Chronic and acute exercise do not alter Ca<sup>2+</sup>regulatory systems and ectonucleotidase activities in rat heart

Delgado, Jerónimo; Saborido, Ana; Morán, María; Megías, Alicia

doi:10.1152/jappl.1999.87.1.152

Cited by 27 publications

(50 citation statements)

References 39 publications

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“…Thus, reduced availability of channels could be tolerated without compromising the Ca 2+ transient (Pott et al 2005(Pott et al , 2007. Furthermore, neither treadmill exercise training for 12 weeks nor exhaustive exercise alters the density of Ca 2+ channels involved in excitationcontraction coupling in rat heart (Delgado et al 1999). Our Wndings demonstrated a remarkable adaptive plasticity of L-type channel characteristics in training rat heart.…”

Section: Evects Of Swimming Training On Calcium Current Characteristicsmentioning

confidence: 73%

“…These data indicate that chronic exercise inXuences the contractile function of diVerent types of cardiac preparations, including LV papillary muscle and isolated myocytes. Exercise training does not induce a change in cardiac Ca 2+ regulatory system (Delgado et al 1999). However, regulatory proteins such as the Na + /H + exchanger, Na + /Ca 2+ exchanger and the L-type Ca + channel are not correlated with LV function (Renna et al 2006).…”

Section: Evects Of Swimming Training On Calcium Current Characteristicsmentioning

confidence: 99%

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Swimming training can affect intrinsic calcium current characteristics in rat myocardium

et al. 2008

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Endurance exercise is widely assumed to improve cardiac function in humans, but the mechanisms involved in such changes are not clearly understood. The purpose of this study is to determine whether training elicits adaptations at the level of the L-type Ca(2+) channel. Sprague-Dawley rats performed swimming training at either moderate intensity (MOD) or high intensity (HIGH) during 8 weeks. The trained rats were studied by echocardiography and the whole-cell L-type Ca(2+) currents (I (Ca,L)) characteristics in a single cell were measured by standard whole-cell patch-clamp recording technique. Echocardiography showed that septal and posterior wall thickness in MOD and HIGH increased with the increased LV mass by 43 and 41%, respectively (P < 0.05). Training (P < 0.05) increased mean myocyte capacitance (approximately 38% in MOD and HIGH) and myocyte length (approximately 20% longer in MOD and 26% longer in HIGH), thus providing electrophysiological and morphological evidence that the training elicited LV cardiocyte hypertrophy. Mean peak I (Ca,L) was not different in three groups. However, whole-cell I (Ca,L) density was decreased in MOD and HIGH versus sedentary (P < 0.05), but there was no significant difference between MOD and HIGH. The present study provides the evidence of a training adaptation in intrinsic I (Ca,L) characteristics in ventricular myocardium, which demonstrates a remarkable adaptive plasticity of L-type channel characteristics in training rat heart.

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Section: Evects Of Swimming Training On Calcium Current Characteristicsmentioning

confidence: 73%

Section: Evects Of Swimming Training On Calcium Current Characteristicsmentioning

confidence: 99%

Swimming training can affect intrinsic calcium current characteristics in rat myocardium

et al. 2008

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“…In our previous study using male Wistar rats as an animal model, none of the three different exercise intensities employed (moderate, high, and interval running) in a 3-month treadmill training program altered various indicators of the Ca 2+ regulatory system (density of L-type and SR Ca 2+ channels and SR Ca 2+ -ATPase activity) significantly [4]. It could not be inferred from this investigation, however, whether the observed lack of changes would have persisted with longer exercise programs.…”

Section: Introductionmentioning

confidence: 83%

“…Adaptation of these important enzymes to exercise training has been studied rarely. Whilst no changes in Mg 2+ -ATPase and 5'-nucleotidase activities are detected in the heart of rats after 3 months of treadmill training at different exercise intensities [4], the response to longer training periods is unknown.…”

Section: Introductionmentioning

confidence: 99%

Ca2+ regulatory systems in rat myocardium are altered by 24 weeks treadmill training

Morán

Saborido

Megías

2003

Pflugers Arch - Eur J Physiol

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The present study was conducted to investigate the effects of long-term exercise training on the main components involved in excitation-contraction coupling and relaxation in rat myocardium. Twenty male Wistar rats were divided into sedentary (S) and treadmill-trained (T) groups. Group T was trained for 24 weeks, 5 days/week (25 m/min, 45-60 min, 0% slope). 48 h after the last exercise session, animals were killed and ventricular and soleus muscle homogenates were obtained. The citrate synthase activity in soleus muscle was significantly increased (163%) in T compared with S rats ( P<0.01), confirming the exercise training efficacy. Although heart weight and cardiac oxidative capacity were not modified by exercise training, the binding of [(3)H] ryanodine and the dihydropyridine [(3)H]PN200-110 to cardiac homogenates, and sarcoplasmic reticulum Ca(2+)-ATPase activity were increased significantly in the ventricular homogenates from T compared with S animals ( P<0.01). Western blot analysis of ventricular homogenates failed to show significant alterations in dihydropyridine receptor and Ca(2+)-ATPase levels in T animals, but revealed an increase of ryanodine receptor density in this group ( P<0.01). The activity of the ectoenzymes 5'-nucleotidase and Mg(2+)-ATPase was not affected by training ( P>0.05). In conclusion, long-term treadmill training induces adaptive changes in some of the components of myocardial rat excitation-contraction coupling and relaxation systems that could contribute to the improvement of cardiac function.

