An androgenic steroid decreases left ventricular compliance in rats

1995 ◽  
Vol 268 (3) ◽  
pp. H1096-H1105 ◽  
Author(s):  
B. Trifunovic ◽  
G. R. Norton ◽  
M. J. Duffield ◽  
P. Avraam ◽  
A. J. Woodiwiss
Keyword(s):  
Cardiac Contractility ◽  
Chronic Administration ◽  
Elastic Stiffness ◽  
Left Ventricular ◽  
Heart Weight ◽  
Control Group ◽  
Nandrolone Decanoate ◽  
Androgenic Steroid ◽  
Strain Relation ◽  
Stiffness Constant

The effect of chronic administration of an androgenic steroid on left ventricular (LV) compliance and contractility was studied in rats. Rats received a biweekly intramuscular injection of nandrolone decanoate (5 mg/kg; steroid group) or the vehicle (control group) for 3 mo. Cardiac performance was measured in anesthetized open-chest ventilated rats. LV compliance was determined from the slope of the LV end-diastolic pressure (LVEDP) vs. LV end-diastolic (LVED) strain relation measured in the long and short axes of the LV. LV regional myocardial compliance was determined from the slope of the LVED stress vs. LVED strain relation (myocardial elastic stiffness constant). Cardiac contractility was determined from the slope of the LV end-systolic (LVES) pressure vs. LVES strain relation. Systolic performance was also assessed from the slope of the pressure-length area (PL area) or stroke work vs. LVED strain and LVEDP relations. Nandrolone decanoate decreased body weight, heart weight, and plasma testosterone concentrations but increased the heart weight-to-body weight ratio. Nandrolone decanoate decreased LV compliance (slope of LVEDP vs. LVED strain relation in long and short axes; steroid vs. control, P < 0.01). This occurred as a result of an increased regional myocardial stiffness (myocardial elastic stiffness constant; steroid vs. control, P < 0.01), which resulted in a reduced cardiac systolic performance (PL area vs. LVEDP, slope of steroid vs. control group, P < 0.005). Diastolic geometry (LV wall thickness-to-radius ratio) and cardiac contractility were unchanged with steroid administration. In conclusion, chronic administration of the androgenic steroid nandrolone decanoate decreases LV myocardial compliance and thus overall cardiac performance without altering contractility in rats.

scholarly journals Insulin Preconditioning Elevates p-Akt and Cardiac Contractility after Reperfusion in the Isolated Ischemic Rat Heart

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Tamaki Sato ◽  
Hiroaki Sato ◽  
Takeshi Oguchi ◽  
Hisashi Fukushima ◽  
George Carvalho ◽  
...  
Keyword(s):  
Myocardial Dysfunction ◽  
Cardiac Contractility ◽  
Left Ventricular ◽  
Control Group ◽  
Optimal Timing ◽  
Insulin Administration ◽  
Rat Hearts ◽  
Reperfusion Period ◽  
Pressure Development ◽  
And Control

Insulin induces cardioprotection partly via an antiapoptotic effect. However, the optimal timing of insulin administration for the best quality cardioprotection remains unclear. We tested the hypothesis that insulin administered prior to ischemia provides better cardioprotection than insulin administration after ischemia. Isolated rat hearts were prepared using Langendorff method and divided into three groups. The Pre-Ins group (Pre-Ins) received 0.5 U/L insulin prior to 15 min no-flow ischemia for 20 min followed by 20 min of reperfusion. The Post-Ins group (Post-Ins) received 0.5 U/L insulin during the reperfusion period only. The control group (Control) was perfused with KH buffer throughout. The maximum of left ventricular derivative of pressure development (dP/dt(max)) was recorded continuously. Measurements of TNF-αand p-Akt in each time point were assayed by ELISA. After reperfusion, dP/dt(max) in Pre-Ins was elevated, compared with Post-Ins at 10 minutes after reperfusion and Control at all-time points. TNF-αlevels at 5 minutes after reperfusion in the Pre-Ins were lower than the others. After 5 minutes of reperfusion, p-Akt was elevated in Pre-Ins compared with the other groups. Insulin administration prior to ischemia provides better cardioprotection than insulin administration only at reperfusion. TNF-αsuppression is possibly mediated via p-Akt leading to a reduction in contractile myocardial dysfunction.

