MiRNAs regulate cardiac development, hypertrophy, and angiogenesis, but their role in cardiac hypertrophy (CH) induced by aerobic training has not previously been studied. Aerobic training promotes physiological CH preserving cardiac function. This study assessed involvement of miRNAs-29 in CH of trained rats. Female Wistar rats (n ϭ 7/group) were randomized into three groups: sedentary (S), training 1 (T1), training 2 (T2). T1: swimming sessions of 60 min/5 days/wk/10 wk. T2: similar to T1 until 8th wk. On the 9th wk rats swam 2ϫ/day, and on the 10th wk 3ϫ/day. MiRNAs analysis was performed by miRNA microarray and confirmed by real-time PCR. We assessed: markers of training, CH by ratio of left ventricle (LV) weight/body wt and cardiomyocytes diameter, pathological markers of CH (ANF, skeletal ␣-actin, ␣/␤-MHC), collagen I and III (COLIAI and COLIIIAI) by real-time PCR, protein collagen by hydroxyproline (OH-proline) concentration, CF and CH by echocardiography. Training improved aerobic capacity and induced CH. MiRNAs-1, 133a, and 133b were downregulated as observed in pathological CH, however, without pathological markers. MiRNA-29c expression increased in T1 (52%) and T2 (123%), correlated with a decrease in COLIAI and COLIIIAI expression in T1 (27%, 38%) and T2 (33%, 48%), respectively. MiRNA-29c was inversely correlated to OH-proline concentration (r ϭ 0.61, P Ͻ 0.05). The E/A ratio increased in T2, indicating improved LV compliance. Thus, these results show that aerobic training increase miR-29 expression and decreased collagen gene expression and concentration in the heart, which is relevant to the improved LV compliance and beneficial cardiac effects, associated with aerobic high performance training. cardiac hypertrophy; collagen; molecular markers; swimming training; physiological cardiac hypertrophy; diastolic function microRNAs (miRNAs) are recognized as a new class of gene expression regulators, consisting of short RNAs, singlestranded, that do not synthesize proteins.MiRNAs are currently potential therapeutic targets and biomarkers in cardiovascular research of various physiological and pathological processes (2,3,(33)(34)(35)(36)(37)40). The action of miRNAs occurs at the posttranscriptional level. MiRNAs negatively regulate the expression of their target genes by coupling to the 3=-untranslated regions (3=-UTR) of mRNA expressed by the target gene (direct modulation) or in the 3=-UTR of mRNA related with the expression of target gene (indirect modulation), which represses its translation into protein (18,19).There are several studies involving miRNAs in pathological cardiac hypertrophy (CH) (2, 3, 29, 35, 36). MiRNAs-1, 133a, and 133b are the best known and highly expressed in heart (36) and already have several targets genes validated, as transcription factors, proteins involved in cellular growth and division, rearrangement of myofibrils and cardiac contractility (34). Carè et al. (2) reported that the decreased expression of miRNA-1 and 133 in vivo and in vitro has a critical role in hypertro...

This study showed that aerobic training promotes an increase in the expression of miRNA-126 and that this may be related to exercise-induced cardiac angiogenesis, by indirect regulation of the VEGF pathway and direct regulation of its targets that converged in an increase in angiogenic pathways, such as MAPK and PI3K/Akt/eNOS.

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