A Comparison of Two Exercise Training Programs on Cardiac Responsiveness to β-Stimulation in Obesity

2005 ◽  
Vol 230 (3) ◽  
pp. 180-188 ◽  
Author(s):  
Joan F. Carroll ◽  
Jeremy J. Thaden ◽  
Allison M. Wright
Keyword(s):  
Exercise Training ◽  
Isolated Heart ◽  
Training Volume ◽  
Adrenergic Stimulation ◽  
Isolated Hearts ◽  
Response Data ◽  
New Zealand White Rabbits ◽  
Obese Control ◽  
Developed Pressure ◽  
Post Hoc

We demonstrated previously that exercise training did not restore normal cardiac β-adrenergic responsiveness in obese rabbits. This study tested the hypothesis that an increased training volume was required to attenuate obesity-related reductions in isolated heart responsiveness to isoproterenol. Female New Zealand White rabbits were divided into lean control, lean exercise-trained, obese control, and obese exercise-trained groups. For the exercise-trained groups, total treadmill work over 12 weeks was increased 27% when compared with lean and obese animals trained with lower total training volume. After 12 weeks, Langendorff isolated hearts were used to study developed pressure, +dP/dtmax, and –dP/dtmax responses to isoproterenol (10−9 – 3 × 10−7 M). Concentration-response data were fit to a sigmoidal function using a four-parameter logistic equation. Controls were compared with animals trained under the low– and high–training volume programs using one-way analysis of variance and Tukey's post-hoc test; separate analyses were conducted for lean and obese rabbits. In both lean and obese groups trained under the high–training volume program, EC50 values for +dP/daytmax and –dP/dtmax were higher compared with same-weight controls and animals trained under the low–training volume program, indicating that contractility and relaxation responsiveness to isoproterenol was reduced by the higher training volume. Therefore, these data indicate that increased training volume failed to attenuate obesity-related decrements in isolated heart responsiveness to β-adrenergic stimulation and caused reduced sensitivity to isoproterenol in both lean and obese animals.

Cardiac nicotinic receptors show β-subunit dependent compensatory changes

2021 ◽  
Author(s):  
Katarina Targosova ◽  
Matej Kucera ◽  
Zuzana Kilianova ◽  
Lubica Slobodova ◽  
Kristina Szmicsekova ◽  
...  
Keyword(s):  
Heart Rate ◽  
Muscarinic Receptors ◽  
Nicotinic Receptors ◽  
Isolated Heart ◽  
High Dose ◽  
Β Subunit ◽  
Adrenergic Stimulation ◽  
Relative Expression ◽  
Isolated Hearts ◽  
Heart Functions

Nicotinic receptors (NR) play an important role in the cholinergic regulation of heart functions, and converging evidence suggests a diverse repertoire of NR subunits in the heart. A recent hypothesis about the plasticity of β NR subunits suggests that β2 and β4 subunits may substitute for each other. In our study, we assessed the hypothetical β subunit interchangeability in the heart at the level of mRNA. Using two mutant mice strains lacking β2 or β4 NR subunits, we examined the relative expression of NR subunits and other key cholinergic molecules. We investigated the physiology of isolated hearts perfused by Langendorff's method at basal conditions and after cholinergic and/or adrenergic stimulation. Lack of β2 NR subunit was accompanied with decreased relative expression of β4 and α3 subunits. No other cholinergic changes were observed at the level of mRNA, except for increased M3 and decreased M4 muscarinic receptors. Isolated hearts lacking β2 NR subunit showed different dynamics in heart rate response to indirect cholinergic stimulation. In hearts lacking β4 NR subunit, increased levels of β2 subunits were observed together with decreased mRNA for acetylcholine-synthetizing enzyme and M1 and M4 muscarinic receptors. Changes in the expression levels in β4-/- hearts were associated with increased basal heart rate and impaired response to a high dose of acetylcholine upon adrenergic stimulation. In support of the proposed plasticity of cardiac NRs, our results confirmed subunit-dependent compensatory changes to missing cardiac NRs subunits with consequences on isolated heart physiology.

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.