Chronically Administered Acetaminophen and the Ischemia/Reperfused Myocardium

2003 ◽  
Vol 228 (6) ◽  
pp. 674-682 ◽  
Author(s):  
R. Golfetti ◽  
T. Rork ◽  
G. Merrill
Keyword(s):  
Creatine Kinase ◽  
Tap Water ◽  
Chronic Administration ◽  
Left Ventricular ◽  
Low Flow ◽  
Control Group ◽  
Coronary Perfusion ◽  
In Vitro Production

Male and female Hartley strain guinea pigs weighing 280 ± 10 g were given acetaminophen-treated water ad libitum for 10 days. Sham-treated control animals were given similar quantities of untreated tap water (vehicle-treated control group). On Day 10, hearts were extracted, instrumented, and exposed to an ischemia (low-flow, 20 min)/reperfusion protocol. Our objective was to compare and contrast ventricular function, coronary circulation, and selected biochemical and histological indices in the two treatment groups. Left ventricular developed pressure in the early minutes of reperfusion was significantly greater in the presence of acetaminophen, e.g., at 1 min, 40 ± 4 vs 21 ± 3 mmHg ( P < 0.05). Coronary perfusion pressure was significantly less from 3 to 40 min of reperfusion in the presence of acetaminophen. Creatine kinase release in vehicle-treated hearts rose from 42 ± 14 (baseline) to 78 ± 25 units/liter by the end of ischemia. Corresponding values in acetaminophen-treated hearts were 36 ± 8 and 44 ± 14 units/liter. Acetaminophen significantly ( P < 0.05) attenuated release of creatine kinase. Chemiluminescence, an indicator of the in vitro production of peroxynitrite via the in vivo release of superoxide and nitric oxide, was also significantly attenuated by acetaminophen. Electron microscopy indicated a well-preserved myofibrillar ultrastructure in the postischemic myocardium of acetaminophen-treated hearts relative to vehicle-treated hearts (e.g., few signs of contraction bands, little or no evidence of swollen mitochondria, and well-defined light and dark bands in sarcomeres with acetaminophen; opposite with vehicle). We conclude that chronic administration of acetaminophen provides cardioprotection to the postischemic, reperfused rodent myocardium.

scholarly journals Does the β 2 -Agonist Clenbuterol Help to Maintain Myocardial Potential to Recover During Mechanical Unloading?

Circulation ◽  
2005 ◽  
Vol 112 (9_supplement) ◽  
Author(s):  
Hiroshi Tsuneyoshi ◽  
Wnimunk Oriyanhan ◽  
Hideo Kanemitsu ◽  
Reiko Shiina ◽  
Takeshi Nishina ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Chronic Administration ◽  
Left Ventricular ◽  
Control Group ◽  
Assist Device ◽  
Mechanical Unloading ◽  
Myocardial Apoptosis ◽  
Plasmic Reticulum ◽  
And Function ◽  
Myocardial Atrophy

Objective— Chronic mechanical unloading induces left ventricular (LV) atrophy, which may impair functional recovery during support with an LV-assist device. Clenbuterol, a β 2 -adrenergic receptor (AR) agonist, is known to induce myocardial hypertrophy and might prevent LV atrophy during LV unloading. Furthermore, β 2 -AR stimulation is reported to improve Ca 2+ handling and contribute to antiapoptosis. However, there is little information on the effects of clenbuterol during LV unloading. Methods and Results— We investigated LV atrophy and function after LV unloading produced by heterotopic heart transplantation in isogenic rats. After transplantation, rats were randomized to 1o f 2 groups (n=10 each). The clenbuterol group received 2 mg·kg −1 ·d −1 of the drug for 2 weeks; the control group received normal saline. The weight of unloaded control hearts was 48% less than that of host hearts after 2 weeks of unloading. Clenbuterol significantly increased the weight of the host hearts but did not prevent unloading-induced LV atrophy. Papillary muscles were isolated and stimulated, and there was no difference in developed tension between the 2 groups. However, the inotropic response to the β-AR agonist isoproterenol significantly improved in the clenbuterol group. The mRNA expression of myocardial sarco(endo)plasmic reticulum Ca 2+ -ATPase 2a (SERCA2a) and fetal gene shift (myosin heavy chain [MHC] mRNA isozyme) was also significantly improved by clenbuterol treatment. There was no difference in β 1 -AR mRNA expression between the 2 groups. In contrast, β 2 -AR mRNA was significantly decreased in the clenbuterol-treated, unloaded heart. This indicates that clenbuterol may downregulate β 2 -ARs. In the evaluation of apoptosis, mRNA expression of caspase-3, which is the central pathway for apoptosis, tended to be better in the clenbuterol group. Conclusions— During complete LV unloading, clenbuterol did not prevent myocardial atrophy but improved gene expression (SERCA2a, β-MHC) and β-adrenergic responsiveness and potentially prevented myocardial apoptosis. However, chronic administration of clenbuterol may be associated with downregulation of β 2 -ARs.

