scholarly journals Molecular Mechanisms of Nigella sativa- and Nigella sativa Exercise-Induced Cardiac Hypertrophy in Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Lubna Ibrahim Al Asoom
Keyword(s):  
Exercise Training ◽  
Cardiac Hypertrophy ◽  
Molecular Mechanisms ◽  
Nigella Sativa ◽  
Male Rats ◽  
Cell Diameter ◽  
Vigorous Exercise ◽  
Physiological Cardiac Hypertrophy ◽  
Igf I ◽  
Exercise Induced

Background. In our lab, we demonstrated cardiac hypertrophy induced by long-term administration of Nigella sativa (Ns) with enhanced function. Therefore, we aim to investigate the molecular mechanisms of Ns-induced cardiac hypertrophy, compare it with that induced by exercise training, and explore any possible synergistic effect of these two interventions. Method. Twenty adult Wistar male rats were divided into control (C), Ns-fed (N.s.), exercise-trained (Ex.), Ns-fed exercise-trained (N.s.Ex.) groups. 800 mg/kg of Ns was administered orally to N.s. rats. Ex. rats were trained on a treadmill with speed 18 m/min and grade 32° for two hours daily, and the N.s.Ex. group underwent both interventions. After 8 weeks, Immunohistochemical slides of the left ventricles were prepared using rat growth hormone (GH), insulin-like growth factor I (IGF-I), angiotensin-II receptors 1 (AT-I), endothelin-I (ET-1), Akt-1, and Erk-1. Cell diameter and number of nuclei were measured. Results. Cardiomyocyte diameter, number of nuclei, GH, and Akt were significantly higher in N.s, Ex., and N.s.Ex groups compared with the controls. IGF-I, AT-1, and ET-1 were significantly higher in Ex. rats only compared with the controls. Erk-1 was lower in N.s., Ex., and N.s.Ex. compared with the controls. Conclusion. We can conclude that Ns-induced cardiac hypertrophy is mediated by the GH-IGF I-PI3P-Akt pathway. Supplementation of Ns to exercise training protocol can block the upregulation of AT-I and ET-1. The combined N.s. exercise-induced cardiac hypertrophy might be a superior model of physiological cardiac hypertrophy and be used as a prophylactic therapy for athletes who are engaged in vigorous exercise activity.

Rat model of exercise-induced cardiac hypertrophy: hemodynamic characterization using left ventricular pressure-volume analysis

2013 ◽  
Vol 305 (1) ◽  
pp. H124-H134 ◽  
Author(s):  
Tamás Radovits ◽  
Attila Oláh ◽  
Árpád Lux ◽  
Balázs Tamás Németh ◽  
László Hidi ◽  
...  
Keyword(s):  
Exercise Training ◽  
Cardiac Hypertrophy ◽  
Rat Model ◽  
Left Ventricular ◽  
Heart Weight ◽  
Stroke Work ◽  
Functional Changes ◽  
Exercise Induced

Long-term exercise training is associated with characteristic structural and functional changes of the myocardium, termed athlete's heart. Several research groups investigated exercise training-induced left ventricular (LV) hypertrophy in animal models; however, only sporadic data exist about detailed hemodynamics. We aimed to provide functional characterization of exercise-induced cardiac hypertrophy in a rat model using the in vivo method of LV pressure-volume (P-V) analysis. After inducing LV hypertrophy by swim training, we assessed LV morphometry by echocardiography and performed LV P-V analysis using a pressure-conductance microcatheter to investigate in vivo cardiac function. Echocardiography showed LV hypertrophy (LV mass index: 2.41 ± 0.09 vs. 2.03 ± 0.08 g/kg, P < 0.01), which was confirmed by heart weight data and histomorphometry. Invasive hemodynamic measurements showed unaltered heart rate, arterial pressure, and LV end-diastolic volume along with decreased LV end-systolic volume, thus increased stroke volume and ejection fraction (73.7 ± 0.8 vs. 64.1 ± 1.5%, P < 0.01) in trained versus untrained control rats. The P-V loop-derived sensitive, load-independent contractility indexes, such as slope of end-systolic P-V relationship or preload recruitable stroke work (77.0 ± 6.8 vs. 54.3 ± 4.8 mmHg, P = 0.01) were found to be significantly increased. The observed improvement of ventriculoarterial coupling (0.37 ± 0.02 vs. 0.65 ± 0.08, P < 0.01), along with increased LV stroke work and mechanical efficiency, reflects improved mechanoenergetics of exercise-induced cardiac hypertrophy. Despite the significant hypertrophy, we observed unaltered LV stiffness (slope of end-diastolic P-V relationship: 0.043 ± 0.007 vs. 0.040 ± 0.006 mmHg/μl) and improved LV active relaxation (τ: 10.1 ± 0.6 vs. 11.9 ± 0.2 ms, P < 0.01). According to our knowledge, this is the first study that provides characterization of functional changes and hemodynamic relations in exercise-induced cardiac hypertrophy.

