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., Y. Wang, U. Wisloff, O. J. Kemi., and Obsahuje bibliografii a bibliografické odkazy
The aim of the study was to assess whether angiotensin converting enzyme (ACE) inhibition with captopril prevents the development of hypertension and myocardial hypertrophy and affects nitric oxide synthase (NOS) activity in rats. Animals were divided into five groups: control, two groups receiving NG-nitro-L-arginine methyl ester (L-NAME) 20 or 40 mg/kg/day, a group receiving captopril 100 mg/kg/day and a group concomitantly treated with 40 mg/kg/day L-NAME plus 100 mg/kg/day captopril. After four weeks, systolic blood pressure (SBP) significantly increased in both L-NAME groups by 30 % and 34 %, respectively. In the captopril group, SBP significantly decreased by 30 % and in the captopril plus L-NAME group SBP was not changed as compared to the controL Although left ventricular weight/body weight (LVW/BW) ratio in both L-NAME groups was significantly elevated by 19 % and 29 %, respectively, no alterations in LVW/BW ratio were found in the captopril group and captopril plus L-NAME group. In both groups receiving L-NAME, NOS activity significantly decreased by 17 % and 69 % in the heart, by 14 % and 26 % in the aorta, by 60 % and 73 % in the brain and by 13 % and 30 % in the kidney, respectively. Captopril did not influence NO synthase activity in any of the studied tissues. We conclude that captopril prevents the development of hypertension and LV hypertrophy without affecting NO formation.
The effect of 4 weeks’ inhibition of NO synthase by nitro-L-arginine methyl ester (L-NAME) on haemodynamic parameters and cGMP and cAMP content was studied in rat tissues. L-NAME in both 20 mg/kg/day and 40 mg/kg/day doses significantly increased systolic blood pressure by 28 % and 30 % and decreased the heart rate by 14 % and 23 %, respectively, after the first week. These changes persisted during the following three weeks. Left ventricular weight/body weight (LVW/BW) ratio was significantly elevated in both L-NAME-treated groups by 19 % and 29 %, respectively. Radioimmunoassay was used to determine the cGMP and cAMP content Cyclic GMP content in animals treated by L-NAME (20 mg/kg/day and 40 mg/kg/day) decreased significantly by 13 % and 22 % in the left ventricle, by 28 % and 62 % in the aorta, by 20 % and 34 % in the brain, and by 10 % and 15 % in the kidney, respectively. On the other hand, the cAMP content increased in both L-NAME treated groups by 8 % and 9 % in the left ventricle, by 28 % and 46 % in the aorta, and by 23 % and 32 % in the brain, respectively. There were no significant changes in kidney cAMP content as compared to control animals. The results suggest a simultaneous decrease of cGMP and increase of cAMP content in the majority of studied tissues during NO-deficient hypertension.
This study aimed to examine how regular aerobic training can affect the muscle hypertrophy induced by overloading. Male C57BL/6J mice were randomly divided into three groups: rest group, low-intensity aerobic exercise group, and high-intensity aerobic exercise group. Mice in the exercise groups were assigned to run at a speed of 10 m/min (low-intensity) or 25 m/min (high-intensity) for 30 min/day, five days/week, for four weeks. Then, the right hind leg gastrocnemius muscles were surgically removed to overload the plantaris and soleus muscles, while the left hind leg was subjected to a sham-operation. Both the plantaris and soleus muscles grew larger in the overloaded legs than those in the sham-operated legs. Muscle growth increased in the plantaris muscles in the low-intensity exercise group compared to that in the rest or high-intensity exercise groups at one and two weeks after overloading. This enhancement was not observed in the soleus muscles. Consistently, we observed changes in the expression of proteins involved in anabolic intracellular signaling, including Akt, mechanistic target of rapamycin (mTOR), and p70S6K, in the plantaris muscles. Our data showed for the first time that chronic low-intensity aerobic exercise precipitates overload-induced muscle growth., Siriguleng, T. Koike, Y. Natsume, S. Iwama, Y. Oshida., and Obsahuje bibliografii
This study aimed to examine the effect of eicosapentaenoic acid (EPA) on skeletal muscle hypertrophy induced by muscle overload and the associated intracellular signaling pathways. Male C57BL/6J mice were randomly assigned to oral treatment with either EPA or corn oil for 6 weeks. After 4 weeks of treatment, the gastrocnemius muscle of the right hindlimb was surgically removed to overload the plantaris and soleus muscles for 1 or 2 weeks. We examined the effect of EPA on the signaling pathway associated with protein synthesis using the soleus muscles. According to our analysis of the compensatory muscle growth, EPA administration enhanced hypertrophy of the soleus muscle but not hypertrophy of the plantaris muscle. Nevertheless, EPA administration did not enhance the expression or phosphorylation of Akt, mechanistic target of rapamycin (mTOR), or S6 kinase (S6K) in the soleus muscle. In conclusion, EPA enhances skeletal muscle hypertrophy, which can be independent of changes in the AKT-mTOR-S6K pathway.
A pressure overload was induced in 2-day-old male rats by abdominal aortic constriction, and the phospholipid composition of the left ventricle (LV) and the right ventricle (RV) were determined. Sixty days after the surgery, body weights was lower and LV weight were higher in aorta-constricted (AC) rats in comparison with sham- operated animals. Increased ventricular/body weight ratios indicated a significant degree of hypertrophy of LV and smaller hypertrophy of RV. The concentrations of total phospholipids (PL), choline phosphoglycerides (PC), ethanolamine phosphoglycerides (PE), diphosphatidylglycerol (DPG) and phosphatidylinositol (PI) were decreased in both ventricles of AC rats. The concentrations of sphingomyelin (SM) and plasmalogen PE (PLPE) increased in LV only. The changes in phospholipid composition in the developing pressure-overloaded myocardium may contribute to altered membrane functions connected with heart hypertrophy.
This study aimed to compare the effects of three different resistance exercise models on the quadriceps muscle crosssectional area, as well as on mTOR phosphorylation and other pivotal molecules involved in the upstream regulation of mTOR. Twenty-four male Wistar rats were divided into untrained (control), endurance resistance training, strength resistance training, and hypertrophy resistance training (HRT) groups (n=6). After 12 weeks of training, the red portion of the quadriceps was removed for histological and Western blot analyses. The results showed that the quadriceps weight and cross-sectional areas in the exercised groups were higher than those of the untrained rats. However, the HRT group presented better results than the other two experimental groups. This same pattern was observed for mTOR phosphorylation and for the most pivotal molecules involved in the upstream control of mTOR (increase of PKB, 14-3-3, ERK, p38 MAPK, and 4E-BP1 phosphorylation, and reduction of tuberin, sestrin 2, REDD1, and phospho AMPK). In summary, our study showed that HRT leads to high levels of mTOR phosphorylation as well as of other proteins involved in the upstream regulation of mTOR., T. F. Luciano, S. O. Marques, B. L. Pieri, D. R. de Souza, L. V. Araújo, R. T. Nesi, D. L. Scheffer, V. H. Comin, R. A. Pinho, A. P. Muller, C. T. de Souza., and Obsahuje bibliografii