Inhaled nitric oxide prevents left ventricular impairment during endotoxemia

1998 ◽  
Vol 85 (6) ◽  
pp. 2018-2024 ◽  
Author(s):  
Satoshi Ishihara ◽  
John A. Ward ◽  
Osamu Tasaki ◽  
Basil A. Pruitt ◽  
Cleon W. Goodwin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Left Ventricle ◽  
Cardiac Contractility ◽  
Ringer Solution ◽  
Left Ventricular ◽  
Control Group ◽  
Baseline Levels ◽  
Lv Volume

We evaluated the effect of long-term inhalation of nitric oxide (NO) on cardiac contractility after endotoxemia by using the end-systolic elastance of the left ventricle (LV) as a load-independent contractility index. Chronic instrumentation in 12 pigs included implantation of two pairs of endocardial dimension transducers to measure LV volume and a micromanometer to measure LV pressure. One week later, the animals were divided into a control group ( n = 6) or a NO group ( n = 6). All animals received intravenous Escherichia coliendotoxin (10 μg ⋅ kg−1 ⋅ h−1) and equivalent lactated Ringer solution. NO inhalation (20 parts/million) was begun 30 min after the initiation of endotoxemia and was continued for 24 h. In both groups, tachycardia, pulmonary hypertension, and systemic hyperdynamic changes were noted. The end-systolic elastance in the control group was significantly decreased beyond 7 h. NO inhalation maintained the end-systolic elastance at baseline levels and prevented its impairment. These findings indicate that NO exerts a protective effect on LV contractility in this model of endotoxemia.

Positive inotropy due to lowering cyclic GMP is also mediated by increases in cyclic AMP in control and hypertrophic hearts

1998 ◽  
Vol 76 (6) ◽  
pp. 605-612 ◽  
Author(s):  
Karen L Naim ◽  
Prem Rabindranauth ◽  
Harvey R Weiss ◽  
James Tse ◽  
Richard J Leone, Jr. ◽  
...  
Keyword(s):  
Cyclic Amp ◽  
Guanylate Cyclase ◽  
Cyclic Gmp ◽  
Current Model ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Heart Weight ◽  
Control Group ◽  
Inotropic Effects ◽  
Significant Change

The aim of the current study was to determine if lowering myocardial cyclic GMP by guanylate cyclase inhibition would add independently to the positive inotropic effects caused by raising cyclic AMP and if these effects are modified in left ventricular hypertrophy (LVH) produced by aortic valve plication. Isoproterenol (ISO) (0.1 mg·kg-1·min-1) was infused into a branch of the left anterior descending coronary artery of seven control and eight hypertrophy open-chest anesthetized dogs. After 10 min, simultaneous infusion of methylene blue (MB) (2 mg·kg-1·min-1) was initiated at the same site. Hypertrophy increased heart weight and heart weight / body weight ratio. While both drugs increased left ventricular dP/dtmax, no additional global effects were observed in either group. Changes in regional variables followed the same pattern in both groups, i.e., ISO produced an increase that was enhanced by the addition of MB. ISO increased segment shortening, with a significant change in the control group. ISO increased regional force in both groups. The addition of MB increased force above ISO levels, with a significant change in the LVH group. ISO increased regional minute work (g·mm·min-1) (control, 1779 ± 428 to 2541 ± 500; LVH, 1157 ± 253 to 1839 ± 404) and O2 consumption. MB further increased regional work (control, 2993 ± 952; LVH, 2416 ± 853) and O2 consumption. ISO raised cyclic AMP (pmoles·g-1) (control, 468 ± 41 to 580 ± 84; LVH, 445 ± 43 to 562 ± 71) and had no effect on cyclic GMP (pmoles·g-1) (control, baseline 3.27 ± 0.22, ISO 2.87 ± 0.23; LVH, baseline 6.84 ± 1.12, ISO 5.66 ± 0.54). The addition of MB lowered cyclic GMP (control, 2.41 ± 0.26; LVH, 3.68 ± 0.35), but also increased cyclic AMP (control, 1021 ± 121; LVH, 1107 ± 134). Similar results were observed in control hearts using a specific soluble guanylate cyclase inhibitor (ODQ) in terms of changes in local work, O2 consumption, and cyclic nucleotides. Thus, at least part of the positive inotropic response to lowering cyclic GMP was mediated by changes in cyclic AMP in the current model. This was true in both control and LVH animals, although baseline cyclic GMP levels were higher, and a larger reduction in cyclic GMP was observed with MB in the LVH group.Key words: guanylate cyclase, coronary blood flow, myocardial shortening, myocardial work, myocardial O2 consumption, dog.