Comparison of Nigella sativa- and Exercise-Induced Models of Cardiac Hypertrophy: Structural and Electrophysiological Features

2014 ◽  
Vol 14 (3) ◽  
pp. 208-213 ◽  
Author(s):  
Lubna Ibrahim Al-Asoom ◽  
Basil Abdulrahman Al-Shaikh ◽  
Abdullah Omar Bamosa ◽  
Mohammad Nabil El-Bahai
Keyword(s):  
Cardiac Hypertrophy ◽  
Nigella Sativa ◽  
Exercise Induced

scholarly journals Supra-physiological dose of testosterone induces pathological cardiac hypertrophy

2016 ◽  
Vol 229 (1) ◽  
pp. 13-23 ◽  
Author(s):  
Prapawadee Pirompol ◽  
Vassana Teekabut ◽  
Wattana Weerachatyanukul ◽  
Tepmanas Bupha-Intr ◽  
Jonggonnee Wattanapermpool
Keyword(s):  
Cardiac Hypertrophy ◽  
Weight Ratio ◽  
Male Rats ◽  
Cross Sectional ◽  
Physiological Level ◽  
Testosterone Treatment ◽  
Pathological Cardiac Hypertrophy ◽  
Physiological Cardiac Hypertrophy ◽  
Hypertrophy Of The Heart ◽  
Contractile Activation

Testosterone and androgenic anabolic steroids have been misused for enhancement of physical performance despite many reports on cardiac sudden death. Although physiological level of testosterone provided many regulatory benefits to human health, including the cardiovascular function, supra-physiological levels of the hormone induce hypertrophy of the heart with unclear contractile activation. In this study, dose- and time-dependent effects of high-testosterone treatment on cardiac structure and function were evaluated. Adult male rats were divided into four groups of testosterone treatment for 0, 5, 10, and 20 mg/kg BW for 4, 8, or 12 weeks. Increases in both percentage heart:body weight ratio and cardiomyocyte cross-sectional area in representing hypertrophy of the heart were significantly shown in all testosterone-treated groups to the same degree. In 4-week-treated rats, physiological cardiac hypertrophy was apparent with an upregulation of α-MHC without any change in myofilament contractile activation. In contrast, pathological cardiac hypertrophy was observed in 8- and 12-week testosterone-treated groups, as indicated by suppression of myofilament activation and myocardial collagen deposition without transition of MHC isoforms. Only in 12-week testosterone-treated group, eccentric cardiac hypertrophy was demonstrated with unaltered myocardial stiffness, but significant reductions in the phosphorylation signals of ERK1/2 and mTOR. Results of our study suggest that the outcome of testosterone-induced cardiac hypertrophy is not dose dependent but is rather relied on the factor of exposure to duration in inducing maladaptive responses of the heart.

scholarly journals Animal models in the study of exercise-induced cardiac hypertrophy

2010 ◽  
pp. 633-644 ◽  
Author(s):  
Y Wang ◽  
U Wisloff ◽  
OJ Kemi
Keyword(s):  
Animal Models ◽  
Exercise Training ◽  
Cardiac Hypertrophy ◽  
Wheel Running ◽  
Experimental Models ◽  
Laboratory Animals ◽  
Training Models ◽  
Advantages And Disadvantages ◽  
Experimental Approaches ◽  
Exercise Induced

Exercise training-induced cardiac hypertrophy occurs following a program of aerobic endurance exercise training and it is considered as a physiologically beneficial adaptation. To investigate the underlying biology of physiological hypertrophy, we rely on robust experimental models of exercise training in laboratory animals that mimic the training response in humans. A number of experimental strategies have been established, such as treadmill and voluntary wheel running and swim training models that all associate with cardiac growth. These approaches have been applied to numerous animal models with various backgrounds. However, important differences exist between these experimental approaches, which may affect the interpretation of the results. Here, we review the various approaches that have been used to experimentally study exercise training-induced cardiac hypertrophy; including the advantages and disadvantages of the various models.

