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 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 Sarcalumenin is essential for maintaining cardiac function during endurance exercise training

2009 ◽  
Vol 297 (2) ◽  
pp. H576-H582 ◽  
Author(s):  
Qibin Jiao ◽  
Yunzhe Bai ◽  
Toru Akaike ◽  
Hiroshi Takeshima ◽  
Yoshihiro Ishikawa ◽  
...  
Keyword(s):  
Exercise Training ◽  
Cardiac Function ◽  
Endurance Exercise ◽  
Maximal Exercise ◽  
Storage System ◽  
Critical Role ◽  
Pressure Overload ◽  
Sodium Calcium Exchanger ◽  
Expression Levels ◽  
Echocardiographic Examination

Sarcalumenin (SAR), a Ca2+-binding protein located in the longitudinal sarcoplasmic reticulum (SR), regulates Ca2+ reuptake into the SR by interacting with cardiac sarco(endo)plasmic reticulum Ca2+-ATPase 2a (SERCA2a). We have previously demonstrated that SAR deficiency induced progressive heart failure in response to pressure overload, despite mild cardiac dysfunction in sham-operated SAR knockout (SARKO) mice ( 26 ). Since responses to physiological stresses often differ from those to pathological stresses, we examined the effects of endurance exercise on cardiac function in SARKO mice. Wild-type (WT) and SARKO mice were subjected to endurance treadmill exercise training (∼65% of maximal exercise ability for 60 min/day) for 12 wk. After exercise training, maximal exercise ability was significantly increased by 5% in WT mice ( n = 6), whereas it was significantly decreased by 37% in SARKO mice ( n = 5). Cardiac function assessed by echocardiographic examination was significantly decreased in accordance with upregulation of biomarkers of cardiac stress in SARKO mice after training. After training, expression levels of SERCA2a protein were significantly downregulated by 30% in SARKO hearts, whereas they were significantly upregulated by 59% in WT hearts. Consequently, SERCA2 activity was significantly decreased in SARKO hearts after training. Furthermore, the expression levels of other Ca2+-handling proteins, including phospholamban, ryanodine receptor 2, calsequestrin 2, and sodium/calcium exchanger 1, were significantly decreased in SARKO hearts after training. These results indicate that SAR plays a critical role in maintaining cardiac function under physiological stresses, such as endurance exercise, by regulating Ca2+ transport activity into the SR. SAR may be a primary target for exercise-related adaptation of the Ca2+ storage system in the SR to preserve cardiac function.

scholarly journals Exercise: Teaching myocytes new tricks

2017 ◽  
Vol 123 (2) ◽  
pp. 460-472 ◽  
Author(s):  
Scott K. Powers
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Cardiac Myocytes ◽  
Endurance Exercise ◽  
Ischemia Reperfusion ◽  
Muscle Fibers ◽  
Cardiac Phenotype ◽  
Endurance Exercise Training ◽  
Skeletal Muscle Fibers ◽  
Exercise Induced

Endurance exercise training promotes numerous cellular adaptations in both cardiac myocytes and skeletal muscle fibers. For example, exercise training fosters changes in mitochondrial function due to increased mitochondrial protein expression and accelerated mitochondrial turnover. Additionally, endurance exercise training alters the abundance of numerous cytosolic and mitochondrial proteins in both cardiac and skeletal muscle myocytes, resulting in a protective phenotype in the active fibers; this exercise-induced protection of cardiac and skeletal muscle fibers is often referred to as “exercise preconditioning.” As few as 3–5 consecutive days of endurance exercise training result in a preconditioned cardiac phenotype that is sheltered against ischemia-reperfusion-induced injury. Similarly, endurance exercise training results in preconditioned skeletal muscle fibers that are resistant to a variety of stresses (e.g., heat stress, exercise-induced oxidative stress, and inactivity-induced atrophy). Many studies have probed the mechanisms responsible for exercise-induced preconditioning of cardiac and skeletal muscle fibers; these studies are important, because they provide an improved understanding of the biochemical mechanisms responsible for exercise-induced preconditioning, which has the potential to lead to innovative pharmacological therapies aimed at minimizing stress-induced injury to cardiac and skeletal muscle. This review summarizes the development of exercise-induced protection of cardiac myocytes and skeletal muscle fibers and highlights the putative mechanisms responsible for exercise-induced protection in the heart and skeletal muscles.