Abstract 098: Blocking Cardiac Gq-Receptor Coupling Prevents Adverse Remodeling and Preserves Myocardial Function after Ischemic Injury in Mice and Promotes Repair via Cardiac Regeneration

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Erhe Gao ◽  
Lin Zuo ◽  
Xiying Shang ◽  
Matthieu Boucher ◽  
Yonghong Lei ◽  
...  
Keyword(s):  
Cardiac Contractility ◽  
Ischemic Injury ◽  
Cardiac Regeneration ◽  
Border Zone ◽  
Heart Weight ◽  
Control Group ◽  
Inhibitory Peptide ◽  
Littermate Control ◽  
Functional Changes ◽  
Adverse Remodeling

Background: Studies have shown that the heterotrimeric G protein, Gq, is a critical molecule in the development of myocardial hypertrophy and heart failure (HF). In the present study, we examined whether Gq signaling is also a critical pathological trigger for adverse remodeling and HF after ischemic injury. Using cardiac-specific transgenic mice with expression of a specific Gq inhibitory peptide (GqI) that blocks Gq-GPCR coupling allowed us to investigate whether Gq inhibition can alter cardiac structure and functional changes after myocardial infarction (MI). Methods and Results: Cardiac-specific GqI transgenic (TG) and non-transgenic littermate control (NLC) mice were subjected to MI. Serial echocardiography performed before ischemia as well as 2, 4, 8 weeks after MI injury show that TG mice develop less progressive LV enlargement and dysfunction. The % LV EF and FS were significantly improved in the TG compared to NLC mice at 8 weeks post-MI. Consistently, cardiac contractility (+dP/dt) and relaxation (-dP/dt) were significantly improved in TG mice also when stimulated with isoproterenol. The LVEDP, the heart weight to body weight (BW) and lung to BW ratios were significantly less in TG mice, indicating that HF was limited with GqI expression. Moreover, TG mice have smaller infarcts, less LV dimensions and lower fibrosis in both the border zone and remote area with clearly more viable tissue in the scar region. Constantly, there are more micro-vessel and more BrdU(+) cardiomyocytes in the scar area and border zone at the 2 week post-MI in TG group. Western blot shows a consistent decrease in phosphorylated PKC substrates and higher levels of activated Akt in TG mice. Over expression of the GqI in cultured H9c2 myoblasts did lead to higher level of Ki67 positive cells (38.06±2.46%) than a control group (21.78±2.64%) and FACS analysis showed that Gq inhibition increased the % of H9c2 cells in S phase and G2/M phase compared to control cells. Conclusion: These data indicate cardiac specific Gq inhibition protects the heart against adverse LV remodeling and HF progression after MI. Mechanisms attributed to GqI expression appear to include improved myocyte survival, less fibrosis, and promotion of angiogenesis and cardiac repair through regeneration.

scholarly journals Cardiac Contractility Modulation Attenuates Chronic Heart Failure in a Rabbit Model via the PI3K/AKT Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-8 ◽  
Author(s):  
Qingqing Hao ◽  
Feifei Zhang ◽  
Yudan Wang ◽  
Yingxiao Li ◽  
Xiaoyong Qi
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Cardiac Contractility ◽  
Rabbit Model ◽  
The Body ◽  
Heart Weight ◽  
Akt Pathway ◽  
Control Group ◽  
Cardiac Contractility Modulation ◽  
Positive Effects

