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.

Effect of diazoxide on flavoprotein oxidation and reactive oxygen species generation during ischemia-reperfusion: a study on Langendorff-perfused rat hearts using optic fibers

2008 ◽  
Vol 294 (5) ◽  
pp. H2088-H2097 ◽  
Author(s):  
Philippe Pasdois ◽  
Bertrand Beauvoit ◽  
Liliane Tariosse ◽  
Béatrice Vinassa ◽  
Simone Bonoron-Adèle ◽  
...  
Keyword(s):  
Ischemia Reperfusion ◽  
Reactive Oxygen Species Generation ◽  
Left Ventricular ◽  
Rate Pressure Product ◽  
Control Group ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Optic Fibers ◽  
The One ◽  
Isolated Perfused Rat Hearts

This study analyzed the oxidant generation during ischemia-reperfusion protocols of Langendorff-perfused rat hearts, preconditioned with a mitochondrial ATP-sensitive potassium channel (mitoKATP) opener (i.e., diazoxide). The autofluorescence of mitochondrial flavoproteins, and that of the total NAD(P)H pool on the one hand and the fluorescence of dyes sensitive to H2O2 or O2•− [i.e., the dihydrodichlorofluoroscein (H2DCF) and dihydroethidine (DHE), respectively] on the other, were noninvasively measured at the surface of the left ventricular wall by means of optic fibers. Isolated perfused rat hearts were subjected to an ischemia-reperfusion protocol. Opening mitoKATP with diazoxide (100 μM) 1) improved the recovery of the rate-pressure product after reperfusion (72 ± 2 vs. 16.8 ± 2.5% of baseline value in control group, P < 0.01), and 2) attenuated the oxidant generation during both ischemic (−46 ± 5% H2DCF oxidation and −40 ± 3% DHE oxidation vs. control group, P < 0.01) and reperfusion (−26 ± 2% H2DCF oxidation and −23 ± 2% DHE oxidation vs. control group, P < 0.01) periods. All of these effects were abolished by coperfusion of 5-hydroxydecanoic acid (500 μM), a mitoKATP blocker. During the preconditioning phase, diazoxide induced a transient, reversible, and 5-hydroxydecanoic acid-sensitive flavoprotein and H2DCF (but not DHE) oxidation. In conclusion, the diazoxide-mediated cardioprotection is supported by a moderate H2O2 production during the preconditioning phase and a strong decrease in oxidant generation during the subsequent ischemic and reperfusion phases.

Regular Moderate Exercise Training Prevents Decrease of CD4+ T-Lymphocytes Induced by a Single Bout of Strenuous Exercise in Mice

2003 ◽  
Vol 28 (3) ◽  
pp. 370-381 ◽  
Author(s):  
Sai Chuen Fu ◽  
Lin Qin ◽  
Chi Kam Leung ◽  
Barbara Pui Chan ◽  
Kai Ming Chan
Keyword(s):  
T Lymphocytes ◽  
Exercise Training ◽  
Strenuous Exercise ◽  
Control Group ◽  
Moderate Exercise ◽  
Handling Stress ◽  
Flow Cytometric ◽  
Single Bout ◽  
Leukocyte Populations ◽  
Moderate Exercise Training

The biphasic effects of exercise training on the immune system have been studied extensively and represented by the well-known J-shaped curve with respect to training intensity. However, the relationship and interactions between "beneficial" exercise training and "harmful" strenuous exercise have not been researched. This study was designed to determine whether regular moderate exercise training could affect the changes of percentage of T-lymphocytes induced by a single bout of strenuous exercise. A protocol to run uphill on a 10° tilted treadmill for 4 weeks was employed as moderate exercise training in mice, while a sedentary control group of mice was exposed to the same handling stress without training. The trained and untrained mice were then exposed to a single bout of strenuous exercise until exhaustion. Total leukocytes were collected from spleen and peripheral blood at 0 hr, 3 hrs, and 24 hrs postexhaustion, as well as from the control groups. Flow cytometric analyses were conducted to determine the percentages of selected leukocyte populations. It was demonstrated that moderate exercise training prevented the decrease of CD4+ but stimulated the increase of CD25+CD8+ T-lymphocytes induced by a single bout of strenuous exercise, indicating an adaptive response that can affect changes of leukocyte subpopuplations. Key words: CD8, flow cytometry, exhaustion, splenic T-cell

Adaptation of the left ventricle to exercise-induced hypertrophy

1987 ◽  
Vol 62 (3) ◽  
pp. 1097-1110 ◽  
Author(s):  
F. C. White ◽  
M. D. McKirnan ◽  
E. A. Breisch ◽  
B. D. Guth ◽  
Y. M. Liu ◽  
...  
Keyword(s):  
Exercise Training ◽  
Stroke Volume ◽  
Time Derivative ◽  
Left Ventricular ◽  
O2 Consumption ◽  
Moderate Exercise ◽  
Heavy Exercise ◽  
Morphometric Measurements ◽  
Exercise Induced ◽  
Moderate Exercise Training