Effects of exercise training on the vascular reactivity of the whole kidney circulation in rabbits

2004 ◽  
Vol 97 (2) ◽  
pp. 683-688 ◽  
Author(s):  
Roger De Moraes ◽  
Giovanni Gioseffi ◽  
Antonio C. L. Nóbrega ◽  
Eduardo Tibiriçá
Keyword(s):  
Exercise Training ◽  
Vascular Reactivity ◽  
Perfusion Pressure ◽  
Rabbit Kidney ◽  
Constant Flow ◽  
Renal Circulation ◽  
New Zealand White Rabbits ◽  
Vascular Beds ◽  
Renal Vascular ◽  
Isolated Kidneys

Exercise training is known to improve vasodilating mechanisms mediated by endothelium-dependent relaxing factors in the cardiac and skeletal muscle vascular beds. However, the effects of exercise training on visceral vascular reactivity, including the renal circulation, are still unclear. We used the experimental model of the isolated perfused rabbit kidney, which involves both the renal macro- and microcirculation, to test the hypothesis that exercise training improves vasodilator mechanisms in the entire renal circulation. New Zealand White rabbits were pen confined (Sed; n = 24) or treadmill trained (0% grade) for 5 days/wk at a speed of 18 m/min during 60 min over a 12-wk period (ExT; n = 24). Kidneys isolated from Sed and ExT rabbits were continuously perfused in a nonrecirculating system under conditions of constant flow and precontracted with norepinephrine (NE). We assessed the effects of exercise training on renal vascular reactivity using endothelial-dependent [acetylcholine (ACh) and bradykinin (BK)] and -independent [sodium nitroprusside (SNP)] vasodilators. ACh induced marked and dose-related vasodilator responses in kidneys from Sed rabbits, the reduction in perfusion pressure reaching 41 ± 8% ( n = 6; P < 0.05). In the kidneys from ExT rabbits, vasodilation induced by ACh was significantly enhanced to 54 ± 6% ( n = 6; P < 0.05). In contrast, BK-induced renal vasodilation was not enhanced by training [19 ± 8 and 13 ± 4% reduction in perfusion pressure for Sed and ExT rabbits, respectively ( n = 6; P > 0.05)]. Continuous perfusion of isolated kidneys from ExT animals with Nω-nitro-l-arginine methyl ester (l-NAME; 300 μM), an inhibitor of nitric oxide (NO) biosynthesis, completely blunted the additional vasodilation elicited by ACh [reduction in perfusion pressure of 54 ± 6 and 38 ± 5% for ExT and l-NAME + ExT, respectively ( n = 6; P < 0.05)]. On the other hand, l-NAME infusion did not affect ACh-induced vasodilation in Sed animals. Exercise training also increased renal vasodilation induced by SNP [36 ± 7 and 45 ± 10% reduction in perfusion pressure for Sed and ExT rabbits, respectively ( n = 6; P < 0.05)]. It is concluded that exercise training alters the rabbit kidney vascular reactivity, enhancing endothelium-dependent and -independent renal vasodilation. This effect seems to be related not only to an increased bioavailability of NO but also to the enhanced responsiveness of the renal vascular smooth muscle to NO.

Myocardial reperfusion injury management: erythropoietin compared with postconditioning

2009 ◽  
Vol 297 (6) ◽  
pp. H2035-H2043 ◽  
Author(s):  
Sophie Tamareille ◽  
Nehmat Ghaboura ◽  
Frederic Treguer ◽  
Dalia Khachman ◽  
Anne Croué ◽  
...  
Keyword(s):  
Infarct Size ◽  
Reperfusion Injury ◽  
Isolated Heart ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Myocardial Reperfusion ◽  
Myocardial Reperfusion Injury ◽  
Gsk 3Β ◽  
Developed Pressure

