Inhibiting MicroRNA-497 Improves the Effects of Exercise Training on Myocardial Infarction

2020 ◽  
Vol 41 (07) ◽  
pp. 475-483
Author(s):  
Zhenci Li ◽  
Jing Lv ◽  
Yizhi Pan ◽  
Yi Luo ◽  
Zhen Liu ◽  
...  

AbstractExercise training (ET) could improve myocardial infarction (MI), and microRNA-497 is highly associated with MI. This study aimed to investigate whether the regulation of miR-497 is involved in the positive effects of ET on MI. MI rat models induced by left anterior descending (LAD) were subjected to interval training and infarct size was observed. Blood and myocardial samples were collected from the rats for determining the expressions of miR-497. To evaluate the functions of miR-497, miR-497 agomir and antagomir were injected accordingly into grouped rats during ET, and subsequently, the expressions of apoptotic and inflammatory factors were determined. ET reduced the infarct size in MI rats and inhibited the levels of miR-497. MiR-497 agomir injection enlarged the infarct size, and reversed the shrunk infarct size induced by ET. However, miR-497 antagomir further promoted the positive effect on MI improved by ET. Chloride voltage-gated channel 3 (CLCN3) was identified as the most possible target for miR-497. Moreover, ET improving MI also involved the regulation of apoptotic and inflammatory factors. The mechanisms underlying the positive effects of ET on MI were highly associated with the regulation of miR-497.

2020 ◽  
pp. 1-12
Author(s):  
S. Rahmati-Ahmadabad ◽  
M.-A. Azarbayjani ◽  
D.R. Broom ◽  
M. Nasehi

This study examined the independent and combined effects of high-intensity interval training (HIIT) and flaxseed oil supplementation on cognitive/executive functions in middle-aged rats. Hippocampal neurotropic brain factor (BDNF) and tyrosine kinase receptor B (TrkB) gene expression were also measured. Animals were randomly divided into groups including no exercise control and saline (CS), no exercise control and flaxseed oil supplement (CF), exercise training-and saline (TS) and exercise training and flaxseed oil supplement (TF). The training groups undertook a program of HIIT (10 weeks, five sessions per week) and the supplement groups received flaxseed oil supplement (300 mg/kg). The results showed that HIIT and flaxseed oil supplementation independently had positive effects on memory and learning (P<0.05). HIIT and flaxseed oil independently decreased immobility behaviour and increased hippocampal BDNF and TrkB genes expression (P<0.05). HIIT and flaxseed oil combination had a greater effect on some variables (hippocampal TrkB gene expression, memory and immobility) compared to each intervention alone (P<0.05). In conclusion, HIIT and flaxseed oil can independently improve cognitive/executive functions. In addition, HIIT had a greater positive effect than flaxseed oil supplementation on memory and immobility. The combination of HIIT and flaxseed oil supplement had a more positive effect compared to each intervention alone on memory, and immobility. Hippocampal BDNF gene expression did not significantly differ in the combination or independent groups. Thus, future work is needed on several other genes in different segments of the brain to find the additive-mechanisms involved in memory and immobility regulation and younger and older species of rat should be examined.


2021 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Abdolhamid Zokaei ◽  
Mehran Ghahramani

Background: The creatine phosphokinase-MB (CPK-MB) isoenzyme level is useful in determining the myocardial infarction (MI) extent and time. Evidence indicates the possible effect of exercise training on reducing the amount of CPK-MB, but the proper intensity of exercise is still unclear. Objectives: In this study the effect of intensity of exercise training on creatinine kinas after a myocardial infarction in plasma levels of male Wistar rats was comparing. Methods: Thirty two male Wistar rats at 10 weeks of age were divided in to four groups [low (N = 8), moderate (N = 8), and high (N = 8) intensity interval training and a control (N = 8) group (no exercise)]. Six weeks later, rats became MI patients through surgery. CPK-MB plasma levels were investigated before training, immediately after training for six weeks as well as 12 hours after MI. The data were analyzed by ANOVA with repeated measure and Tukey (α ≥ 0.05). Results: The results showed that changes in CK enzyme at 12 hours after MI in LIIT (113.88 ± 19.25), MIIT (135.88 ± 35.58) and HIIT (105.75 ± 19.05) were statistically significant compared to the control group (124.62 ± 23.41) only in 12 hours after MI and this reduction in the low-intensity interval training group was significant than the other two groups (P = 0.0001). Conclusions: In this study, six weeks of interval training with each intensity was likely to make cardiac cells resistant to necrosis resulting in low levels of the CPK-MB enzyme compared to the control group after the myocardial infarction event.


