Increased cholinergic activity under conditions of low estrogen leads to adverse cardiac remodeling

2020 ◽  
Author(s):  
Vanessa P. Teixeira ◽  
Kiany Miranda ◽  
Sergio Scalzo ◽  
Cibele Rocha-Resende ◽  
Mário Morais Silva ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Postmenopausal Women ◽  
Ventricular Myocytes ◽  
Left Ventricular ◽  
Genetically Engineered ◽  
Cardiac Response ◽  
Cholinesterase Inhibition ◽  
Functional Changes ◽  
Concentric Hypertrophy ◽  
The Impact

Cholinesterase inhibitors are used in postmenopausal women for the treatment of neurodegenerative diseases. Despite their widespread use in the clinical practice, little is known about the impact of augmented cholinergic signaling on cardiac function under reduced estrogen conditions. To address this gap, we subjected a genetically engineered murine model of systemic vesicular acetylcholine transporter overexpression (Chat-ChR2) to ovariectomy and evaluated cardiac parameters. Left-ventricular function was similar between Chat-ChR2 and wild-type (WT) mice. Following ovariectomy, WT mice showed signs of cardiac hypertrophy. Conversely, ovariectomized (OVX) Chat-ChR2 mice evolved to cardiac dilation and failure. Transcript levels for cardiac stress markers ANP and BNP were similarly upregulated in WT/OVX and Chat-ChR2/OVX mice. 17β-Estradiol (E2) treatment normalized cardiac parameters in Chat-ChR2/OVX to the Chat-ChR2/SHAM levels, providing a link between E2 status and the aggravated cardiac response in this model. To investigate the cellular basis underlying the cardiac alterations, ventricular myocytes were isolated and their cellular area and contractility were assessed. Myocytes from WT/OVX mice were wider than WT/SHAM, an indicative of concentric hypertrophy, but their fractional shortening was similar. Conversely, Chat-ChR2/OVX myocytes were elongated, and presented contractile dysfunction. E2 treatment again prevented the structural and functional changes in Chat-ChR2/OVX myocytes. We conclude that hypercholinergic mice under reduced estrogen conditions do not develop concentric hypertrophy, a critical compensatory adaptation, evolving towards cardiac dilation and failure. This study emphasizes the importance of understanding the consequences of cholinesterase inhibition, used clinically to treat dementia, for cardiac function in postmenopausal women.

Cardiac response to doxorubicin and dexrazoxane in intact and ovariectomized young female rats at rest and after swim training

2012 ◽  
Vol 302 (10) ◽  
pp. H2048-H2057 ◽  
Author(s):  
Annie Calvé ◽  
Rami Haddad ◽  
Sarah-Neiel Barama ◽  
Melissa Meilleur ◽  
Igal A. Sebag ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Adult Survivors ◽  
Young Female ◽  
Cardiac Response ◽  
Female Rats ◽  
Cancer Therapies ◽  
Sprague Dawley ◽  
Cardiac Damage ◽  
Ovx Rats ◽  
The Impact

The impact of cancer therapies on adult cardiac function is becoming a concern as more children survive their initial cancer. Cardiovascular disease is now a significant problem to adult survivors of childhood cancer. Specifically, doxorubicin (DOX) may be particularly harmful in young girls. The objective of this study was to characterize DOX damage and determine the ability of dexrazoxane (DEX) to reduce DOX-mediated cardiac damage in sedentary and swim-trained female rats. Female Sprague-Dawley rats were left intact or ovariectomized (OVX) at weaning then injected with DEX (60 mg/kg) before DOX (3 mg/kg), DOX alone, or PBS. Rats were separated into sedentary and swim cohorts. Body weight was reduced in DOX:DEX- but not PBS- or DOX-treated rats. Echocardiographic parameters were similar in sedentary rats. Swim training revealed greater concentric remodeling in DOX-treated rats and reduced fractional shortening in DOX:DEX-treated rats. Calsequestrin 2 was reduced with DOX and increased with DOX:DEX postswim. Sarco(endo)plasmic reticulum Ca2+-ATPase 2a was reduced and calsequestrin 2 reduced further by swim training only in intact rats. OVX rats were heavier and developed eccentric remodeling post-swim with DOX and eccentric hypertrophy with DOX:DEX. Changes in SERCA2a and calsequestrin 2 expression were not observed. Ovariectomized DOX- and DOX:DEX-treated rats stopped growing during swim training. DEX coinjection did not relieve DOX-mediated cardiotoxicity in intact or hormone-deficient rats. DOX-mediated reductions in growth, cardiac function, and expression of calcium homeostasis proteins were exacerbated by swim. DEX coadministration did not substantially relieve DOX-mediated cardiotoxicity in young female rats. Ovarian hormones reduce DOX-induced cardiotoxicity.

