Endurance Training in the Spontaneously Hypertensive Rat: Conversion of Pathological into Physiological Cardiac Hypertrophy (original) (raw)
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Endurance Training in the Spontaneously Hypertensive Rat
Hypertension, 2009
The effect of endurance training (swimming 90 min/d for 5 days a week for 60 days) on cardiac hypertrophy was investigated in the spontaneously hypertensive rat (SHR). Sedentary SHRs (SHR-Cs) and normotensive Wistar rats were used as controls. Exercise training enhanced myocardial hypertrophy assessed by left ventricular weight/tibial length (228±7 versus 251±5 mg/cm in SHR-Cs and exercised SHRs [SHR-Es], respectively). Myocyte cross-sectional area increased ≈40%, collagen volume fraction decreased ≈50%, and capillary density increased ≈45% in SHR-Es compared with SHR-Cs. The mRNA abundance of atrial natriuretic factor and myosin light chain 2 was decreased by the swimming routine (100±19% versus 41±10% and 100±8% versus 61±9% for atrial natriuretic factor and myosin light chain 2 in SHR-Cs and SHR-Es, respectively). The expression of sarcoplasmic reticulum Ca 2+ pump was significantly augmented, whereas that of Na + /Ca 2+ exchanger was unchanged (93±7% versus 167±8% and 158±13% ve...
2010
Sprint training attenuates myocyte hypertrophy and improves Ca 2ϩ homeostasis in postinfarction myocytes. J. Appl. Physiol. 84(2): 544-552, 1998.-Myocytes isolated from rat hearts 3 wk after myocardial infarction (MI) had decreased Na ϩ /Ca 2ϩ exchange currents (I Na/Ca ; 3 Na ϩ out:1 Ca 2ϩ in) and sarcoplasmic reticulum (SR)-releasable Ca 2ϩ contents. These defects in Ca 2ϩ regulation may contribute to abnormal contractility in MI myocytes. Because exercise training elicits positive adaptations in cardiac contractile function and myocardial Ca 2ϩ regulation, the present study examined whether 6-8 wk of high-intensity sprint training (HIST) would ameliorate some of the cellular maladaptations observed in post-MI rats with limited exercise activity (Sed). In MI rats, HIST did not affect citrate synthase activities of plantaris muscles but significantly increased the percentage of cardiac ␣-myosin heavy chain (MHC) isoforms (57.2 Ϯ 1.9 vs. 49.3 Ϯ 3.5 in MI-HIST vs. MI-Sed, respectively; P Յ 0.05). At the single myocyte level, HIST attenuated cellular hypertrophy observed post-MI, as evidenced by reductions in cell lengths (112 Ϯ 4 vs. 130 Ϯ 5 µm in MI-HIST vs. MI-Sed, respectively; P Յ 0.005) and cell capacitances (212 Ϯ 8 vs. 242 Ϯ 9 pF in MI-HIST vs. MI-Sed, respectively; P Յ 0.015). Reverse I Na/Ca was significantly lower (P Յ 0.0001) in myocytes from MI-Sed rats compared with those from rats that were sham operated and sedentary. HIST significantly increased reverse I Na/Ca (P Յ 0.05) without affecting the amount of Na ϩ /Ca 2ϩ exchangers (detected by immunoblotting) in MI myocytes. SR-releasable Ca 2ϩ content, as estimated by integrating forward I Na/Ca during caffeine-induced SR Ca 2ϩ release, was also significantly increased (P Յ 0.02) by HIST in MI myocytes. We conclude that the enhanced cardiac output and stroke volume in post-MI rats subjected to HIST are mediated, at least in part, by reversal of cellular maladaptations post-MI.
Armaghane Danesh Bimonthly Journal, 2021
Background & aim: Protein synthesis and degradation are dynamically regulated processes that to control the accretion or loss of muscle mass. However, the mechanisms responsible exercise-induced heart hypertrophy remains elusive. The aim of the present study was to investigate the effect of aerobic training on expression of some indices of myocardial hypertrophy and atrophy in male rats Methods: In this experimental study conducted in 2018, 16 wistar male rats 10 weeks old with 299.74±19.32 g weight were randomly classified into control and training groups. Training group performed an aerobic running program (at 10-18 m/min, 10-40 min/day, and 5 days/week) on a motor-driven treadmill for six weeks. At the end of six week's heart tissue samples were collected and used for determination of gene expression (AMPactivated protein kinase, fork head Box O3, Muscle atrophy F-box and Muscle RING finger 1). Data were analyzed using Independent t test at p<0.05. Result: Six weeks aerobic training significant increased the heart AMP-activated protein kinase in rats (p=0.014). Also heart fork head Box O3 (p=0.022), Muscle atrophy F-box (p=0.032) and Muscle RING finger 1 (p=0.028) was significantly decrease than training group. Conclusion: Aerobic exercise improved the heart structure by improving the parameters that affect cardiac size, possibly improving cardiac function.
