scholarly journals pH recovery from a proton load in rat cardiomyocytes: effects of chronic exercise

2018 ◽  
Vol 314 (2) ◽  
pp. H285-H292 ◽  
Author(s):  
Vennetia R. Danes ◽  
Josephine Anthony ◽  
Kaveh Rayani ◽  
Kenneth W. Spitzer ◽  
Glen F. Tibbits
Keyword(s):  
Exercise Training ◽  
Exercise Tolerance ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Trained Group ◽  
Sedentary Control ◽  
Control Groups ◽  
Rat Cardiomyocytes ◽  
Extrusion Rate ◽  
Proton Load

The ability of cardiomyocytes to recover from a proton load was examined in the hearts of exercise-trained and sedentary control rats in CO2/[Formula: see text]-free media. Acidosis was created by the NH4Cl prepulse technique, and intracellular pH (pHi) was determined using fluorescence microscopy on carboxy-SNARF-1 AM-loaded isolated cardiomyocytes. CO2-independent pHi buffering capacity (βi) was measured by incrementally reducing the extracellular NH4Cl concentration in steps of 50% from 20 to 1.25 mM. βi increased as pHi decreased in both exercise-trained and sedentary control groups. However, the magnitude of increase in βi as a function of pHi was found to be significantly ( P < 0.001) greater in the exercise-trained group compared with the sedentary control group. The rate of pHi recovery from an imposed proton load was found to not be different between the exercise-trained and control groups. The Na+/H+ exchanger-dependent H+ extrusion rate during the recovery from an imposed proton load, however, was found to be significantly greater in the exercise-trained group compared with the control group. By increasing βi and subsequently the Na+/H+ exchanger-dependent H+ extrusion rate, exercise training may provide cardiomyocytes with the ability to better handle an intracellular excess of H+ generated during hypoxia/ischemic insults and may serve in a cardioprotective role. These data may be predictive of two positive outcomes: 1) increased exercise tolerance by the heart and 2) a protective mechanism that limits the degree of myocardial acidosis and subsequent damage that accompanies ischemia-reperfusion stress. NEW & NOTEWORTHY The enhanced ability to deal with acidosis conferred by exercise training is likely to improve exercise tolerance and outcomes in response to myocardial ischemia-reperfusion injury.

Exercise training improves myocardial tolerance to in vivo ischemia-reperfusion in the rat

1998 ◽  
Vol 275 (5) ◽  
pp. R1468-R1477 ◽  
Author(s):  
Scott K. Powers ◽  
Haydar A. Demirel ◽  
Heather K. Vincent ◽  
Jeff S. Coombes ◽  
Hisashi Naito ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Ischemia Reperfusion ◽  
Experimental Studies ◽  
Control Group ◽  
Sprague Dawley ◽  
Endurance Exercise Training ◽  
Nonprotein Thiols

Experimental studies examining the effects of regular exercise on cardiac responses to ischemia and reperfusion (I/R) are limited. Therefore, these experiments examined the effects of endurance exercise training on myocardial biochemical and physiological responses during in vivo I/R. Female Sprague-Dawley rats (4 mo old) were randomly assigned to either a sedentary control group or to an exercise training group. After a 10-wk endurance exercise training program, animals were anesthetized and mechanically ventilated, and the chest was opened by thoracotomy. Coronary occlusion was achieved by a ligature around the left coronary artery; occlusion was maintained for 20 min, followed by a 10-min period of reperfusion. Compared with untrained, exercise-trained animals maintained higher ( P < 0.05) peak systolic blood pressure throughout I/R. Training resulted in a significant ( P < 0.05) increase in ventricular nonprotein thiols, heat shock protein (HSP) 72, and the activities of superoxide dismutase (SOD), phosphofructokinase (PFK), and lactate dehydrogenase. Furthermore, compared with untrained controls, left ventricles from trained animals exhibited lower levels ( P < 0.05) of lipid peroxidation after I/R. These data demonstrate that endurance exercise training improves myocardial contractile performance and reduces lipid peroxidation during I/R in the rat in vivo. It appears likely that the improvement in the myocardial responses to I/R was related to training-induced increases in nonprotein thiols, HSP72, and the activities of SOD and PFK in the myocardium.

