after MI associated to imbalance in the redox state (pro-oxidative) [3]. MI-induced increase in D3 activity was associated with lower T3 concentration in cardiomyocytes, whereas plasma T3 levels were unchanged [4]. Long-term effects caused by increased D3 activity as a result of imbalance in the redox state appear to contribute to pathologic ventricular remodeling and lower cardiac function [5]
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