scholarly journals Cardiac and Pulmonary Vascular Remodeling in Endurance Open Water Swimmers Assessed by Cardiac Magnetic Resonance: Impact of Sex and Sport Discipline

2021 ◽  
Vol 8 ◽  
Author(s):  
Vanessa Martínez ◽  
María Sanz-de la Garza ◽  
Blanca Domenech-Ximenos ◽  
César Fernández ◽  
Ana García-Alvarez ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Pulmonary Artery ◽  
Open Water ◽  
Left Ventricular ◽  
Endurance Athletes ◽  
Cardiac Response ◽  
Pulmonary Vasculature ◽  
Exercise Induced ◽  
Pulmonary Remodeling ◽  
The Impact

Background: The cardiac response to endurance exercise has been studied previously, and recent reports have described the extension of this remodeling to the pulmonary vasculature. However, these reports have focused primarily on land-based sports and few data are available on exercise-induced cardio-pulmonary adaptation in swimming. Nor has the impact of sex on this exercise-induced cardio-pulmonary remodeling been studied in depth. The main aim of our study was to evaluate cardiac and pulmonary circulation remodeling in endurance swimmers. Among the secondary objectives, we evaluate the impact of sex and endurance sport discipline on this cardio-pulmonary remodeling promoted by exercise training.Methods:Resting cardiovascular magnetic resonance imaging was performed in 30 healthy well-trained endurance swimmers (83.3% male) and in 19 terrestrial endurance athletes (79% male) to assess biventricular dimensions and function. Pulmonary artery dimensions and flow as well as estimates of pulmonary vascular resistance (PVR) were also evaluated.Results:In relation to the reference parameters for the non-athletic population, male endurance swimmers had larger biventricular and pulmonary artery size (7.4 ± 1.0 vs. 5.9 ± 1.1 cm2, p < 0.001) with lower biventricular ejection fraction (EF) (left ventricular (LV) EF: 58 ± 4.4 vs. 67 ± 4.5 %, p < 0.001; right ventricular (RV) EF: 60 ± 4 vs. 66 ± 6 %, p < 0.001), LV end-diastolic volume (EDV): 106 ± 11 vs. 80 ± 9 ml/m2, p < 0.001; RV EDV: 101 ± 14 vs. 83 ± 12 ml/m2, p < 0.001). Significantly larger LV volume and lower LV EF were also observed in female swimmers (LV EF: 60 ± 5.3 vs. 67 ± 4.6 %, p = 0.003; LV EDV: 90 ± 17.6 vs. 75± 8.7 ml/m2, p = 0.002). Compared to terrestrial endurance athletes, swimmers showed increased LV indexed mass (75.0 ± 12.8 vs. 61.5 ± 10.0 g/m2, p < 0.001). The two groups of endurance athletes had similar pulmonary artery remodeling.Conclusions: Cardiac response to endurance swimming training implies an adaptation of both ventricular and pulmonary vasculature, as in the case of terrestrial endurance athletes. Cardio-pulmonary remodeling seems to be less extensive in female than in male swimmers.

Targeted inactivation of Gαi does not alter cardiac function or β-adrenergic sensitivity

2001 ◽  
Vol 280 (2) ◽  
pp. H569-H575 ◽  
Author(s):  
Mohit Jain ◽  
Chee Chew Lim ◽  
Kohzo Nagata ◽  
Vannessa M. Davis ◽  
David S. Milstone ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Ventricular Myocytes ◽  
Ex Vivo ◽  
Cardiac Response ◽  
Similar Degree ◽  
Wild Type ◽  
Isolated Hearts ◽  
Targeted Inactivation ◽  
Contractile Performance