Regional differences in effects of exercise training on contractile and biochemical properties of rat cardiac myocytes

2003 ◽  
Vol 95 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Gary M. Diffee ◽  
Daniel F. Nagle
Keyword(s):  
Exercise Training ◽  
Cardiac Myocytes ◽  
Endurance Exercise ◽  
Biochemical Properties ◽  
Ventricular Wall ◽  
Sprague Dawley ◽  
Cellular Mechanisms ◽  
Endurance Exercise Training ◽  
Improved Function ◽  
Rat Cardiac Myocytes

Myocardial function is enhanced by endurance exercise training, but the cellular mechanisms underlying this improved function remain unclear. A number of studies have shown that the characteristics of cardiac myocytes vary across the width of the ventricular wall. We have previously shown that endurance exercise training alters the Ca2+ sensitivity of tension as well as contractile protein isoform expression in rat cardiac myocytes. We tested the hypothesis that these effects of training are not uniform across the ventricular wall but are more pronounced in the subendocardial (Endo) region of the myocardium. Female Sprague-Dawley rats were divided into sedentary control (C) and exercise trained (T) groups. T rats underwent 11 wk of progressive treadmill exercise. Myocytes were isolated from the Endo region of the myocardium and from the subepicardial (Epi) region of both T and C hearts. We found an increase in the Ca2+ sensitivity of tension in T cells compared with C cells, but this difference was larger in the Endo cells than in the Epi cells. In addition, we found a training-induced increase in atrial myosin light chain 1 (aMLC1) expression that was larger in the Endo compared with Epi samples. We conclude that effects of exercise training on myocyte contractile and biochemical properties are greater in myocytes from the Endo region of the myocardium than those from the Epi region. In addition, these results provide evidence that the increase in aMLC1 expression may be responsible for some of the training-induced increase in myocyte Ca2+ sensitivity of tension.

scholarly journals Expressions Profiles of the Proteins Associated with Carbohydrate Metabolism in Rat Liver Regeneration

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Li Yin ◽  
Cuifang Chang ◽  
Cunshuan Xu
Keyword(s):  
Liver Regeneration ◽  
Signaling Pathways ◽  
Carbohydrate Metabolism ◽  
Motif Discovery ◽  
Critical Role ◽  
Remnant Liver ◽  
Absolute Quantitation ◽  
New Thinking ◽  
Isobaric Tags ◽  
First Time

Liver has a very amazing ability to regenerate from the remnant liver after injury or partial hepatectomy (PH). Carbohydrate metabolism plays a critical role in regeneration. Many signaling pathways are involved in the metabolism process. We analyzed the changes of proteins at 0–36 h after PH in rats using isobaric tags for relative and absolute quantitation (iTRAQ) coupled with LC-MS/MS-based quantitative proteomics strategy. The results showed that 110 proteins and 5 signaling pathways related to carbohydrate metabolism in rat LR changed significantly. Based on a motif discovery method performed by iRegulon, we identified for the first time that the transcription factor SPIB whose motif was enriched among the differentiated genes associated with carbohydrate metabolism may play an important role in liver regeneration for the first time. The findings of this research provide a molecular basis for further unrevealing the mechanism of regeneration at priming stage (0–6 h) and proliferation stage (6–36 h) of LR in rats. At the same time, our studies provide more novel evidence for the signaling pathways which regulate carbohydrate metabolism from proteomics level. This study can provide some new thinking of liver regeneration and treatment of diseases associated with glucose metabolism.

Endurance exercise training decreases capillary basement membrane width in older nondiabetic and diabetic adults

1996 ◽  
Vol 80 (3) ◽  
pp. 747-753 ◽  
Author(s):  
J. R. Williamson ◽  
P. L. Hoffmann ◽  
W. M. Kohrt ◽  
R. J. Spina ◽  
A. R. Coggan ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Basement Membrane ◽  
Glucose Tolerance ◽  
Endurance Exercise ◽  
Older Men ◽  
Sedentary Control ◽  
Men And Women ◽  
Endurance Exercise Training ◽  
Older Men And Women

The objectives of these studies were to 1) evaluate the relationships among age, glucose intolerance, and skeletal muscle capillary basement membrane (CBM) width (CBMW) and 2) determine the effects of exercise training on CBMW by comparing values of young (28 +/- 4 yr) and older (63 +/- 7 yr) athletes with those of age-matched sedentary control subjects and by measuring CBMW in older men and women before and after a 9-mo endurance-exercise training program. CBMW was measured in tissue samples obtained from the gastrocnemius muscle. CBMW in sedentary 64 +/- 3-yr-old subjects was 25% thicker than in sedentary 24 +/- 3-yr-old subjects. CBMW was similar in young and older athletes and was thinner than the CBMW of age-matched sedentary control subjects. There were no differences in CBMW among older sedentary individuals with normal or impaired glucose tolerance or mild non-insulin-dependent diabetes mellitus. Nine months of endurance exercise training reduced CBMW in older men and women by 30-40%, to widths that were not different from those of the young subjects; this response was independent of glucose tolerance status. These findings suggest that habitual exercise prevents the thickening of the skeletal muscle CBM that is characteristic of advancing age. Moreover, the thickening of the CBM appears to be readily reversed as a result of exercise training, even in older individuals.