Ischemic postconditioning (IPost) and erythropoietin (EPO) have been shown to attenuate myocardial reperfusion injury using similar signaling pathways. The aim of this study was to examine whether EPO is as effective as IPost in decreasing postischemic myocardial injury in both Langendorff-isolated-heart and in vivo ischemia-reperfusion rat models. Rat hearts were subjected to 25 min ischemia, followed by 30 min or 2 h of reperfusion in the isolated-heart study. Rats underwent 45 min ischemia, followed by 24 h of reperfusion in the in vivo study. In both studies, the control group ( n = 12; ischemia-reperfusion only) was compared with IPost ( n = 16; 3 cycles of 10 s reperfusion/10 s ischemia) and EPO ( n = 12; 1,000 IU/kg) at the onset of reperfusion. The following resulted. First, in the isolated hearts, IPost or EPO significantly improved postischemic recovery of left ventricular developed pressure. EPO induced better left ventricular developed pressure than IPost at 30 min of reperfusion (73.18 ± 10.23 vs. 48.11 ± 7.92 mmHg, P < 0.05). After 2 h of reperfusion, the infarct size was significantly lower in EPO-treated hearts compared with IPost and control hearts (14.36 ± 0.60%, 19.11 ± 0.84%, and 36.21 ± 4.20% of the left ventricle, respectively; P < 0.05). GSK-3β phosphorylation, at 30 min of reperfusion, was significantly higher with EPO compared with IPost hearts. Phosphatidylinositol 3-kinase and ERK1/2 inhibitors abolished both EPO- and IPost-mediated cardioprotection. Second, in vivo, IPost and EPO induced an infarct size reduction compared with control (40.5 ± 3.6% and 28.9 ± 3.1%, respectively, vs. 53.7 ± 4.3% of the area at risk; P < 0.05). Again, EPO decreased significantly more infarct size and transmurality than IPost ( P < 0.05). In conclusion, with the use of our protocols, EPO showed better protective effects than IPost against reperfusion injury through higher phosphorylation of GSK-3β.

Abstract 33: Prostaglandin E2 Reduces Cardiac Contractility via EP3 Receptor

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Xiaosong Gu ◽  
Jiang Xu ◽  
Xiao-Ping Yang ◽  
Edward Peterson ◽  
Pamela Harding
Keyword(s):  
Prostaglandin E2 ◽  
Cardiac Contractility ◽  
Peak Height ◽  
Left Ventricular ◽  
Reduced Ejection Fraction ◽  
Langendorff Preparation ◽  
Cell Contractility ◽  
Isolated Hearts ◽  
Developed Pressure ◽  
Ep3 Receptor

Prostaglandin E2 (PGE2) EP receptors EP3 and EP4 are present in the heart and signal via decreased and increased cAMP production, respectively. Previously we reported that cardiomyocyte-specific EP4 KO mice develop a phenotype of dilated cardiomyopathy with reduced ejection fraction. We thus hypothesized that PGE2 decreases contractility via EP3. To test this hypothesis, the effects of PGE2 and the EP1/EP3 agonist sulprostone (sulp) were examined in the mouse langendorff preparation and in adult mouse cardiomyocytes (AVM) using the IonOptix cell contractility system. Isolated hearts of 18-20 wk old male C57Bl/6 mice were mounted and equilibrated for 10 min, then perfused with PGE2 (10 -6 mol/l) or sulp (10 -6 mol/l) for 30 min. Values at the end of equilibration were set to 100%. Compared to vehicle, PGE2 decreased +dp/dt (77.8±3% vs 96.7±3%, p<0.01) and left ventricular developed pressure, LVDP (77.2±2% vs 96.8±3%, p<0.001). Sulp decreased +dp/dt (75.9±2% vs 96.7±3%, p<0.001), -dp/dt (72.2±1% vs 85.7±1%, p<0.01) and LVDP (70.9±1% vs 96.8±3%, p<0.001). The effects of both PGE2 and sulp were reversed by the EP3 antagonist, L789,106 (10 -6 mol/l). Myocyte contractility was evaluated on the IonOptix system with pacing at 1Hz. Treatment with PGE2 (10 -9 M) for 10 min reduced contractility as measured by peak height (3.69 ± 0.48% for vehicle vs 2.00 ± 0.22% for PGE2, p < 0.05 ), departure velocity (-171.9 ± 22.9 um/sec for vehicle vs -106.3± 12.5 um/sec for PGE2, p < 0.05) and return velocity (87.7 ± 16.3 um/sec for vehicle vs 36.7 ± 6.6 um/sec for PGE2, p < 0.05) with similar effects noted for sulp. Sulp reduced change in peak height (4.79 ± 1.15% for vehicle vs 1.81 ± 0.37% for sulp, p < 0.05), departure velocity (-169.1 ± 35.8 um/sec for vehicle vs -59.4 ± 10.3 um/sec for sulp, p < 0.05) and return velocity (86.5 ± 23.8 um/sec for vehicle vs 16.9 ± 14.7 um/sec for sulp, p < 0.05). We then examined the acute effects of PGE2 and sulp on expression of phosphorylated phospholamban (PLN) and SERCA using Western blot. Treatment of AVM for 15min with either PGE2 or sulp decreased expression of phosphorylated PLN corrected to total PLN, by 67% and 43%. SERCA2a expression was unaffected. In conclusion, PGE2 and sulp reduce contractility via the EP3 receptor through effects on PLN.