Inhibitory Gαi protein increases in the myocardium during hypertrophy and has been associated with β-adrenergic receptor (β-AR) desensitization, contractile dysfunction, and progression of cardiac disease. The role of Gαi proteins in mediating basal cardiac function and β-AR response in nonpathological myocardium, however, is uncertain. Transgenic mice with targeted inactivation of Gαi2 or Gαi3 were examined for in vivo cardiac function with the use of conscious echocardiography and for ex vivo cardiac response to inotropic stimulation with the use of Langendorff blood-perfused isolated hearts and adult ventricular cardiomyocytes. Echocardiography revealed that percent fractional shortening and heart rate were similar among wild-type, Gαi2 -null, and Gαi3 -null mice. Comparable baseline diastolic and contractile performance was also observed in isolated hearts and isolated ventricular myocytes from wild-type mice and mice lacking Gαi proteins. Isoproterenol infusion enhanced diastolic and contractile performance to a similar degree in wild-type, Gαi2 -null, and Gαi3 -null mice. These data demonstrate no observable role for inhibitory G proteins in mediating basal cardiac function or sensitivity to β-AR stimulation in nonpathological myocardium.

The impact of endurance exercise training on left ventricular systolic mechanics

2008 ◽  
Vol 295 (3) ◽  
pp. H1109-H1116 ◽  
Author(s):  
Aaron L. Baggish ◽  
Kibar Yared ◽  
Francis Wang ◽  
Rory B. Weiner ◽  
Adolph M. Hutter ◽  
...  
Keyword(s):  
Exercise Training ◽  
Ejection Fraction ◽  
Endurance Exercise ◽  
Systolic Function ◽  
Radial Strain ◽  
Left Ventricular ◽  
Functional Changes ◽  
Endurance Exercise Training ◽  
Lv Systolic Function ◽  
The Impact

Although exercise training-induced changes in left ventricular (LV) structure are well characterized, adaptive functional changes are incompletely understood. Detailed echocardiographic assessment of LV systolic function was performed on 20 competitive rowers (10 males and 10 females) before and after endurance exercise training (EET; 90 days, 10.7 ± 1.1 h/wk). Structural changes included LV dilation (end-diastolic volume = 128 ± 25 vs. 144 ± 28 ml, P < 0.001), right ventricular (RV) dilation (end-diastolic area = 2,850 ± 550 vs. 3,260 ± 530 mm2, P < 0.001), and LV hypertrophy (mass = 227 ± 51 vs. 256 ± 56 g, P < 0.001). Although LV ejection fraction was unchanged (62 ± 3% vs. 60 ± 3%, P = not significant), all direct measures of LV systolic function were altered. Peak systolic tissue velocities increased significantly (basal lateral S′Δ = 0.9 ± 0.6 cm/s, P = 0.004; and basal septal S′Δ = 0.8 ± 0.4 cm/s, P = 0.008). Radial strain increased similarly in all segments, whereas longitudinal strain increased with a base-to-apex gradient. In contrast, circumferential strain (CS) increased in the LV free wall but decreased in regions adjacent to the RV. Reductions in septal CS correlated strongly with changes in RV structure (ΔRV end-diastolic area vs. ΔLV septal CS; r2 = 0.898, P < 0.001) and function (Δpeak RV systolic velocity vs. ΔLV septal CS, r2 = 0.697, P < 0.001). EET leads to significant changes in LV systolic function with regional heterogeneity that may be secondary to concomitant RV adaptation. These changes are not detected by conventional measurements such as ejection fraction.

Cardiac response to pressure overload in 129S1/SvImJ and C57BL/6J mice: temporal- and background-dependent development of concentric left ventricular hypertrophy

2007 ◽  
Vol 292 (5) ◽  
pp. H2119-H2130 ◽  
Author(s):  
Cordelia J. Barrick ◽  
Mauricio Rojas ◽  
Robert Schoonhoven ◽  
Susan S. Smyth ◽  
David W. Threadgill
Keyword(s):  
Heart Failure ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Cardiac Response ◽  
Dependent Manner ◽  
Geometric Patterns ◽  
Concentric Hypertrophy ◽  
Eccentric Hypertrophy

