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 Endurance exercise training normalizes repolarization and calcium-handling abnormalities, preventing ventricular fibrillation in a model of sudden cardiac death

2012 ◽  
Vol 113 (11) ◽  
pp. 1772-1783 ◽  
Author(s):  
Ingrid M. Bonilla ◽  
Andriy E. Belevych ◽  
Arun Sridhar ◽  
Yoshinori Nishijima ◽  
Hsiang-Ting Ho ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Cardiac Death ◽  
Outward Current ◽  
Calcium Handling ◽  
Transient Outward Current ◽  
Cellular Electrophysiology ◽  
Endurance Exercise Training

The risk of sudden cardiac death is increased following myocardial infarction. Exercise training reduces arrhythmia susceptibility, but the mechanism is unknown. We used a canine model of sudden cardiac death (healed infarction, with ventricular tachyarrhythmias induced by an exercise plus ischemia test, VF+); we previously reported that endurance exercise training was antiarrhythmic in this model (Billman GE. Am J Physiol Heart Circ Physiol 297: H1171–H1193, 2009). A total of 41 VF+ animals were studied, after random assignment to 10 wk of endurance exercise training (EET; n = 21) or a matched sedentary period ( n = 20). Following (>1 wk) the final attempted arrhythmia induction, isolated myocytes were used to test the hypotheses that the endurance exercise-induced antiarrhythmic effects resulted from normalization of cellular electrophysiology and/or normalization of calcium handling. EET prevented VF and shortened in vivo repolarization ( P < 0.05). EET normalized action potential duration and variability compared with the sedentary group. EET resulted in a further decrement in transient outward current compared with the sedentary VF+ group ( P < 0.05). Sedentary VF+ dogs had a significant reduction in repolarizing K+ current, which was restored by exercise training ( P < 0.05). Compared with controls, myocytes from the sedentary VF+ group displayed calcium alternans, increased calcium spark frequency, and increased phosphorylation of S2814 on ryanodine receptor 2. These abnormalities in intracellular calcium handling were attenuated by exercise training ( P < 0.05). Exercise training prevented ischemically induced VF, in association with a combination of beneficial effects on cellular electrophysiology and calcium handling.

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.

Protective effect of glycine on renal injury induced by ischemia-reperfusion in vivo

2002 ◽  
Vol 282 (3) ◽  
pp. F417-F423 ◽  
Author(s):  
Ming Yin ◽  
Zhi Zhong ◽  
Henry D. Connor ◽  
Hartwig Bunzendahl ◽  
William F. Finn ◽  
...  
Keyword(s):  
Renal Injury ◽  
Cell Injury ◽  
Ischemia Reperfusion Injury ◽  
Interstitial Fibrosis ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Renal Tubular Cell ◽  
Sprague Dawley

Although glycine prevents renal tubular cell injury in vitro, its effect in vivo is not clear. The purpose of this study was to investigate whether a bolus injection of glycine given before reperfusion plus continuous dietary supplementation afterward would reduce renal injury caused by ischemia-reperfusion. Female Sprague-Dawley rats received a semisynthetic powdered diet containing 5% glycine and 15% casein (glycine group) or 20% casein (control group). Two days later, renal ischemia was produced by cross-clamping the left renal vessels for 15 min, followed by reperfusion. The right kidney was removed before reperfusion. The postischemic glomerular filtration rate (GFR) showed that renal function was less impaired and recovered more quickly in rats receiving glycine. For example, at day 7, GFR in controls (0.31 ± 0.03 ml · min−1 · 100 g−1) was about one-half that of glycine-treated rats (0.61 ± 0.06 ml · min−1 · 100 g−1, P < 0.05). Furthermore, tubular injury and cast formation observed in controls was minimized by glycine (pathology score, 3.2 ± 0.4 vs. 1.0 ± 0.4, P < 0.05). Urinary lactate dehydrogenase (LDH) concentration was elevated by ischemia-reperfusion in the control group (260 ± 22 U/l), but values were significantly lower by about fourfold (60 ± 30 U/l) in glycine-fed rats. Similarly, free radical production in urine was significantly lower in glycine-treated animals. Importantly, on postischemic day 1, binding of pimonidazole, an in vivo hypoxia marker, was increased in the outer medulla in controls; however, this phenomenon was prevented by glycine. Two weeks later, mild leukocyte infiltration and interstitial fibrosis were still observed in controls, but not in kidneys from glycine-treated rats. In conclusion, these results indicate that administration of glycine indeed reduces mild ischemia-reperfusion injury in the kidney in vivo, in part by decreasing initial damage and preventing chronic hypoxia.