scholarly journals Moderate exercise prevents impaired Ca2+ handling in heart of CO-exposed rat: implication for sensitivity to ischemia-reperfusion

2010 ◽  
Vol 299 (6) ◽  
pp. H2076-H2081 ◽  
Author(s):  
C. Farah ◽  
G. Meyer ◽  
L. André ◽  
J. Boissière ◽  
S. Gayrard ◽  
...  
Keyword(s):  
Exercise Training ◽  
Antioxidant Status ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Moderate Exercise ◽  
Plasmic Reticulum ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Exercise Induced ◽  
Moderate Exercise Training

Sustained urban carbon monoxide (CO) exposure exacerbates heart vulnerability to ischemia-reperfusion via deleterious effects on the antioxidant status and Ca2+ homeostasis of cardiomyocytes. The aim of this work was to evaluate whether moderate exercise training prevents these effects. Wistar rats were randomly assigned to a control group and to CO groups, living during 4 wk in simulated urban CO pollution (30–100 parts/million, 12 h/day) with (CO-Ex) or sedentary without exercise (CO-Sed). The exercise procedure began 4 wk before CO exposure and was maintained twice a week in standard filtered air during CO exposure. On one set of rats, myocardial ischemia (30 min) and reperfusion (120 min) were performed on isolated perfused rat hearts. On another set of rats, myocardial antioxidant status and Ca2+ handling were evaluated following environmental exposure. As a result, exercise training prevented CO-induced myocardial phenotypical changes. Indeed, exercise induced myocardial antioxidant status recovery in CO-exposed rats, which is accompanied by a normalization of sarco(endo)plasmic reticulum Ca2+-ATPase 2a expression and then of Ca2+ handling. Importantly, in CO-exposed rats, the normalization of cardiomyocyte phenotype with moderate exercise was associated with a restored sensitivity of the myocardium to ischemia-reperfusion. Indeed, CO-Ex rats presented a lower infarct size and a significant decrease of reperfusion arrhythmias compared with their sedentary counterparts. To conclude, moderate exercise, by preventing CO-induced Ca2+ handling and myocardial antioxidant status alterations, reduces heart vulnerability to ischemia-reperfusion.

Measuring Learning using an Untrained Control Group: Comment on R. Reber and Perruchet

2003 ◽  
Vol 56 (1) ◽  
pp. 117-123 ◽  
Author(s):  
Zoltán Dienes ◽  
Gerry Altmann
Keyword(s):  
Control Group ◽  
Trained Group ◽  
Control Groups

R. Reber and Perruchet (this issue) argue that use of control groups without training is unsound for establishing that learning has occurred. We show that inferring learning from a difference between a trained group and an untrained control in no way relies on their implausible additivity assumption, and that untrained control groups can be an invaluable aid to the researcher.

scholarly journals Leucine imparts cardioprotective effects by enhancing mTOR activity and mitochondrial fusion in a myocardial ischemia/reperfusion injury murine model

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Atsushi Morio ◽  
Rie Tsutsumi ◽  
Shiho Satomi ◽  
Takashi Kondo ◽  
Hirotsugu Miyoshi ◽  
...  
Keyword(s):  
Infarct Size ◽  
High Fat Diet ◽  
Ischemia Reperfusion ◽  
Mitochondrial Fusion ◽  
Control Group ◽  
Obese Mice ◽  
High Fat ◽  
Rat Cardiomyocytes ◽  
Cardioprotective Effects ◽  
Mtor Activity