Left ventricular hypertrophy (LVH), a risk factor for cardiovascular morbidity and mortality, is commonly caused by essential hypertension. Three geometric patterns of LVH can be induced by hypertension: concentric remodeling, concentric hypertrophy, and eccentric hypertrophy. Clinical studies suggest that different underlying etiologies, genetic modifiers, and risk of mortality are associated with LVH geometric patterns. Since pressure overload-induced LVH can be modeled experimentally using transverse aortic constriction (TAC) and since C57BL/6J (B6) and 129S1/SvImJ (129S1) strains, which have different baseline cardiovascular phenotypes, are commonly used, we conducted serial echocardiographic studies to assess cardiac function up to 8 wk of post-TAC in male B6, 129S1, and B6129F1 (F1) mice. B6 mice had an earlier onset and more pronounced impairment in contractile function, with corresponding left and right ventricular dilatation, fibrosis, change in expression of hypertrophy marker, and increased liver weights at 5 wk of post-TAC. These observations suggest that B6 mice had eccentric hypertrophy with systolic dysfunction and right-sided heart failure. In contrast, we found that 129S1 and F1 mice delayed transition to decompensated heart failure, with 129S1 mice exhibiting preserved systolic function until 8 wk of post-TAC and relatively mild alterations in histology and markers of hypertrophy at 5 wk post-TAC. Consistent with concentric hypertrophy, our results show that these strains manifest different cardiac responses to pressure overload in a time-dependent manner and that genetic susceptibility to initial concentric hypertrophy is dominant to eccentric hypertrophy. These results also imply that genetic background differences can complicate interpretation of TAC studies when using mixed genetic backgrounds.

scholarly journals Breast Cancer Promotes Cardiac Dysfunction Through Deregulation of Cardiomyocyte Ca 2+ ‐Handling Protein Expression That is Not Reversed by Exercise Training

2021 ◽  
Vol 10 (5) ◽  
Author(s):  
Tassia S. R. da Costa ◽  
Ursula Urias ◽  
Marcelo V. Negrao ◽  
Camila P. Jordão ◽  
Clévia S. Passos ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Exercise Training ◽  
Cardiac Function ◽  
Protein Expression ◽  
Exercise Capacity ◽  
Tolerance Test ◽  
Left Ventricular ◽  
T Antigen ◽  
Significant Difference ◽  
The Impact

Background Patients treated for breast cancer have a high incidence of cardiovascular complications. In this study, we evaluated the impact of breast cancer on cardiac function and cardiomyocyte Ca 2+ ‐handling protein expression. We also investigated whether exercise training (ET) would prevent these potential alterations. Methods and Results Transgenic mice with spontaneous breast cancer (mouse mammary tumor virus–polyomavirus middle T antigen [MMTV‐PyMT+], n=15) and littermate mice with no cancer (MMTV‐PyMT−, n=14) were studied. For the ET analysis, MMTV‐PyMT+ were divided into sedentary (n=10) and exercise‐trained (n=12) groups. Cardiac function was evaluated by echocardiography with speckle‐tracking imaging. Exercise tolerance test was conducted on a treadmill. Both studies were performed when the tumor became palpable and when it reached 1 cm 3 . After euthanasia, Ca 2+ ‐handling protein expression (Western blot) was evaluated. Exercise capacity was reduced in MMTV‐PyMT+ compared with MMTV‐PyMT− ( P interaction =0.031). Longitudinal strain ( P group <0.001) and strain rate ( P group =0.030) were impaired. Cardiomyocyte phospholamban was increased ( P =0.011), whereas phospho‐phospholamban and sodium/calcium exchanger were decreased ( P =0.038 and P =0.017, respectively) in MMTV‐PyMT+. No significant difference in sarcoplasmic or endoplasmic reticulum calcium 2 ATPase (SERCA2a) was found. SERCA2a/phospholamban ratio was reduced ( P =0.007). ET was not associated with increased exercise capacity. ET decreased left ventricular end‐systolic diameter ( P group =0.038) and end‐diastolic volume ( P group =0.026). Other morphological and functional cardiac parameters were not improved by ET in MMTV‐PyMT+. ET did not improve cardiomyocyte Ca 2+ ‐handling protein expression. Conclusions Breast cancer is associated with decreased exercise capacity and subclinical left ventricular dysfunction in MMTV‐PyMT+, which is at least partly associated with dysregulation of cardiomyocyte Ca 2+ handling. ET did not prevent or reverse these changes.