Journal of Molecular and Cellular Cardiology, 2013
The aim of the present study was to verify the effects of low-intensity endurance training and detraining on the mechanical and molecular properties of cardiomyocytes from spontaneously hypertensive rats (SHRs). Male SHRs and normotensive control Wistar rats at 16-weeks of age were randomly divided into eight groups of eight animals: NC8 and HC8 (normotensive and hypertensive control for 8 weeks); NT8 and HT8 (normotensive and hypertensive trained at 50-60% of maximal exercise capacity for 8 weeks); NC12 and HC12 (normotensive and hypertensive control for 12 weeks); NDT and HDT (normotensive and hypertensive trained for 8 weeks and detrained for 4 weeks). The total exercise time until fatigue (TTF) was determined by a maximal exercise capacity test. Resting heart rate (RHR) and systolic arterial pressure (SAP) were measured. After the treatments, animals were killed by cervical dislocation and left ventricular myocytes were isolated by enzymatic dispersion. Isolated cells were used to determine intracellular global Ca 2+ ([Ca 2+ ] i) transient and cardiomyocyte contractility (1 Hz;~25°C). [Ca 2+ ] i regulatory proteins were measured by Western blot, and the markers of pathologic cardiac hypertrophy by quantitative real-time polymerase chain reaction (q-RT-PCR). Exercise training augmented the TTF (NC8, 11.4± 1.5 min vs. NT8, 22.5±1.4 min; HC8, 11.7±1.4 min vs. HT8, 24.5±1.3 min; Pb 0.05), reduced RHR (NT8initial, 340± 8 bpm vs. NT8final, 322 ±10 bpm; HT8initial, 369 ±8 bpm vs. HT8final, 344±10 bpm; Pb 0.05), and SBP in SHR animals (HC8, 178±3 mm Hg vs. HT8, 161±4 mm Hg; Pb 0.05). HC8 rats showed a slower [Ca 2+ ] i transient (Tpeak, 83.7± 1.8 ms vs. 71.7±2.4 ms; T50%decay, 284.0± 4.3 ms vs. 264.0±4.1 ms; Pb 0.05) and cell contractility (Vshortening, 86.1 ±6.7 μm/s vs. 118.6±6.7 μm/s; Vrelengthening, 57.5± 7.4 μm/s vs. 101.3± 7.4 μm/s; Pb 0.05), and higher expression of ANF (300%; P b 0.05), skeletal α-actin (250%; Pb 0.05) and a decreased α/β-MHC ratio (70%; Pb 0.05) compared to NC8. Exercise training increased [Ca 2+ ] i transient (NC8, 2.39 ±0.06 F/F 0 vs.
Swimming training increases cardiac vagal activity and induces cardiac hypertrophy in rats
Brazilian Journal of Medical and Biological Research, 2004
The effect of swimming training (ST) on vagal and sympathetic cardiac effects was investigated in sedentary (S, N = 12) and trained (T, N = 12) male Wistar rats (200-220 g). ST consisted of 60-min swimming sessions 5 days/week for 8 weeks, with a 5% body weight load attached to the tail. The effect of the autonomic nervous system in generating training-induced resting bradycardia (RB) was examined indirectly after cardiac muscarinic and adrenergic receptor blockade. Cardiac hypertrophy was evaluated by cardiac weight and myocyte morphometry. Plasma catecholamine concentrations and citrate synthase activity in soleus muscle were also determined in both groups. Resting heart rate was significantly reduced in T rats (355 ± 16 vs 330 ± 20 bpm). RB was associated with a significantly increased cardiac vagal effect in T rats (103 ± 25 vs 158 ± 40 bpm), since the sympathetic cardiac effect and intrinsic heart rate were similar for the two groups. Likewise, no significant difference was observed for plasma catecholamine concentrations between S and T rats. In T rats, left ventricle weight (13%) and myocyte dimension (21%) were significantly increased, suggesting cardiac hypertrophy. Skeletal muscle citrate synthase activity was significantly increased by 52% in T rats, indicating endurance conditioning. These data suggest that RB induced by ST is mainly mediated parasympathetically and differs from other training modes, like running, that seems to mainly decrease intrinsic heart rate in rats. The increased cardiac vagal activity associated with ST is of clinical relevance, since both are related to increased life expectancy and prevention of cardiac events.