Adenosine antagonism decreases metabolic but not functional recovery from ischemia

1991 ◽  
Vol 260 (1) ◽  
pp. H193-H200 ◽  
Author(s):  
D. A. Angello ◽  
J. P. Headrick ◽  
N. M. Coddington ◽  
R. M. Berne
Keyword(s):  
Functional Recovery ◽  
Left Ventricular ◽  
Low Flow ◽  
Ischemia And Reperfusion ◽  
Constant Flow ◽  
Hemodynamic Parameters ◽  
Isolated Hearts ◽  
Rat Hearts ◽  
Adenosine Antagonism ◽  
Developed Pressure

The effect of adenosine receptor antagonism on function and metabolism was examined in isolated hearts during low flow ischemia and reperfusion. Isovolumic rat hearts perfused at constant flow were subjected to 30 min of ischemia followed by 30 min of reperfusion. Infusion of vehicle or 10 microM 8-phenyltheophylline (8-PT) was initiated 10 min before ischemia and maintained throughout reperfusion. 8-PT infusion had no significant effects on hemodynamic parameters or metabolism preischemia. During ischemia, left ventricular developed pressure declined to approximately 15% of preischemic values in control and 8-PT hearts, and ATP and PCr decreased to approximately 73 and 60% of preischemic values. Inorganic phosphate (Pi) increased to 353 = 41 and 424 +/- 53% of preischemic values in control and 8-PT hearts, respectively. After reperfusion, function recovered to greater than 95% of preischemic levels in control and 8-PT hearts. Unlike control hearts, recovery of metabolites was significantly different during reperfusion in 8-PT hearts (P less than 0.05); ATP, phosphocreatine, and Pi recovered to 82 +/- 8, 71 +/- 8, and 281 +/- 27% of preischemic values, respectively. Venous purine washout was significantly greater (P less than 0.05) during reperfusion in 8-PT hearts (327 +/- 113 nmol) than in control hearts (127 +/- 28 nmol). Blockade of adenosine receptors appears to adversely affect metabolic but not functional recovery in the ischemic-reperfused myocardium.

Modulation of mouse cardiac function in vivo by eNOS and ANP

2000 ◽  
Vol 278 (3) ◽  
pp. H971-H981 ◽  
Author(s):  
Robert Gyurko ◽  
Peter Kuhlencordt ◽  
Mark C. Fishman ◽  
Paul L. Huang
Keyword(s):  
Cardiac Function ◽  
Isolated Heart ◽  
Cardiac Contractility ◽  
Enos Gene ◽  
Wild Type ◽  
Adrenergic Stimulation ◽  
Microvascular Endothelium ◽  
Ventricular Relaxation ◽  
Nos Inhibitors