Abstract Background Coronary artery disease is a leading cause of morbidity and mortality among patients with diabetes. Previously, we demonstrated that branched-chain amino acids (BCAAs) showed cardioprotective effects against cardiac ischemia/reperfusion (I/R) injury. A recent study suggested that leucine (Leu), a BCAA, is a key amino acid involved in mammalian target of rapamycin (mTOR) activity and mitochondrial function. However, whether Leu has cardioprotective effects on diabetic hearts is unclear. In this study, we examined the preconditioning effect of Leu treatment on high-fat diet (HFD)-induced obese mouse which simulate prediabetic heart. Methods In vivo mice models of I/R injury were divided into the following groups: control, mTOR+/−, and high-fat diet (HFD)-induced obese groups. Mice were randomly administered with Leu, the mTOR inhibitor rapamycin (Rap), or Leu with Rap. Isolated rat cardiomyocytes were subjected to simulated I/R injury. Biochemical and mitochondrial functional assays were performed to evaluate the changes in mTOR activity and mitochondrial dynamics caused by Leu treatment. Results Leu-treated mice showed a significant reduction in infarct size when compared with the control group (34.8% ± 3.8% vs. 43.1% ± 2.4%, n = 7, p < 0.05), whereas Rap-treated mice did not show the protective effects of Leu. This preconditioning effect of Leu was attenuated in mTOR+/− mice. Additionally, Leu increased the percentage of fused mitochondria and the mitochondrial volume, and decreased the number of mitochondria per cell in isolated cardiomyocytes. In HFD-induced obese mice, Leu treatment significantly reduced infarct size (41.0% ± 1.1% vs. 51.0% ± 1.4%, n = 7, p < 0.05), which was not induced by ischemic preconditioning, and this effect was inhibited by Rap. Furthermore, we observed enhanced mTOR protein expression and mitochondrial fusion with decreased reactive oxygen species production with Leu treatment in HFD-induced obese mice, but not in mTOR+/− mice. Conclusions Leu treatment improved the damage caused by myocardial I/R injury by promoting mTOR activity and mitochondrial fusion on prediabetic hearts in mice.

Effect of insulin on adipocyte lipolysis in exercise-trained rats

1993 ◽  
Vol 74 (6) ◽  
pp. 2935-2939 ◽  
Author(s):  
K. Suda ◽  
T. Izawa ◽  
T. Komabayashi ◽  
M. Tsuboi ◽  
S. Era
Keyword(s):  
Exercise Training ◽  
Adrenergic Receptors ◽  
Insulin Dose ◽  
Displacement Rate ◽  
Control Group ◽  
Trained Group ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Low Concentrations ◽  
Cgp 12177

The effect of exercise training on the antilipolytic action of insulin was studied in rat adipocytes. Exercise training enhanced lipolysis induced by norepinephrine. Insulin dose dependently inhibited norepinephrine- (1 microM) stimulated lipolysis in both groups. Its inhibition rate was significantly greater in the trained than in the control group. Thus, exercise training enhanced the antilipolytic action of insulin. In the control group, insulin (1,000 microU/ml) reduced the displacement rate of [3H]CGP-12177 binding to adipocytes by low concentrations of (-)-norepinephrine. The slope factor without insulin was 0.76, whereas that with insulin was 0.95. In the trained group, insulin did not affect the competition binding of (-)-norepinephrine for [3H]CGP-12177. The displacement rate of [3H]CGP-12177 binding from adipocytes by low concentrations of (-)-norepinephrine was significantly greater in the trained than in the control group. The number of surface beta-adrenergic receptors per adipocyte was smaller in the trained than in the control group. Cilostamide, which blocks the antilipolytic action of insulin, restored lipolysis in both groups. The recovery rate was significantly greater in the trained than in the control group. These findings suggest that the enhanced antilipolytic action by insulin in the trained group occurs at a site distal to the binding of norepinephrine to beta-adrenergic receptors and that it is due to the increased activity of particulate low-Michaelis constant phosphodiesterase.