2015 ◽  
Vol 37 (1) ◽  
pp. 162-175 ◽  
Author(s):  
Lichan Tao ◽  
Yihua Bei ◽  
Shenghui Lin ◽  
Haifeng Zhang ◽  
Yanli Zhou ◽  
...  

Background/Aims: Acute myocardial infarction (AMI) represents a major cause of morbidity and mortality worldwide. Exercise has been proved to reduce myocardial ischemia-reperfusion (I/R) injury However it remains unclear whether, and (if so) how, exercise could protect against AMI. Methods: Mice were trained using a 3-week swimming protocol, and then subjected to left coronary artery (LCA) ligation, and finally sacrificed 24 h after AMI. Myocardial infarct size was examined with triphenyltetrazolium chloride staining. Cardiac apoptosis was determined by TUNEL staining. Mitochondria density was checked by Mito-Tracker immunofluorescent staining. Quantitative reverse transcription polymerase chain reactions and Western blotting were used to determine genes related to apoptosis, autophagy and myocardial energy metabolism. Results: Exercise training reduces myocardial infarct size and abolishes AMI-induced autophagy and apoptosis. AMI leads to a shift from fatty acid to glucose metabolism in the myocardium with a downregulation of PPAR-α and PPAR-γ. Also, AMI induces an adaptive increase of mitochondrial DNA replication and transcription in the acute phase of MI, accompanied by an activation of PGC-1α signaling. Exercise abolishes the derangement of myocardial glucose and lipid metabolism and further enhances the adaptive increase of mitochondrial biogenesis. Conclusion: Exercise training protects against AMI-induced acute cardiac injury through improving myocardial energy metabolism and enhancing the early adaptive change of mitochondrial biogenesis.


Author(s):  
Núria Argudo ◽  
Anna Rodó-Pin ◽  
Juana Martínez-Llorens ◽  
Ester Marco ◽  
Laura Visa ◽  
...  

ABSTRACT Patients requiring surgery for locally advanced esophagogastric cancer often require neoadjuvant therapy (NAT), which may have a detrimental impact on cardiorespiratory reserve. The aims of this study were to investigate the feasibility and tolerability of a 5-week preoperative high-intensity interval training program after NAT, and to assess the potential effects of the training protocol on exercise capacity, muscle function, and health-related quality of life (HRQL). We prospectively studied consecutive patients with resectable locally advanced esophageal and gastric cancer in whom NAT was planned (chemo- or chemoradiotherapy). Feasibility was assessed with the TELOS (Technological, Economics, Legal, Operational, and Scheduling) components, and data on exercise tolerability (attendance and occurrence of adverse or unexpected events). Exercise capacity was assessed with peak oxygen uptake (VO2peak) in a cardiopulmonary exercise test at baseline, post-NAT, and following completion of a high-intensity interval exercise training (25 sessions). Changes in muscle strength and HRQL were also assessed. Of 33 recruited subjects (mean age 65 years), 17 received chemoradiotherapy and 16 chemotherapy. All the TELOS components were addressed before starting the intervention; from a total of 17 questions considered as relevant for a successful implementation, seven required specific actions to prevent potential concerns. Patients attended a mean of 19.4 (6.4) exercise sessions. The predefined level of attendance (≥15 sessions of scheduled sessions) was achieved in 27 out of 33 (81.8%) patients. Workload progression was adequate in 24 patients (72.7%). No major adverse events occurred. VO2peak decreased significantly between baseline and post-NAT (19.3 vs. 15.5 mL/Kg/min, P &lt; 0.05). Exercise led to a significant improvement of VO2peak (15.5 vs. 19.6 mL/kg/min, P &lt; 0.05). Exercise training was associated with clinically relevant improvements in some domains of HRQL, with the social and role function increasing by 10.5 and 11.6 points, respectively, and appetite loss and fatigue declining by 16 and 10.5, respectively. We conclude that a structured exercise training intervention is feasible and safe following NAT in patients with esophagogastric cancer, and it has positive effects to restore exercise capacity to baseline levels within 5 weeks with some improvements in HRQL.