To study the role of endothelial nitric oxide synthase (eNOS) in cardiac function, we compared eNOS expression, contractility, and relaxation in the left ventricles of wild-type and eNOS-deficient mice. eNOS immunostaining is localized to the macro- and microvascular endothelium throughout the myocardium in wild-type mice and is absent in eNOS−/− mice. Whereas blood pressure is elevated in eNOS−/− mice, baseline cardiac contractility (dP/d t max) is similar in wild-type and eNOS−/− mice (9,673 ± 2,447 and 9,928 ± 1,566 mmHg/s, respectively). The β-adrenergic agonist isoproterenol (Iso) at doses of ≥1 ng causes enhanced increases in dP/d t max in eNOS−/− mice compared with wild-type controls in vivo ( P < 0.01) as well as in Langendorff isolated heart preparations ( P < 0.02). β-Adrenergic receptor binding (Bmax) is not significantly different in the two groups of animals (Bmax = 41.4 ± 9.4 and 36.1 ± 5.1 fmol/mg for wild-type and eNOS−/−). Iso-stimulated ventricular relaxation is also enhanced in the eNOS−/− mice, as measured by dP/d t min in the isolated heart. However, baseline ventricular relaxation is normal in eNOS−/− mice (τ = 5.2 ± 1.0 and 5.6 ± 1.5 ms for wild-type and eNOS−/−, respectively), whereas it is impaired in wild-type mice after NOS inhibition (τ = 8.3 ± 2.4 ms). cGMP levels in the left ventricle are unaffected by eNOS gene deletion (wild-type: 3.1 ± 0.8 pmol/mg, eNOS−/−: 3.1 ± 0.6 pmol/mg), leading us to examine the level of another physiological regulator of cGMP. Atrial natriuretic peptide (ANP) expression is markedly upregulated in the eNOS−/− mice, and exogenous ANP restores ventricular relaxation in wild-type mice treated with NOS inhibitors. These results suggest that eNOS attenuates both inotropic and lusitropic responses to β-adrenergic stimulation, and it also appears to regulate baseline ventricular relaxation in conjunction with ANP.

scholarly journals P784 Cardiac remodelling in elite rowers - insights from novel echocardiographic techniques

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
G Kleinnibbelink ◽  
N M Panhuyzen-Goedkoop ◽  
H G Hulshof ◽  
A P J Van Dijk ◽  
K P George ◽  
...  
Keyword(s):  
Exercise Training ◽  
Elite Athlete ◽  
Left Ventricular ◽  
Cardiac Remodelling ◽  
Physiological Adaptation ◽  
Training Volume ◽  
Short Term ◽  
Apical Rotation ◽  
Elite Rowers ◽  
The Impact

Abstract Funding Acknowledgements No financial support Background Chronic exercise training leads to cardiac remodelling; the so-called Athlete’s Heart. Previous studies are often limited by a cross-sectional design whilst longitudinal training studies are often constrained to the assessment of non-athletes. Echocardiography provides comprehensive assessment of mechanics and may give additional insight into short-term changes in training volume in the elite athlete. Purpose To examine the impact of a short-term (9 months) increase in training volume on cardiac structure and mechanics in elite international competing rowers. Methods As part of the work-up to the 2012 Olympic Games, twenty-seven elite rowers (26.4 ± 3.7 years, 19 male) underwent baseline echocardiography prior to and post (9-months) a planned increase in training volume. Conventional echocardiographic indices including mechanics of all cardiac chambers were assessed. Results In response to increased training volume, there was a significant increase in left ventricular (LV) size (IVSd 9.2 ± 1.2 to 9.7 ± 1.1 mm, p = 0.001; PWd 8.3 ± 1.3 to 8.7 ± 1.4 mm, p = 0.013), LVIDd (56.5 ± 4.6 to 57.9 ± 4.2 mm, p = 0.001), and LVMi (90.2 ± 17.8 to 100.8 ± 17.1 g/m2, p = 0.000), see table. There was a significant increase in LV twist (9.2 ± 4.5 to 11.2 ± 4.7 °, p = 0.04; basal rotation -4.4 ± 3.1 to -4.5 ± 3.4 °, p = 0.84; apical rotation 5.8 ± 3.4 to 7.1 ± 3.7 °, p = 0.011), see figure, however, there were no changes in any other conventional indices of function or any other cardiac mechanics. There was a significant increase in left atrial (LA) volume (58.8 ± 15.2 to 65.3 ± 17.6 mm, p = 0.01) whilst no changes were observed in right heart structure. Conclusion An increase in exercise training volume in elite rowers across 9-months induced mild balanced structural remodelling of the LV and LA with a concomitant increase in LV twist. Contradictory to findings in non-athletes, there was no increase in right ventricular or atrial structure or function which may be representative of the elite athlete status and possibly already at threshold for physiological adaptation. Abstract P784 Figure.

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