Overexpression of coupling factor 6 attenuates exercise-induced physiological cardiac hypertrophy by inhibiting PI3K/Akt signaling in mice

2012 ◽  
Vol 30 (4) ◽  
pp. 778-786 ◽  
Author(s):  
Shigeki Sagara ◽  
Tomohiro Osanai ◽  
Taihei Itoh ◽  
Kei Izumiyama ◽  
Shuji Shibutani ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Coupling Factor ◽  
Akt Signaling ◽  
Physiological Cardiac Hypertrophy ◽  
Exercise Induced ◽  
Coupling Factor 6

Ischemia-reperfusion-induced calpain activation and SERCA2a degradation are attenuated by exercise training and calpain inhibition

2006 ◽  
Vol 290 (1) ◽  
pp. H128-H136 ◽  
Author(s):  
Joel P. French ◽  
John C. Quindry ◽  
Darin J. Falk ◽  
Jessica L. Staib ◽  
Youngil Lee ◽  
...  
Keyword(s):  
Exercise Training ◽  
Ischemia Reperfusion ◽  
Male Rats ◽  
Calpain Activity ◽  
Cardiac Work ◽  
Calpain Activation ◽  
Protein Levels ◽  
Calpain Inhibition ◽  
Exercise Induced ◽  
Injury Recovery

The Ca2+-activated protease calpain has been shown to play a deleterious role in the heart during ischemia-reperfusion (I/R). We tested the hypothesis that exercise training would minimize I/R-induced calpain activation and provide cardioprotection against I/R-induced injury. Hearts from adult male rats were isolated in a working heart preparation, and myocardial injury was induced with 25 min of global ischemia followed by 45 min of reperfusion. In sedentary control rats, I/R significantly increased calpain activity and impaired cardiac performance (cardiac work during reperfusion = 24% of baseline). Compared with sedentary animals, exercise training prevented the I/R-induced rise in calpain activity and improved cardiac work (recovery = 80% of baseline). Similar to exercise, pharmacological inhibition of calpain activity resulted in comparable cardioprotection against I/R injury (recovery = 86% of baseline). The exercise-induced protection against I/R-induced calpain activation was not due to altered myocardial protein levels of calpain or calpastatin. However, exercise training was associated with increased myocardial antioxidant enzyme activity (Mn-SOD, catalase) and a reduction in oxidative stress. Importantly, exercise training also prevented the I/R-induced degradation of sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA)2a. These findings suggest that increases in endogenous antioxidants may diminish the free radical-mediated damage and/or degradation of Ca2+ handling proteins (such as SERCA2a) typically observed after I/R. In conclusion, these results support the concept that calpain activation is an important component of I/R-induced injury and that exercise training provides cardioprotection against I/R injury, at least in part, by attenuating I/R-induced calpain activation.

Loaded wheel running and muscle adaptation in the mouse

2005 ◽  
Vol 289 (1) ◽  
pp. H455-H465 ◽  
Author(s):  
John P. Konhilas ◽  
Ulrika Widegren ◽  
David L. Allen ◽  
Angelika C. Paul ◽  
Allison Cleary ◽  
...  
Keyword(s):  
Exercise Training ◽  
Wheel Running ◽  
Glycogen Synthase ◽  
Physiological Adaptation ◽  
Muscle Adaptation ◽  
Differential Impact ◽  
Cross Sectional ◽  
Biochemical Adaptation ◽  
Physiological Cardiac Hypertrophy ◽  
Exercise Induced

Voluntary cage wheel exercise has been used extensively to determine the physiological adaptation of cardiac and skeletal muscle in mice. In this study, we tested the effect of different loading conditions on voluntary cage wheel performance and muscle adaptation. Male C57Bl/6 mice were exposed to a cage wheel with no-resistance (NR), low-resistance (LR), or high-resistance (HR) loads for 7 wk. Power output was elevated (3-fold) under increased loading (LR and HR) conditions compared with unloaded (NR) exercise training. Only unloaded (NR) exercise induced an increase in heart mass, whereas only loaded (LR and HR) exercise training induced an increase in skeletal (soleus) muscle mass. Moreover, unloaded and loaded exercise training had a differential impact on the cross-sectional area of muscle fibers, depending on the type of myosin heavy chain expressed by each fiber. The biochemical adaptation of the heart was characterized by a decrease in genes associated with pathological (but not physiological) cardiac hypertrophy and a decrease in calcineurin expression in all exercise groups. In addition, transcriptional activity of myocyte enhancer factor-2 (MEF-2) was significantly decreased in the hearts of the LR group as determined by a MEF-2-dependent transgene driving the expression of β-galactosidase. Phosphorylation of glycogen synthase kinase-3β, protein kinase B (Akt), and p70 S6 kinase was increased only in the hearts of the NR group, consistent with the significant increase in cardiac mass. In conclusion, unloaded and loaded cage wheel exercise have a differential impact on cage wheel performance and muscle (cardiac and skeletal) adaptation.