Cardiac functional and structural adaptations to exercise-induced hypertrophy were studied in 68 pigs. Pigs were exercise trained on a treadmill for 10 wk. Sequential measurements were made of cardiac dimensions, [left ventricular end-diastolic diameter (EDD), changes in diameter (delta D%), wall thickness (WTh), wall thickening (WTh%), left ventricular pressure (LVP), time derivative of pressure (dP/dt), stroke volume, total body O2 consumption (VO2), blood gases, and systemic hemodynamics] at rest and during moderate and severe exercise. Postmortem studies included morphometric measurements of capillary density, arteriolar density, mitochondria, and myofibrils. All of the exercise-trained pigs showed significant increases in aerobic capacity. Maximum O2 consumption (VO2 max) increased by 37.5% in group 1 (moderate exercise training) and 34% in group 3 (heavy exercise training). Cardiac hypertrophy ranged from less than 15% in a group (n = 8) subjected to moderate exercise training to greater than 30% in a group (n = 11) subjected to heavy exercise training. Before training, exercise was characterized by a decreasing EDD during progressive exercise; this was reversed after exercise training. Stroke volume and end-diastolic volumes during exercise showed a highly significant increase after exercise training and hypertrophy. Morphometric measurements showed that mitochondria and cell membranes increased with increasing myocyte growth in all exercise groups, but there was only a partially compensated adaptation of capillary proliferation. Arteriolar number and length increased in all exercise groups. Intrinsic contractility as measured by delta D%, WTh%, or left ventricular dP/dt did not increase with exercise training and in some instances decreased. Therefore, left ventricular adaptation to strenuous exercise in the pig heart is primarily one of changes in left ventricular dimensions and a compensated hypertrophy. Exercise-induced increases in EDD and stroke volume can be accounted for by decreases in peripheral resistance and increased cardiac dimensions.

scholarly journals Moderate exercise training attenuates aging-induced cardiac inflammation, hypertrophy and fibrosis injuries of rat hearts

Oncotarget ◽  
2015 ◽  
Vol 6 (34) ◽  
pp. 35383-35394 ◽  
Author(s):  
Po-Hsiang Liao ◽  
Dennis Jine-Yuan Hsieh ◽  
Chia-Hua Kuo ◽  
Cecilia-Hsuan Day ◽  
Chia-Yao Shen ◽  
...  
Keyword(s):  
Exercise Training ◽  
Moderate Exercise ◽  
Cardiac Inflammation ◽  
Rat Hearts ◽  
Moderate Exercise Training

Reversal of experimental hypoxia-induced pulmonary hypertension by moderate exercise training in mice

Pneumologie ◽  
2011 ◽  
Vol 65 (S 01) ◽  
Author(s):  
D Peters ◽  
C Klöpping ◽  
K Krüger ◽  
C Pilat ◽  
S Katta ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Exercise Training ◽  
Moderate Exercise ◽  
Moderate Exercise Training

scholarly journals Exercise Training Preserves Ischemic Preconditioning in Aged Rat Hearts by Restoring the Myocardial Polyamine Pool

2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Weiwei Wang ◽  
Hao Zhang ◽  
Guo Xue ◽  
Li Zhang ◽  
Weihua Zhang ◽  
...  
Keyword(s):  
Exercise Training ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Polyamine Metabolism ◽  
Aged Rat ◽  
Isolated Hearts ◽  
Age Related ◽  
Rat Hearts ◽  
Myocardial Ischemia Reperfusion

Background. Ischemic preconditioning (IPC) strongly protects against myocardial ischemia reperfusion (IR) injury. However, IPC protection is ineffective in aged hearts. Exercise training reduces the incidence of age-related cardiovascular disease and upregulates the ornithine decarboxylase (ODC)/polyamine pathway. The aim of this study was to investigate whether exercise can reestablish IPC protection in aged hearts and whether IPC protection is linked to restoration of the cardiac polyamine pool.Methods. Rats aging 3 or 18 months perform treadmill exercises with or without gradient respectively for 6 weeks. Isolated hearts and isolated cardiomyocytes were exposed to an IR and IPC protocol.Results. IPC induced an increase in myocardial polyamines by regulating ODC and spermidine/spermine acetyltransferase (SSAT) in young rat hearts, but IPC did not affect polyamine metabolism in aged hearts. Exercise training inhibited the loss of preconditioning protection and restored the polyamine pool by activating ODC and inhibiting SSAT in aged hearts. An ODC inhibitor,α-difluoromethylornithine, abolished the recovery of preconditioning protection mediated by exercise. Moreover, polyamines improved age-associated mitochondrial dysfunctionin vitro.Conclusion. Exercise appears to restore preconditioning protection in aged rat hearts, possibly due to an increase in intracellular polyamines and an improvement in mitochondrial function in response to a preconditioning stimulus.

scholarly journals Moderate exercise training modulates cytokine profile and sleep in elderly people

Cytokine ◽  
2012 ◽  
Vol 60 (3) ◽  
pp. 731-735 ◽  
Author(s):  
R.V.T. Santos ◽  
V.A.R. Viana ◽  
R.A. Boscolo ◽  
V.G. Marques ◽  
M.G. Santana ◽  
...  
Keyword(s):  
Exercise Training ◽  
Elderly People ◽  
Cytokine Profile ◽  
Moderate Exercise ◽  
Moderate Exercise Training

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 training promotes adaptations in coronary blood flow and adenosine production in normotensive rats

Clinics ◽  
2011 ◽  
Vol 66 (12) ◽  
pp. 2105-2111 ◽  
Author(s):  
Fernanda R. Roque ◽  
Ursula Paula Renó Soci ◽  
Katia De Angelis ◽  
Marcele A. Coelho ◽  
Cristina R. Furstenau ◽  
...  
Keyword(s):  
Blood Flow ◽  
Exercise Training ◽  
Coronary Blood Flow ◽  
Moderate Exercise ◽  
Moderate Exercise Training
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