The Akt plays an important role in regulating cardiac growth, myocardial angiogenesis, and cell death in cardiac myocytes. However, there are few studies to focus on the responses of the Akt pathway to cardiac contractility modulation (CCM) in a chronic heart failure (HF) model. In this study, the effects of CCM on the treatment of HF in a rabbit model were investigated. Thirty six-month-old rabbits were randomly separated into control, HF, and CCM groups. The rabbits in HF and CCM groups were pressure uploaded, which can cause an aortic constriction. Then, CCM was gradually injected to the myocardium of rabbits in the CCM group, and this process lasted for four weeks with six hours per day. Rabbit body weight, heart weight, and heart beating rates were recorded during the experiment. To assess the CCM impacts, rabbit myocardial histology was examined as well. Additionally, western blot analysis was employed to measure the protein levels of Akt, FOXO3, Beclin, Pi3k, mTOR, GSK-3β, and TORC2 in the myocardial histology of rabbits. Results showed that the body and heart weight of rabbits decreased significantly after suffering HF when compared with those in the control group. However, they gradually recovered after CCM application. The CCM significantly decreased collagen volume fraction in myocardial histology of HF rabbits, indicating that CCM therapy attenuated myocardial fibrosis and collagen deposition. The levels of Akt, FOXO3, Beclin, mTOR, GSK-3β, and TORC2 were significantly downregulated, but Pi3k concentration was greatly upregulated after CCM utilization. Based on these findings, it was concluded that CCM could elicit positive effects on HF therapy, which was potentially due to the variation in the Pi3k/Akt signaling pathway.

The Beneficial Effects of Trimetazidine on Reperfusion–Induced Arrhythmia in Diabetic Rats

2018 ◽  
Vol 127 (05) ◽  
pp. 320-325 ◽  
Author(s):  
Fatemeh Ramezani-Aliakbari ◽  
Mohammad Badavi ◽  
Mahin Dianat ◽  
Seyed Mard ◽  
Akram Ahangarpour
Keyword(s):  
Infarct Size ◽  
Repeated Measures ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Cardiac Contractility ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Control Group ◽  
Protective Effects ◽  
Sprague Dawley

AbstractTrimetazidine (TMZ), as an anti-ischemic drug, plays a critical role in protecting against cardiovascular complications induced by diabetes. This study was therefore aimed to evaluate the protective effects of TMZ on reperfusion-induced arrhythmias in the diabetic rats. Male Sprague-Dawley rats (250±20 g) were randomly assigned to four (n=8): control rats (C), alloxan induced diabetic rats (D), diabetic rats treated with TMZ (10 mg/kg, D+T10), diabetic rats treated with TMZ (30 mg/kg, D+T30). TMZ was treated orally once daily for 8 weeks. Diabetes was induced by a single intraperitoneal injection of alloxan (120 mg/kg). Ischemia-reperfusion (I/R) was carried out via 30 min of ischemia and following120-min reperfusion. The magnitude and score of arrhythmia, the left ventricular function, infarct size, lactate dehydrogenase (LDH), myocardial creatine kinase (CK-MB) and troponin (cTnI) were measured. The findings were evaluated by two-way repeated measures and one-way ANOVA followed by LSD post hoc test and Fisher's exact test for incidence percentage. The duration, incidence and score of arrhythmia (p<0.001), infarct size (p<0.01) were significantly increased, the cardiac contractility (±dp/dt), LDH, CK-MB (p<0.001) and cTnI (p<0.05) were significantly decreased in the diabetic rats in comparison with the control group. However, treatment with TMZ in the diabetic rats was significantly improved the duration (p<0.001), incidence and score of arrhythmia,±dp/dt LDH, CK-MB, cTnI (p<0.05) and infarct size (p<0.01) in comparison with the untreated diabetic group. The present study indicates anti-arrhythmic effect of TMZ in reducing arrhythmias induced by reperfusion in the diabetic rats.

scholarly journals Ophiopogon japonicas (Linn. f.) Ker-Gawl. extract ameliorates chronic heart failure in rats