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.

Exercise induces a cardiac mitochondrial phenotype that resists apoptotic stimuli

2008 ◽  
Vol 294 (2) ◽  
pp. H928-H935 ◽  
Author(s):  
Andreas N. Kavazis ◽  
Joseph M. McClung ◽  
David A. Hood ◽  
Scott K. Powers
Keyword(s):  
Exercise Training ◽  
Endurance Exercise ◽  
Mitochondrial Permeability Transition Pore ◽  
Mitochondrial Permeability Transition ◽  
Ischemia Reperfusion ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Oxygen Species ◽  
Antiapoptotic Proteins ◽  
Exercise Induced

Ischemia-reperfusion-induced calcium overload and production of reactive oxygen species can trigger apoptosis by promoting the release of proapoptotic factors via the mitochondrial permeability transition pore. While it is clear that endurance exercise provides cardioprotection against ischemia-reperfusion-induced injury, it is unknown if exercise training directly alters mitochondria phenotype and confers protection against apoptotic stimuli in both subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria. We hypothesized that exercise training increases expression of endogenous antioxidant enzymes and other antiapoptotic proteins, resulting in a SS and IMF mitochondrial phenotype that resists apoptotic stimuli. Mitochondria isolated from hearts of sedentary ( n = 8) and exercised-trained ( n = 8) adult male rats were studied. Endurance exercise increased the protein levels of primary antioxidant enzymes in both SS and IMF mitochondria. Furthermore, exercise increased the levels of antiapoptotic proteins in the heart, including the apoptosis repressor with a caspase recruitment domain and inducible heat shock protein 70. Importantly, our findings reveal that endurance exercise training attenuates reactive oxygen species-induced cytochrome c release from heart mitochondria. These changes are accompanied by a lower maximal rate of mitochondrial permeability transition pore opening ( Vmax) and prolonged time to Vmax in both SS and IMF cardiac mitochondria. These novel findings reveal that endurance exercise promotes biochemical alterations in cardiac SS and IMF mitochondria, resulting in a phenotype that resists apoptotic stimuli. Furthermore, these results are consistent with the concept that exercise-induced mitochondrial adaptations contribute to exercise-induced cardioprotection.

Aerobic exercise training reduces cardiac function in adult male offspring exposed to prenatal hypoxia

2015 ◽  
Vol 309 (5) ◽  
pp. R489-R498 ◽  
Author(s):  
Laura M. Reyes ◽  
Raven Kirschenman ◽  
Anita Quon ◽  
Jude S. Morton ◽  
Amin Shah ◽  
...  
Keyword(s):  
Exercise Training ◽  
Cardiac Function ◽  
Preventive Intervention ◽  
Ex Vivo ◽  
Ischemia Reperfusion ◽  
Cardiac Performance ◽  
Male Offspring ◽  
Aerobic Exercise Training ◽  
Sprague Dawley ◽  
Oxygen Control

Intrauterine growth restriction (IUGR) has been associated with increased susceptibility to myocardial ischemia-reperfusion (I/R) injury. Exercise is an effective preventive intervention for cardiovascular diseases; however, it may be detrimental in conditions of compromised health. The aim of this study was to determine whether exercise training can improve cardiac performance after I/R injury in IUGR offspring. We used a hypoxia-induced IUGR model by exposing pregnant Sprague-Dawley rats to 21% oxygen (control) or hypoxic (11% oxygen; IUGR) conditions from gestational day 15 to 21. At 10 wk of age, offspring were randomized to a sedentary group or to a 6-wk exercise protocol. Transthoracic echocardiography assessments were performed after 6 wk. Twenty-four hours after the last bout of exercise, ex vivo cardiac function was determined using a working heart preparation. With exercise training, there was improved baseline cardiac performance in male control offspring but a reduced baseline cardiac performance in male IUGR exercised offspring ( P < 0.05). In male offspring, exercise decreased superoxide generation in control offspring, while in IUGR offspring, it had the polar opposite effect (interaction P ≤ 0.05). There was no effect of IUGR or exercise on cardiac function in female offspring. In conclusion, in male IUGR offspring, exercise may be a secondary stressor on cardiac function. A reduction in cardiac performance along with an increase in superoxide production in response to exercise was observed in this susceptible group.

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