2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Diego Fernando Batista ◽  
Bertha Furlan Polegato ◽  
Renata Candido da Silva ◽  
Renan Turini Claro ◽  
Paula Shmidt Azevedo ◽  
...  

The objective of this study was to analyze the impact of different modalities and intensities of exercise training on cardiac remodeling started early after experimental myocardial infarction (MI). Male Wistar rats, weighing 200–250 g, were subjected to experimental MI. After 5 days, the animals were allocated into three experimental groups and observed for three months: S (sedentary control animals), C (animals subjected to continuous low-intensity training), and HIT (animals subjected to high-intensity interval training). Low-intensity exercise training was performed at a treadmill speed corresponding to 40% VO2 max, which was kept unchanged throughout the entire session (i.e., continuous low-intensity training). High-intensity interval training was performed in such a way that rats run during 3 min at 60% VO2 max, followed by 4-minute intervals at 85% VO2 max (i.e., high-intensity interval training). After the follow-up period, we studied hypertrophy and ventricular geometry, functional alterations in vivo and in vitro, oxidative stress, apoptosis, and cardiac energetic metabolism. Our data showed that both high-intensity interval and continuous low-intensity modalities improved cardiac energetic metabolism variables in comparison with sedentary infarcted animals. In addition, high-intensity interval training decreased cardiac oxidative stress, associated with improved diastolic function. On the other hand, the continuous low-intensity group showed impairment of cardiac function. Therefore, altogether, our data suggest that high-intensity interval training could be the best modality for early physical exercise after MI and should be better studied in this clinical scenario.


2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
A Sigl ◽  
K Esefeld ◽  
F Latsch ◽  
M Halle

Abstract Funding Acknowledgements Type of funding sources: None. Background Deterioration of left ventricular function after acute myocardial infarction is common, particular in ST-elevation myocardial infarction (STEMI). This often leads to heart failure with reduced ejection fraction (HFrEF). Exercise training has shown to be beneficial in stable chronic heart failure patients. However, effects of exercise training have been rarely investigated during very early phases of STEMI.  Purpose The Exercise in Acute Myocardial Infarction (Ex-AMI) pilot study wanted to investigate whether exercise training has beneficial effects on ventricular remodeling under the following conditions: a) started early after myocardial infarction  b) exclusively after STEMI c) performed with higher intensity.  The hypothesis of this study was that exercise training early after acute myocardial infarction performed for 24 weeks is superior to usual care, regarding the improvement of echocardiographic parameters. It was also assumed that higher-intensity interval training is more effective than moderate continuous training.  Methods   Therefore, we randomized 19 patients with STEMI (58.0 ± 7.1 years, 5% female) and left ventricular ejection fraction (LVEF) &lt;55% to: 1. Moderate continuous training (MCT; 50-60% VO2peak; n = 6) 2. Higher intensity interval training (HIIT; MCT interspersed by intervals of 80-85% VO2peak; n = 6)  3. Usual care (UC; n = 7)  Exercise groups (EG: MCT and HIIT) started seven days after STEMI (run-in period for two weeks, followed by a tailored supervised exercise program for 22 weeks). Three-dimensional echocardiography and cardiopulmonary exercise testing were performed at the beginning and at the end of the training period. Patients were also continuously monitored for adverse events. Results At baseline, LVEF (46.3 ± 6,5%) as well as exercise capacity (VO2peak: 17.8 ± 4.4·kg-1·min-1) were impaired. In both exercise groups (EG: MCT and HIIT) LVEF improved significantly more than in the control group (mean change +7.3 ± 3.5% in EG vs. 2.3 ± 2.3% in UC; p = 0.007). Furthermore HIIT was not superior to MCT (mean change 7.6 ± 3.6% in HIIT vs. 6.7 ± 4.1% in MCT; p = 0.78) in terms of LVEF. There were no training associated adverse events.  Conclusion Exercise training early after acute STEMI seems to have anti-remodeling effects. There is a need for more randomized controlled trials to confirm these findings, in order to find the optimal timing and dose of exercise after STEMI. Abstract Figure. Changes in LVEF (in %) after 24 weeks