Methionine protects from myocardial ischemia/reperfusion injury

2014 ◽  
Vol 2 (2) ◽  
pp. 87-97
Keyword(s):  
Reperfusion Injury ◽  
Surgical Procedure ◽  
Troponin I ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Injury ◽  
Treated Group ◽  
Control Group ◽  
Control Groups ◽  
Severity Scores

Ischemia-reperfusion of cardiac tissues may lead to a prominent damage of the myocyte through either necrosis or apoptosis that seems to be the predominant modes of death during this period. In this study, we investigated the effects of L-Methionine in regional ischemia/ reperfusion injury and apoptosis. Dwale-sprague rats were divided into four groups (six rats per group). Sham group, rats were subjected for all surgical procedure without ligation of the left interior descending coronary artery (LAD). Control group, in which LAD was ligated. Control vehicle and L-methionine treated groups, rats pretreated with normal saline and L-methionine (100 mg/kg, IP ), respectively, for 7 days then subjected to the surgical procedure with ligation of LAD for 25 minutes followed by 120 minutes reperfusion. At the end of reperfusion, cardiac tissue TNF-α, IL-1β, IL-6 and ssDNA, as well as plasma cardiac troponin I (cTnI) were measured. It has been found that L-methionine treated group showed significant reduction (P˂0.05) in TNFα, IL-1β, IL-6, ssDNA and cTnI with respect to the control groups. Histopathology study revealed that the treatment with L-methionine significantly (P˂0.05) improved cardiac injury as compared with control groups and the total severity scores showed that the cardiac injury was mild (score 1) in 50.0%, moderate (score 2) in 33.3% and sever (score 3) in 16.7% of L-methionine treated group. It is concluded that L-methionine reduces inflammatory reaction associated with ischemia/reperfusion injury induced by LAD ligation in addition to its reduction for cardiac injury induced by ischemia reperfusion.

scholarly journals Shenxian-Shengmai Oral Liquid Reduces Myocardial Oxidative Stress and Protects Myocardium from Ischemia-Reperfusion Injury

2018 ◽  
Vol 48 (6) ◽  
pp. 2503-2516 ◽  
Author(s):  
Yixiu Zhao ◽  
Xin Zhang ◽  
Jing Luan ◽  
Buchang Zhao ◽  
Na An ◽  
...  
Keyword(s):  
Ischemia Reperfusion ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Neonatal Rat ◽  
Ventricular Pressure ◽  
Control Group ◽  
Maximal Increase ◽  
Rat Cardiomyocytes ◽  
Increase Rate ◽  
Oral Liquid