scholarly journals Exercise Pills for Drug Addiction: Forced Moderate Endurance Exercise Inhibits Methamphetamine-Induced Hyperactivity through the Striatal Glutamatergic Signaling Pathway in Male Sprague Dawley Rats

2021 ◽  
Vol 22 (15) ◽  
pp. 8203
Author(s):  
Suryun Jung ◽  
Youjeong Kim ◽  
Mingyu Kim ◽  
Minjae Seo ◽  
Suji Kim ◽  
...  
Keyword(s):  
Exercise Training ◽  
Signaling Pathway ◽  
Endurance Exercise ◽  
Exercise Group ◽  
Treadmill Running ◽  
Sprague Dawley ◽  
Exercise Treatment ◽  
Endurance Exercise Training ◽  
Sprague Dawley Rats ◽  
Gsk 3Β

Physical exercise reduces the extent, duration, and frequency of drug use in drug addicts during the drug initiation phase, as well as during prolonged addiction, withdrawal, and recurrence. However, information about exercise-induced neurobiological changes is limited. This study aimed to investigate the effects of forced moderate endurance exercise training on methamphetamine (METH)-induced behavior and the associated neurobiological changes. Male Sprague Dawley rats were subjected to the administration of METH (1 mg/kg/day, i.p.) and/or forced moderate endurance exercise (treadmill running, 21 m/min, 60 min/day) for 2 weeks. Over the two weeks, endurance exercise training significantly reduced METH-induced hyperactivity. METH and/or exercise treatment increased striatal dopamine (DA) levels, decreased p(Thr308)-Akt expression, and increased p(Tyr216)-GSK-3β expression. However, the phosphorylation levels of Ser9-GSK-3β were significantly increased in the exercise group. METH administration significantly increased the expression of NMDAr1, CaMKK2, MAPKs, and PP1 in the striatum, and exercise treatment significantly decreased the expression of these molecules. Therefore, it is apparent that endurance exercise inhibited the METH-induced hyperactivity due to the decrease in GSK-3β activation by the regulation of the striatal glutamate signaling pathway.

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.

scholarly journals The Effect of Endurance Exercise Training on Vaspin, Lipid Profile, and Anthropometric Indices in Young People

2019 ◽  
Author(s):  
Mansour Karajibani ◽  
Farzaneh Montazerifar ◽  
Karim Dehghani ◽  
Mehdi Mogharnasi ◽  
Seyed Reza Mousavi Gilani ◽  
...  
Keyword(s):  
Young People ◽  
Exercise Training ◽  
Lipid Profile ◽  
Endurance Exercise ◽  
Intervention Group ◽  
Control Group ◽  
Dietary Intakes ◽  
Anthropometric Indices ◽  
Endurance Exercise Training ◽  
Significant Difference

Background: Exercise training affects the adipose tissue, which may lead to the secretion of adipokines. This study aimed to evaluate the effect of endurance exercise training on vaspin, lipid profiles, and some anthropometric indices among young people. Methods: The participants included 26 young men selected and categorized into the intervention and control groups randomly. The intervention group underwent the endurance activity (aerobic), while the control group had no exercises during the study. Anthropometric indices and dietary intakes were determined by standard and 48-hr recall methods, respectively. Before and after implementation of the exercise training, the participants' fasting blood samples were collected. Lipid profile (including cholesterol, triglyceride, LDL, and HDL) and vaspin levels were determined. Results: A significant difference was observed in body fat percentage of the intervention group after exercise training (P = 0.009). However, no significant differences were observed based on the means of anthropometric indices, lipid profile, and daily energy intake between two groups. With regard to the vaspin levels, a significant difference was observed between the participants' scores before (P = 0.001) and after (P = 0.04) the exercise training in intervention compared to the control group. Conclusion: Endurance exercise program can lead to appropriate changes in some anthropometric indices, lipid profile, and vaspin adipokine in young people. So, exercise training can affect health promotion of people.

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.

Sign in / Sign up

Export Citation Format

Share Document