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“…Adenosine also has an important role as an endogenous determinant of ischemic tolerance by modulating several components of cardiac function (6,41). For example, adenosine has potent cardiac electrophysiological effects, including a negative chronotropic action on the sinus node and a predominant negative dromotropic action on the atrioventricular (AV) node (48).…”

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Acute exercise increases the ventricular arrhythmia threshold via the intrinsic adenosine receptor system in conscious hypertensive rats

Collins¹,

DiCarlo²

2005

American Journal of Physiology-Heart and Circulatory Physiology

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Collins, Heidi L., and Stephen E. DiCarlo. Acute exercise increases the ventricular arrhythmia threshold via the intrinsic adenosine receptor system in conscious hypertensive rats. Am J Physiol Heart Circ Physiol 289: H1020 -H1026, 2005. First published May 6, 2005; doi:10.1152/ajpheart.00156.2005.-Coronary artery occlusioninduced tachyarrhythmias that culminate in ventricular fibrillation are the leading cause of death in developed countries. The intrinsic adenosine receptor system protects the heart from an ischemic insult. Thus the increased functional demands made on the heart during exercise may produce protective adaptations mediated by endogenous adenosine. Therefore, we tested the hypothesis that a single bout of dynamic exercise increases the ventricular arrhythmia threshold (VAT) induced by coronary artery occlusion in conscious hypertensive rats via the intrinsic adenosine receptor system. To test this hypothesis, we recorded the VAT before and on an alternate day after a single bout of dynamic treadmill exercise (12 m/min, 10% grade for 40 min). A single bout of dynamic exercise significantly reduced postexercise arterial pressure (⌬Ϫ24 Ϯ 4 mmHg) and increased VAT (⌬ϩ1.95 Ϯ 0.31 min). Adenosine receptor blockade with the nonselective adenosine receptor antagonists theophylline or aminophylline (10 mg/kg) attenuated the cardioprotective effects of a single bout of dynamic exercise. Results suggest that strategies that increase myocardial ATP requirements leading to adenosine production provide protection against coronary artery occlusion. coronary artery occlusion; cardioprotective strategies THE CARDIOVASCULAR RESPONSE to dynamic, whole body exercise places profound demands on the heart. For example, cardiac output can increase four-to fivefold. The increase in cardiac output is primarily mediated by an increase in heart rate (HR) and to a lesser extent by an increase in stroke volume. The increase in stroke volume is primarily mediated by an increase in end-diastolic volume (Frank-Starling mechanism) and, in part, to a reduction in end-systolic volume (increased contractility mediated by adrenergic stimulation). These cardiovascular responses markedly increase myocardial oxygen consumption and accordingly, coronary blood flow can increase four-to fivefold (46). There is a tight relationship between myocardial oxygen consumption and coronary blood flow that suggests that products of metabolism mediate local control of coronary blood flow. Adenosine, a breakdown product of ATP, has been proposed as the major mediator of local coronary blood flow (3). Specifically, adenosine is the vasodilatory metabolite that links coronary blood flow to myocardial metabolism (3).Adenosine also has an important role as an endogenous determinant of ischemic tolerance by modulating several components of cardiac function (6, 41). For example, adenosine has potent cardiac electrophysiological effects, including a negative chronotropic action on the sinus node and a predominant negative dromotropic action on the atriovent...

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Chronic and acute exercise do not alter Ca²⁺regulatory systems and ectonucleotidase activities in rat heart

Cited by 27 publications

References 39 publications

Swimming training can affect intrinsic calcium current characteristics in rat myocardium

Swimming training can affect intrinsic calcium current characteristics in rat myocardium

Ca2+ regulatory systems in rat myocardium are altered by 24 weeks treadmill training

Acute exercise increases the ventricular arrhythmia threshold via the intrinsic adenosine receptor system in conscious hypertensive rats

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Chronic and acute exercise do not alter Ca2+regulatory systems and ectonucleotidase activities in rat heart

Cited by 27 publications

References 39 publications

Swimming training can affect intrinsic calcium current characteristics in rat myocardium

Swimming training can affect intrinsic calcium current characteristics in rat myocardium

Ca2+ regulatory systems in rat myocardium are altered by 24 weeks treadmill training

Acute exercise increases the ventricular arrhythmia threshold via the intrinsic adenosine receptor system in conscious hypertensive rats

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Chronic and acute exercise do not alter Ca²⁺regulatory systems and ectonucleotidase activities in rat heart