2021 ◽  
Vol 18 (9) ◽  
pp. 1853-1857
Author(s):  
Hu-zhi Cai ◽  
Yan-ping Tang ◽  
Xin-yu Chen ◽  
Hai-bo Xie ◽  
Qing-yang Chen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Normal Control Group ◽  
Heart Weight ◽  
Control Group ◽  
High Dose ◽  
Chronic Congestive Heart Failure ◽  
Whole Heart

Purpose: To investigate the effect of Ophiopogon japonicas (Linn. f.) Ker-Gawl. extract (OJKE) on oxidative stress and hemodynamics in chronic congestive heart failure (CHF) rats. Methods: The rats were modelled to congestive heart failure (except normal group) , and then randomly divided into normal control group, model (untreated) group, captopril group, high-dose, middle-dose and low-dose of OJKE groups. They were treated for 4 weeks as appropriate for each group. At the end of treatment, the hemodynamic function, whole heart weight index, and blood creatinine kinase (CK), as well as superoxide dismutase (SOD), malondialdehyde (MDA), nitric oxide (NO), nitricoxide synthase (NOS) were determined. Results: Compared with the normal control group, arterial systolic pressure (SBP), diastolic pressure (DBP), mean arterial pressure (MAP), heart rate (HR), left ventricular systolic peak (LVSP), and left ventricular pressure change rate (dp/dt max) significantly decreased (p < 0.05), while left ventricular end diastolic pressure (LVEDP), whole heart weight index, blood CK, MDA, NO, NOS significantly increased in the untreated group (p < 0.05). A high dose of OJKE significantly improved hemodynamic function, lowered MDA (8.33 ± 2.12 nmol/mL) and NO (20.58 ± 3.53 umol/L) levels (p < 0.05), and also decreased CK (0.53±0.37 U/mL) and NOS (22.46±3.29 U/mL) in CHF rats (p < 0.05). Conclusion: OJKE improved adriamycin-induced chronic congestive heart failure in rats significantly.

scholarly journals The Effect of Different Exercise Intensities on T-Box Transcription Factor 5 Gene Expression and Hypertrophy in the Heart Muscle of Male Rats

2020 ◽  
Vol 24 (3) ◽  
pp. 202-211
Author(s):  
Elham Vosadi ◽  
◽  
Mahbobeh Borjian Fard ◽  
Keyword(s):  
Exercise Program ◽  
Left Ventricular ◽  
Heart Weight ◽  
Control Group ◽  
Vo2 Max ◽  
T Box ◽  
Intensive Exercise ◽  
Ventricular Wall Thickness ◽  
Tbx5 Gene ◽  
Intensity Training

Background: Exercise is one of the methods affecting cardiovascular adaptation, but its cellular and molecular pathways and mechanisms are unknown. T-Box Transcription Factor 5 (TBX5) gene seems to be one of the factors involved in regulating cardiac hypertrophy. Objective: The aim of this study was to investigate the effect of an 8-week exercise program with different intensities on the expression of TBX5 gene in the heart of male Wistar rats. Methods: In this experimental study, 24 male adult Wistar rats were divided into three groups of High Intensity Training (HIT), Low Intensity Training and (LIT) and control. Training groups performed the exercise program for 8 weeks, 5 sessions per week. The exercise program for the HIT group consists of running on a treadmill with five 8-min intervals at 85-90% VO2 max intensity divided into 2-min intervals at 50-60% VO2 max intensity, while for the LIT group it was included five 8-min intervals with 50-60% VO2 max intensity divided into 2-min intervals with 45% -50% VO2 max intensity. The control group performed no exercise. The real-time Polymerase Chain Reaction (PCR) analysis was used to measure the expression level of TBX5 gene. The collected data were analyzed by one-way ANOVA and Tukey’s post hoc test. Findings: The heart weight (P≤0.001 and P=0.004), heart-weight to body-weight ratio (P≤0.0001 and P=0.001), and left ventricular wall thickness were significantly higher in the HIT and LIT groups than in the control group (P≤0.0001 and P=0.38 ). The left ventricular wall thickness in the HIT group was significantly higher than in the LIT group (P=0.001). The TBX5 expression in the two training groups were not significantly different from that of control group (P=0.11). Conclusion: It seems that more intensive exercise can have more significant effects on cardiac hypertrophy than less intensive exercise.

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