2018 ◽  
Vol 7 (2) ◽  
pp. 46-55 ◽  
Author(s):  
Babak Ebadi ◽  
Arsalan Damirchi

Myocardial infarction (MI) is the most common type of heart disease. According to recent studies, mitochondrial dysfunction has been suggested as a central player in cardiac disease and evidences point out the association of mitochondrial morphology with development of heart diseases. Exercise training plays a protective role against cardiovascular disease. However, the role of exercise training on proteins involved in mitochondrial dynamics and mitophagy system are not well understood. Therefore, the aim of the present study was to investigate these on cardiac mitochondrial dynamic and mitophagy proteins in rats with myocardial infarction. The present study was post-test design experiment with the control group. after MI with ligation of the left anterior descending coronary artery (LAD) and ensuring the creation of MI by echocardiography, male rats were subjected to high intensity interval training (HIIT), moderate (MIIT), low (LIIT), sedentary myocardial infarction (SED-MI) and healthy control groups. After six weeks exercise, the levels of MFN2, DRP1, Parkin, P62 and PGC-1α proteins were measured by ELISA method. Data analysis showed that proteins levels of MFN2, PGC-1α, Parkin and P62 decreased significantly in SED-MI group compared to healthy control while DRP1 protein levels increased significantly (P≤0.05). Also, MFN2 and PGC-1α proteins increased in MIIT group compared with SED-MI group and DRP1 protein levels were significantly decreased (P≤0.05). Moderate-intensity interval training (MIIT) resulted to improve mitochondrial fusion and fusion proteins in rats with myocardial infarction. While high and low intensity interval training (HIIT, LIIT), despite increasing MFN2 and PGC-1α and reducing DRP1, failed to improve fusion and mitochondrial fission


1999 ◽  
Vol 82 (S 01) ◽  
pp. 68-72 ◽  
Author(s):  
Alessandro Sciahbasi ◽  
Eugenia De Marco ◽  
Attilio Maseri ◽  
Felicita Andreotti

SummaryPreinfarction angina and early reperfusion of the infarct-related artery are major determinants of reduced infarct-size in patients with acute myocardial infarction. The beneficial effects of preinfarction angina on infarct size have been attributed to the development of collateral vessels and/or to post-ischemic myocardial protection. However, recently, a relation has been found between prodromal angina, faster coronary recanalization, and smaller infarcts in patients treated with rt-PA: those with preinfarction angina showed earlier reperfusion (p = 0.006) and a 50% reduction of CKMB-estimated infarct-size (p = 0.009) compared to patients without preinfarction angina. This intriguing observation is consistent with a subsequent observation of higher coronary recanalization rates following thrombolysis in patients with prodromal preinfarction angina compared to patients without antecedent angina. Recent findings in dogs show an enhanced spontaneous lysis of plateletrich coronary thrombi with ischemic preconditioning, which is prevented by adenosine blockade, suggesting an antithrom-botic effect of ischemic metabolites. Understanding the mechanisms responsible for earlier and enhanced coronary recanalization in patients with preinfarction angina may open the way to new reperfusion strategies.A vast number of studies, globally involving ≈17,000 patients with acute myocardial infarction, have unequivocally shown that an infarction preceded by angina evolves into a smaller area of necrosis compared to an infarct not preceded by angina (Table 1) (1). So far, preinfarction angina has been thought to have cardioprotective effects mainly through two mechanisms: collateral perfusion of the infarctzone (2-4), and ischemic preconditioning of the myocardium (5-7). Here we discuss a further mechanism of protection represented by improved reperfusion of the infarct-related artery.


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