Early remodeling of rat cardiac muscle induced by swimming training
Brazilian Journal of Medical and Biological Research, 2006
The aim of the present investigation was to study the effect of acute swimming training with an anaerobic component on matrix metallopeptidase (MMP) activity and myosin heavy chain gene expression in the rat myocardium. Animals (male Wistar rats, weighing approximately 180 g) were trained for 6 h/day in 3 sessions of 2 h each for 1 to 5 consecutive days (N = 5 rats per group). Rats swam in basins 47 cm in diameter and 60 cm deep filled with water at 33 to 35ºC. After the training period a significant increase (P < 0.05) was observed in the heart weight normalized to body weight by about 22 and 35% in the groups that trained for 96 and 120 h, respectively. Blood lactate levels were significantly increased (P < 0.05) in all groups after all training sessions, confirming an anaerobic component. However, lactate levels decreased (P < 0.05) with days of training, suggesting that the animals became adapted to this protocol. Myosin heavy chain-ß gene expression, analyzed by real time PCR and normalized with GAPDH gene expression, showed a significant twofold increase (P < 0.01) after 5 days of training. Zymography analysis of myocardium extracts indicated a single ~60-kDa activity band that was significantly increased (P < 0.05) after 72, 96, and 120 h, indicating an increased expression of MMP-2 and suggesting precocious remodeling. Furthermore, the presence of MMP-2 was confirmed by Western blot analysis, but not the presence of MMP-1 and MMP-3. Taken together, our results indicate that in these training conditions, the rat heart undergoes early biochemical and functional changes required for the adaptation to the new physiological condition by tissue remodeling.
Jorjani Biomedicine Journal, 2020
Background and Objective: Vascular obstruction and impaired blood flow and oxygen delivery cause a myocardial infarction and limit a personchr('39')s function. Therefore, finding a way to create new arteries and replace blocked arteries has always been of interest to researchers, including exercise physiologists. Therefore, this study was conducted to evaluate the effect of eight weeks of moderate-intensity endurance training on the capillary density of the myocardium and ejection fraction and left ventricular shortening fraction in male rats with myocardial infarction. Material and Methods: 16 ten-week-old male wistar rats with mean weight of 250-300gr were allocated to two groups of experimental (60 minutes of interval treadmill running for four minutes at an intensity of 65-70% VO2max and two minutes of active rest at 50-60 percent of VO2max for 5 days a week for 8 weeks) and control group (without any training). Immunohistochemistry was used to measure the capillary density of the myocardium. Ejection fraction and left ventricular shortening fraction were measured by Doppler echocardiography. Data were analyzed in SPSS18 using independent samples t test (α≤ 0.05). Results: The findings showed that there was a significant increase in the capillary density of the myocardium (p=0.000), ejection fraction (P = 0.001) and left ventricular shortening fraction (P = 0.001) in the experimental group as compared with the control group. Conclusion: In general, eight weeks of moderate-intensity endurance training can effectively increase angiogenesis in male Wistar rats after MI.
The journals of gerontology. Series A, Biological sciences and medical sciences, 2017
Exercise training effects on the contractility of aged myocardium have been investigated for more than 20 years, but the data are still unclear. This study evaluated the hypothesis that a swimming training (ST) may improve myocardial inotropism in older rats. Male Wistar rats aged 4 (young)-and 21 (old)-months-old were divided into young untrained (YNT), old untrained (ONT), and old trained (OTR; 6 weeks of ST) groups. Echocardiography and hemodynamic were employed to assess left ventricular morphology and function. Myocardial mechanics was evaluated on papillary muscles. Histological and immunoblotting were carried out to evaluate fibrosis and proteins that modulate the myocardial function. We found that older rats did not show cardiac dysfunction, but ONT group showed lower physical performance during a swimming test (YNT:5±2; ONT:-16±0.4; OTR:51±3; Δ%). Moreover, ONT group showed worse myocardial inotropism, in which it was reversed by ST (Peak developed tension: YNT:6,2±0.7; ONT...