Abstract 519: Talin is Required for Normal Adult Heart Function

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Yoshitake Cho ◽  
Ruixia Li ◽  
Ana M Manso ◽  
Robert S Ross
Keyword(s):  
Heart Failure ◽  
Cardiac Function ◽  
Cardiac Dysfunction ◽  
Cardiac Development ◽  
Heart Function ◽  
Left Ventricular ◽  
Mass Spectrometry Analysis ◽  
Adult Heart ◽  
Spectrometry Analysis ◽  
Functional Changes

Talin (Tln) is a component of muscle costameres that links integrins to other components of the cellular cytoskeleton and plays an important role in maintaining the cellular integrity of cardiac myocytes (CM). There are two talin genes, Tln1 and Tln2, expressed in the heart. Tln1 is ubiquitously expressed, and Tln2 is dominantly expressed in CM. In our previous study, we show that the global deletion of Tln2 in mice (T2KO) caused no structural or functional changes in the heart, presumably because CM Tln1 became up-regulated. However, we found that mice lacking both CM Tln1 and Tln2 exhibit cardiac dysfunction by 4 weeks (w) of age with 100% mortality by 6 months (m), showing Tln plays an essential role in cardiac development and in maintaining cardiac function. In this study, we produced a tamoxifen (Tamo)-inducible mouse model in which Tln1 could be explicitly reduced in the adult CM (T1icKO), and then generate T1icKO:T2KO (T1/2dKO), so that the function of Tln could be assessed in the postnatal heart. T2KO and Tln1/2dKO mice were injected with Tamo at 8w. Echocardiograms were performed to evaluate cardiac function up to 8w post-Tamo injection. While T2KO mice showed normal cardiac function, T1/2dKO exhibited a gradual decrease in function post-Tamo injection. At 8w post-Tamo injection, T1/2dKO mice showed cardiac hypertrophy, fibrosis, and heart failure. To understand the mechanism by which deletion CM talin leads to cardiac dysfunction, left ventricular tissue protein lysates from T2KO and T1/2dKO mice at 4w post-Tamo when cardiac function (echo) and structure were preserved in dKO. The protein lysates were subjected to quantitative mass spectrometry analysis. We found there are 1,100 proteins differentially expressed in T2KO and T1/2dKO hearts. Pathway analysis was performed, and the results showed that proteins involved in vesicle transport, protein folding, and innate immunity are most up-regulated in the T1/2dKO heart. Taken together, our results show that Tln is required for maintaining proper cardiac function in the adult heart. The deletion of Tln in CM results in the up-regulation of multiple intracellular pathways, and we are currently studying the role of each pathway in the pathogenesis of heart failure induced by CM Tln deletion.

scholarly journals Left ventricular volume analysis as a basic tool to describe cardiac function

2018 ◽  
Vol 42 (1) ◽  
pp. 130-139 ◽  
Author(s):  
Peter L. M. Kerkhof ◽  
Tatiana Kuznetsova ◽  
Rania Ali ◽  
Neal Handly
Keyword(s):  
Cardiac Function ◽  
Volume Regulation ◽  
Function Analysis ◽  
Group Analysis ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Ventricular Performance ◽  
Healthy Humans ◽  
End Diastolic Volume ◽  
The Impact

The heart is often regarded as a compression pump. Therefore, determination of pressure and volume is essential for cardiac function analysis. Traditionally, ventricular performance was described in terms of the Starling curve, i.e., output related to input. This view is based on two variables (namely, stroke volume and end-diastolic volume), often studied in the isolated (i.e., denervated) heart, and has dominated the interpretation of cardiac mechanics over the last century. The ratio of the prevailing coordinates within that paradigm is termed ejection fraction (EF), which is the popular metric routinely used in the clinic. Here we present an insightful alternative approach while describing volume regulation by relating end-systolic volume (ESV) to end-diastolic volume. This route obviates the undesired use of metrics derived from differences or ratios, as employed in previous models. We illustrate basic principles concerning ventricular volume regulation by data obtained from intact animal experiments and collected in healthy humans. Special attention is given to sex-specific differences. The method can be applied to the dynamics of a single heart and to an ensemble of individuals. Group analysis allows for stratification regarding sex, age, medication, and additional clinically relevant covariates. A straightforward procedure derives the relationship between EF and ESV and describes myocardial oxygen consumption in terms of ESV. This representation enhances insight and reduces the impact of the metric EF, in favor of the end-systolic elastance concept advanced 4 decades ago.