Background/Aims: Shenxian-shengmai (SXSM) oral liquid, a Chinese patent compound medicine, has been used to treat sinus bradyarrhythmias induced by mild sick sinus syndrome in clinical practice. Myocardial ischemia, in particular in serious or right coronary-related heart diseases, can cause bradyarrhythmias and cardiac dysfunction. Moreover, reperfusion of ischemic myocardium is associated with additional myocardial damage known as myocardial ischemia-reperfusion (I/R) injury. This study was designed to evaluate the effects of SXSM on bradyarrhythmias and cardiac dysfunction induced by myocardial I/R injury, and to explore the underlying mechanisms. Methods: Administration of SXSM to adult male Sprague Dawley (SD) rats was achieved orally by gavage and control rats were given equivalent deionized water every day for 14 days. After the last administration, the heart was connected with the Langendorff perfusion apparatus and both groups were subjected to ischemia for 20 min followed by reperfusion for 40 min to induce myocardial I/R injury. Heart rate (HR), left ventricular developed pressure (LVDP), the maximal increase rate of left ventricular pressure (+dp/dtmax) and the maximal decrease rate of left ventricular pressure (-dp/dtmax) were recorded by a physiological signal acquisition system. The heart treated with ischemic preconditioning (IPC) for 3 times at a range of 5 min/time before ischemia served as a positive control group. The hearts without I/R injury served as control group. After reperfusion, superoxide dismutase (SOD), glutathione (GSH) and glutathione peroxidase (GSH-Px) activities in the myocardium were determined by appropriate assay kits. Myocardial SOD1 and glutamate cysteine ligase catalytic subunit (GCLC) expression were assessed by western blot analysis. For the in vitro study, SXSM serum was prepared according to the serum pharmacological method and neonatal rat cardiomyocytes were isolated from the heart of new born SD rats. Neonatal rat cardiomyocytes were pretreated with SXSM serum and subjected to H2O2 or anoxia/ reoxygenation (A/R) treatment to induce oxidative damage. Cell viability was evaluated using a Cell Counting Kit-8 (CCK8) assay. Levels of reactive oxygen species (ROS), SOD, GSH and GSH-Px in cardiomyocytes were determined by appropriate assay kits. SOD1 and GCLC expression were assessed by western blot analysis. Buthionine-[S, R]-sulfoximine (BSO), a GCLC inhibitor, and SOD1 siRNA were also used for identifying the cardiac protective targets of SXSM. Results: SXSM and ischemic preconditioning (IPC) significantly increased heart rate during myocardial reperfusion and protected cardiac function against myocardial I/R injury, including an increase in left ventricular diastolic pressure (LVDP), the maximal increase rate of left ventricular pressure (+dp/dtmax) and the maximal decrease rate of left ventricular pressure (-dp/dtmax). We also found that SXSM and IPC improved the expansion of myocardial interstitium, the structural abnormality and morphological changes of cardiomyocytes induced by I/R injury. Meanwhile, SXSM protected cardiomyocytes against the oxidative damage induced by H2O2 and A/R injury through reducing intracellular ROS levels. Moreover, SXSM increased SOD activity through enhancing SOD1 expression and increased GSH content through promoting GCLC expression as well as GSH-Px activity. BSO and SOD1 siRNA counteracted anti-arrhythmic and cardiac protective effect of SXSM, suggesting that the therapeutic targets of SXSM might be SOD1 and GCLC. Conclusion: SXSM is effective in protecting the myocardium from I/R injury, with myocardial SOD1 and GCLC being the potential therapeutic targets.

scholarly journals Exercise training induces a cardioprotective phenotype and alterations in cardiac subsarcolemmal and intermyofibrillar mitochondrial proteins

2009 ◽  
Vol 297 (1) ◽  
pp. H144-H152 ◽  
Author(s):  
Andreas N. Kavazis ◽  
Sophie Alvarez ◽  
Erin Talbert ◽  
Youngil Lee ◽  
Scott K. Powers
Keyword(s):  
Exercise Training ◽  
Endurance Exercise ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Mitochondrial Proteins ◽  
Sprague Dawley ◽  
Sedentary Control ◽  
Absolute Quantitation ◽  
Mitochondrial Proteome ◽  
Isobaric Tags

Endurance exercise is known to provide cardioprotection against ischemia-reperfusion-induced myocardial injury, and mitochondrial adaptations may play a critical role in this protection. To investigate exercise-induced changes in mitochondrial proteins, we compared the proteome of subsarcolemmal and intermyofibrillar mitochondria isolated from the myocardium of sedentary (control) and exercise-trained Sprague-Dawley rats. To achieve this goal, we utilized isobaric tags for relative and absolute quantitation, which allows simultaneous identification and quantification of proteins between multiple samples. This approach identified a total of 222 cardiac mitochondrial proteins. Importantly, repeated bouts of endurance exercise resulted in significant alterations in 11 proteins within intermyofibrillar mitochondria (seven increased; four decreased) compared with sedentary control animals. Furthermore, exercise training resulted in significant changes in two proteins within subsarcolemmal mitochondria (one increased; one decreased) compared with sedentary control animals. Differentially expressed proteins could be classified into seven functional groups, and several novel and potentially important cardioprotective mediators were identified. We conclude that endurance exercise induces alterations in mitochondrial proteome that may contribute to cardioprotective phenotype. Importantly, based on our findings, pharmacological or other interventions could be used to develop a strategy of protecting the myocardium during an ischemic attack.

