Resistance Training Regulates Cardiac Function through Modulation of miRNA-214

Abstract

Aims: To determine the effects of resistance training (RT) on the expression of microRNA (miRNA)-214 and its target in sarcoplasmic reticulum Ca2+-ATPase (SERCA2a), and on the morphological and mechanical properties of isolated left ventricular myocytes. Main methods: Male Wistar rats were divided into two groups (n = 7/group): Control (CO) or trained (TR). The exercise-training protocol consisted of: 4 × 12 bouts, 5×/week during 8 weeks, with 80% of one repetition maximum. Key findings: RT increased the left ventricular myocyte width by 15% and volume by 12%, compared with control animals (p < 0.05). The time to half relaxation and time to peak were 8.4% and 4.4% lower, respectively, in cells from TR group as compared to CO group (p < 0.05). RT decreased miRNA-214 level by 18.5% while its target SERCA2a expression were 18.5% higher (p < 0.05). Significance: Our findings showed that RT increases single left ventricular myocyte dimensions and also leads to faster cell contraction and relaxation. These mechanical adaptations may be related to the augmented expression of SERCA2a which, in turn, may be associated with the epigenetic modification of decreased miRNA-214 expression.

Downregulation of miR-26b-5p, miR-204-5p, and miR-497-3p Expression Facilitates Exercise-Induced Physiological Cardiac Hypertrophy by Augmenting Autophagy in Rats

“…Accumulated evidences showed that microRNA (miRNA, miR) networks changed in response to exercise contributed to physiological cardiac hypertrophy (Carè et al, 2007;Fernandes et al, 2011;Fernandes et al, 2015). However, different types of exercise training have been reported to cause changes in different miRNAs (Martinelli et al, 2014;Melo et al, 2015;Ramasamy et al, 2015). MiRNAs could target autophagy-related genes and negatively regulate their activities Aredia and Scovassi, 2017;Chen et al, 2017).…”

Cardioprotective Properties of Aerobic and Resistance Training Against Myocardial Infarction

“…Thus, we may hypothesize that if our training protocol were either more intense or performed as high-volume resistance exercise some degree of cardiovascular dysfunction prevention might have been observed. However, it is not possible to know whether such a positive adaptation, as observed in the study of Melo et al [29] can be maintained after MI. Thus, the lack of studies investigat-ing the cardioprotective mechanisms of resistant ET against an ischemic event prevents a fuller understanding of the issue.…”

“…Recently, it has been demonstrated that resistance ET (80 % of one maximum repetition) increases single left ventricular myocyte dimensions and leads to faster cell contraction and relaxation, related to augmented expression of SERCA2a [29]. Thus, we may hypothesize that if our training protocol were either more intense or performed as high-volume resistance exercise some degree of cardiovascular dysfunction prevention might have been observed.…”

The Role of MicroRNAs in the Cardiac Response to Exercise

“…Of note, miR-222 was upregulated in both HF groups (Souza et al 2015). Other miRNAs, including miR-1, -29, -126, and -214, have also been reported to change in both healthy and diseased hearts after exercise (da Silva et al 2012;Melo et al 2014Melo et al , 2015aZhao 2015). Given limited access to tissue, there are no clinical studies to date examining human cardiac miRNA alterations after exercise.…”

“…For example, Cha et al (2013) showed that miR-145 suppressed reactive oxygen species (ROS)-induced Ca 2þ overload and related signaling by targeting CaMKIId, and thereby protected against ROS-induced cardiomyocyte apoptosis. Resistance training decreased the expression of miR-214 contributing to up-regulation of its target, SERCA2a, which enhances SR Ca 2þ -uptake accelerating cardiomyocyte relaxation and loading the SR with Ca 2þ , thereby improving peak Ca 2þ release and contractility (Melo et al 2015a). Melo et al (2015b) also found that swimming increased miR-1 (targeting NCX1) and decreased miR-214 (targeting NCX1 and SERCA2a) regulating Ca 2þ handling after MI.…”