scholarly journals Impact of Diabetes on Cardiac Function in Patients with High Blood Pressure

2021 ◽  
Vol 18 (12) ◽  
pp. 6553
Author(s):  
Nabila Soufi Taleb Bendiab ◽  
Souhila Ouabdesselam ◽  
Latefa Henaoui ◽  
Marilucy Lopez-Sublet ◽  
Jean-Jacques Monsuez ◽  
...  
Keyword(s):  
Blood Pressure ◽  
High Blood Pressure ◽  
Global Longitudinal Strain ◽  
Left Ventricular ◽  
Left Ventricular Geometry ◽  
Lv Function ◽  
Hypertensive Patients ◽  
Concentric Hypertrophy ◽  
Lv Dysfunction ◽  
The Impact

Background: Although the combination of high blood pressure (HBP) and type 2 diabetes (T2DM) increases the risk of left ventricular (LV) dysfunction, the impact of T2DM on LV geometry and subclinical dysfunction in hypertensive patients and normal ejection fraction (EF) has been infrequently evaluated. Methods: Hypertensive patients with or without T2DM underwent cardiac echocardiography coupled with LV global longitudinal strain (GLS) assessment. Results: Among 200 patients with HBP (mean age 61.7 ± 9.7 years) and EF > 55%, 93 had associated T2DM. Patients with T2DM had a higher body mass index (29.9 ± 5.1 kg/m2 vs. 29.3 ± 4.7 kg/m2, p = 0.025), higher BP levels (158 ± 23/95 ± 13 vs. 142 ± 33/87 ± 12 mmHg, p = 0.003), a higher LV mass index (115.8 ± 32.4 vs. 112.0 ± 24.7 g/m2, p = 0.004), and higher relative wall thickness (0.51 ± 0.16 vs. 0.46 ± 0.12, p = 0.0001). They had more frequently concentric remodeling (20.4% vs. 16.8%, p < 0.001), concentric hypertrophy (53.7% vs. 48.6%, p < 0.001), elevated filling pressures (25.8 vs. 12.1%, p = 0.0001), indexed left atrial volumes greater than 28 mL/m2 (17.2 vs. 11.2%, p = 0.001), and a reduced GLS less than −18% (74.2 vs. 47.7%, p < 0.0001). After adjustment for BP and BMI, T2DM remains an independent determinant factor for GLS decline (OR = 2.26, 95% CI 1.11–4.61, p = 0.023). Conclusions: Left ventricular geometry and subclinical LV function as assessed with GLS are more impaired in hypertensive patients with than without T2DM. Preventive approaches to control BMI and risk of T2DM in hypertensive patients should be emphasized.

Endurance training in the rat. II. Performance of isolated and intact heart

1981 ◽  
Vol 51 (4) ◽  
pp. 941-947 ◽  
Author(s):  
E. O. Fuller ◽  
D. O. Nutter
Keyword(s):  
Cardiac Function ◽  
Endurance Training ◽  
Ventricular Function ◽  
Left Ventricular ◽  
Treadmill Running ◽  
Cardiac Response ◽  
Male Rats ◽  
Isolated Perfused Heart ◽  
Perfused Heart

The effects of isotonic physical training and detraining on cardiac function were studied in young and adult male rats trained by graded treadmill running and compared with sedentary controls. Absolute left ventricular mass was not increased, and ventricular compliance was not altered by training. Ventricular function curves that plotted peak systolic pressure, maximum rate of rise of left ventricular pressure, cardiac output, coronary flow, or stroke work as a function of atrial filling height in the isolated perfused heart did not demonstrate a training effect in either age group. The cardiac response to hypoxia was also comparable in the trained and sedentary rats. The base-line heart rate of anesthetized rats, in which in situ cardiac function was studied, was lower in the trained rats (321 +/- 14 vs. 377 +/- 8, P less than 0.005). Resting hemodynamics and left ventricular function curves generated from pressure-flow data during volume infusion did not differentiate between the hearts of trained and sedentary rats. In conclusion, a moderate level of endurance training did not enhance cardiac contractility when this was assessed under nonexercise conditions in both the isolated perfused heart and intact in situ heart preparations.

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