FoxO1 is required for physiological cardiac hypertrophy induced by exercise but not by constitutively active PI3K

2021 ◽  
Author(s):  
Kate L. Weeks ◽  
Yow Keat Tham ◽  
Suzan G. Yildiz ◽  
Yonali Alexander ◽  
Daniel G. Donner ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Interstitial Fibrosis ◽  
Heart Weight ◽  
Cardiomyocyte Hypertrophy ◽  
Physiological Cardiac Hypertrophy ◽  
Exercise Induced ◽  
Physiological Hypertrophy ◽  
Constitutively Active

The insulin-like growth factor 1 receptor (IGF1R) and phosphoinositide 3-kinase p110a (PI3K) are critical regulators of exercise-induced physiological cardiac hypertrophy, and provide protection in experimental models of pathological remodeling and heart failure. Forkhead box class O1 (FoxO1) is a transcription factor which regulates cardiomyocyte hypertrophy downstream of IGF1R/PI3K activation in vitro, but its role in physiological hypertrophy in vivo was unknown. We generated cardiomyocyte-specific FoxO1 knockout (cKO) mice and assessed the phenotype under basal conditions and settings of physiological hypertrophy induced by 1) swim training, or 2) cardiac-specific transgenic expression of constitutively active PI3K (caPI3KTg+). Under basal conditions, male and female cKO mice displayed mild interstitial fibrosis compared with control (CON) littermates, but no other signs of cardiac pathology were present. In response to exercise training, female CON mice displayed an increase (~21%) in heart weight normalized to tibia length vs untrained mice. Exercise-induced hypertrophy was blunted in cKO mice. Exercise increased cardiac Akt phosphorylation and IGF1R expression, but was comparable between genotypes. However, differences in Foxo3a, Hsp70 and autophagy markers were identified in hearts of exercised cKO mice. Deletion of FoxO1 did not reduce cardiac hypertrophy in male or female caPI3KTg+ mice. Cardiac Akt and FoxO1 protein expression were significantly reduced in hearts of caPI3KTg+ mice, which may represent a negative feedback mechanism from chronic caPI3K, and negate any further effect of reducing FoxO1 in the cKO. In summary, FoxO1 contributes to exercise-induced hypertrophy. This has important implications when considering FoxO1 as a target for treating the diseased heart.

Abstract 421: Cardiac Hypertrophy Induced by Swimming Exercise in Mice and the Cardiac Renin-Angiotensin System: The More, the Better?

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Santiago Alonso L Tobar ◽  
Douglas S Soares ◽  
Graziela H Pinto ◽  
Daniel S Caetano ◽  
Amanda Lopes ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Molecular Mechanisms ◽  
Renin Angiotensin System ◽  
Angiotensin Receptors ◽  
Swimming Training ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Angiotensin Peptides ◽  
Physiological Cardiac Hypertrophy ◽  
Wide Range

Cardiac hypertrophy is an adaptive process which is triggered by different mechanism in order to improve blood flow to organism and it may progress as physiological or pathological. Physical exercise offers a wide range hemodynamic stimulus; consequently it may modulate several molecular mechanisms associated to cardiac hypertrophy, for instance the local cardiac renin-angiotensin system (RAS). Thus, the aim of this study was to analyze the classical (ANGII/AT1) and alternative (ANG1-7/MAS) axis of the RAS in the cardiac muscle of mice submitted to exercise with different volumes/intensity training for the development of cardiac hypertrophy. Therefore, male Balb/c mice were divided in three groups: (i) Sedentary (SED), (ii) swimming training twice a day (T2), and (iii) swimming training three times a day with 2% of body weight overload (T3), for six weeks of training. The cardiac hypertrophy was assessed by the left ventricle weight and tibial length (LV/mm) ratio and cardiomyocytes cross-sectional area. Angiotensin peptides were analyzed by HPLC and angiotensin receptor measured by western blotting. We have also analyzed fibrosis by masson’s tricrome and the fetal genes reactivation was assessed by qRT-PCR. Both swimming training induced cardiac hypertrophy, the CHI for groups was T2 (6.34±0.44 mg/mm) and T3 (6.74 ± 0.70 mg/mm) compared to SED (5.55±0.5 mg/mm, p = 0.002). There was no observed change in the levels of angiotensin peptides ANG-I, ANG-II, and ANG1-7 between training groups and sedentary, however when we analyze angiotensin receptors, group T3 showed higher levels of AT1 when compared to SED (p=0.004), while MASR levels was higher in T2 compared to SED (0.017). Further, there was moderate reactivation of fetal genes as evidenced by increased in MHC-β expression observed in T3, but without fibrosis in either group. Our results suggest that increasing volumes/intensity of exercise beyond moderate does not influence the magnitude or the structural phenotype of physiological cardiac hypertrophy. However, it might promote the activation of molecular mechanisms involved in pathological cardiac hypertrophy.

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