Exercise training and clenbuterol reduce insulin resistance of obese Zucker rats

1993 ◽  
Vol 264 (3) ◽  
pp. E373-E379 ◽  
Author(s):  
C. E. Torgan ◽  
J. T. Brozinick ◽  
E. A. Banks ◽  
M. Y. Cortez ◽  
R. E. Wilcox ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Exercise Training ◽  
Glucose Tolerance ◽  
Glucose Uptake ◽  
Adrenergic Receptor ◽  
Aerobic Exercise Training ◽  
Zucker Rats ◽  
Sedentary Control ◽  
Control Groups ◽  
Beta 2

This study compared the effects of aerobic exercise training and chronic administration of the selective beta 2-adrenergic agonist clenbuterol on whole body and skeletal muscle insulin resistance in obese (fa/fa) Zucker rats. Obese rats were randomly assigned to training, clenbuterol, or sedentary control groups. Lean littermates served as a second control group. After 4-5 wk of treatment, an oral glucose tolerance test was performed, followed 1 wk later by hindlimb perfusion, during which time the rates of glucose uptake and 3-O-methyl-D-glucose (3-MG) transport were assessed in the presence of a submaximal (500 microU/ml) insulin concentration. Training resulted in a significant increase in citrate synthase and cytochrome oxidase activity in the recruited muscles. Clenbuterol induced a large increase in muscle mass but provoked a significant decrease in oxidative enzyme activity and beta-adrenergic receptor density. Both treatments increased glucose tolerance and reduced the postglucose insulin response, with the improvements being more pronounced in the clenbuterol group. However, only exercise training improved insulin-stimulated hindlimb muscle glucose uptake (11.37 +/- 0.65, 8.73 +/- 0.77, and 8.27 +/- 0.41 mumol.g-1.h-1 for trained, clenbuterol, and sedentary control groups, respectively) and 3-MG transport. These results suggest that aerobic exercise training attenuated the insulin-resistant condition in the obese Zucker rat by a mechanism other than or in addition to beta 2-adrenergic receptor activation.

Exercise training preserves coronary flow and reduces infarct size after ischemia-reperfusion in rat heart

2003 ◽  
Vol 95 (6) ◽  
pp. 2510-2518 ◽  
Author(s):  
David A. Brown ◽  
Korinne N. Jew ◽  
Genevieve C. Sparagna ◽  
Timothy I. Musch ◽  
Russell L. Moore
Keyword(s):  
Coronary Artery ◽  
Exercise Training ◽  
Infarct Size ◽  
Coronary Flow ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Control Group ◽  
Mechanical Function ◽  
Sprague Dawley ◽  
Regional Ischemia

The effect of endurance training on the resistance of the heart to left ventricular (LV) functional deficit and infarction after a transient regional ischemia and subsequent reperfusion was examined. Female Sprague-Dawley rats were randomly assigned to an endurance exercise training (Tr) group or a sedentary (Sed) control group. After 20 wk of training, hearts were excised, perfused, and instrumented for assessment of LV mechanical function, and the left anterior descending coronary artery was occluded to induce a transient regional ischemia (1 h) that was followed by 2 h of reperfusion. Throughout much of the regional ischemia-reperfusion protocol, coronary flow rates, diastolic function, and LV developed pressure were better preserved in hearts from Tr animals. During the regional ischemia, coronary flow to myocardium outside the ischemic zone at risk (ZAR) was maintained in Tr hearts, whereas it progressively fell in Sed hearts. On release of the coronary artery ligature, flow to the ZAR was greater in Tr than in Sed hearts. Infarct size, expressed as a percentage of the ischemic ZAR, was significantly smaller in hearts from Tr rats (24 ± 3 vs. 32 ± 2% of ZAR, P < 0.05). Mn- and CuZn-SOD protein expression were higher in the LV myocardium of Tr animals ( P < 0.05 for both isoforms). Our data indicate that long-term exercise training leads to infarct sparing and better maintenance of coronary flow and mechanical function after ischemia-reperfusion.

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