Echocardiographic variables in healthy guineapigs anaesthetized with ketamine-xylazine

Echocardiographic parameters were recorded, measured and statistically analysed on a population of 12 male Hartley albino guineapigs under ketamine-xylazine anaesthesia. Additionally, the effect of body weight on these parameters and the correlation between the parameters were assessed. The mean values of left ventricular internal diameter in end diastole (LVIDD), left ventricular internal diameter in end systole (LVIDS), interventricular septum thickness in diastole (IVSD), interventricular septum thickness in systole (IVSS), left ventricular posterior wall thickness in diastole (LVPWD), left ventricular posterior wall thickness in systole (LVPWS), left atrial diameter (LA), aortic diameter (AO), left ventricular fractional shortening (FS) and left ventricular ejection fraction (EF) were measured or calculated as 6.85+/-0.36, 4.35+/-0.17, 1.75+/-0.31, 2.26+/-0.35, 2.28+/-0.40, 2.80+/-0.58, 4.95+/-0.34, 4.65+/-0.25 mm, 35.62+/-2.62 and 70.87+/-3.01%, respectively. A significant (P<0.01) positive correlation to body weight was found with LVIDD, LVPWD, IVSD, aortic root diameter and LA. Significant correlation was also found between a number of echocardiographic parameters.     

Morphological and functional differences in cardiac parameters between power and endurance athletes: a magnetic resonance imaging study

The present study compared morphological and functional parameters of the left ventricle by magnetic resonance imaging (MRI) in competitive athletes engaged in endurance and power activities and sedentary control subjects. Twenty male subjects, 7 endurance-trained athletes (ETA) (age 23.8+/-3.5 yr), 7 strength-trained athletes (STA) (age 22.8+/-4.0 yr), and 6 sedentary controls (age 24.1+/-2.2 yr) were studied by MRI. In the ETA group body size related left ventricular mass (rel.LVM) was significantly higher than that in the STA group (71.0+/-9.2 vs 57.4+/-15.7 g/m3). The difference between their size related left ventricular wall thickness (rel.LVWT) values (9.37+/-1.0 vs 8.37+/-1.8 mm/m) was near to the level of significance (p=0.057). Relative left ventricular internal diameter (rel.LVID) was significantly higher in the ETA group compared to the STA group (42.3+/-1.0 vs 40.1+/-2.5 mm/m, p<0.05). The muscular quotient (MQ=LVWT/LVID) of the ETA group was not significantly higher compared to the strength athletes. Relative left ventricular end-diastolic volume (LVEDV) was also higher in the ETA group than in the STA group (69.5+/-6.7 vs 59.9+/-8.2 ml/m3, p<0.05) and the controls (53.6+/-3.7, p<0.001). Significantly higher relative stroke volume (SV) was measured in the ETA group compared to the STA group and the controls (41.0+/-5.7; 32.6+/-6.9; 32.0+/-3.2 ml/m3). According to the present data, the strongest impact on LV cavity size and wall thickness is caused by long-term high intensity endurance training. Intense strength training does not necessarily induce wall thickening.     

The echocardiographic study of the rabbit heart left ventricle morpho-functional parameters

Morphometric and functional parameters of the heart left ventricle in rabbits during systole and diastole were investigated by the method of echocardiography. Morphometric parameters were studied on three levels: the mitral valve, the papillary muscles and the apical level. The internal dimension of the left ventricle uniformly decreases in three parallel planes during systole, its maximal reduction being observed on the apical level. During the contraction phase, the posterior wall thickness of the left ventricular and the interventricular septum thickness increases on the basal level to a greater extent than on the apical one. During systole, the interventricular septum movement is greater than the left ventricular posterior wall motion. During the heart cycle, the form of the left ventricular cavity changes from an ellipsoid in diastole to elliptic paraboloid in systole.     

Experimental cardiac tamponade: correlation of pressure, flow velocity, and echocardiographic changes

Seven episodes of experimental cardiac tamponade were induced in five anesthetized closed-chest dogs. Simultaneous pericardial and intracavitary pressures were synchronized with superior vena caval and transvalvular pulsed-Doppler flow tracings. The earliest indication of tamponade was the development of a negative transmural right atrial pressure that occurred during early ventricular diastole and was associated with echocardiographic evidence of right atrial collapse. This was also associated with reversal of diastolic flow in the superior vena cava and with diminished early diastolic flow velocity across the tricuspid as well as the mitral valve. During more advanced cardiac tamponade, the transmural right atrial pressure became negative during both early and late ventricular diastole as well as during isovolumic ventricular systole. This was associated with a disappearance of early diastolic ventricular filling and right ventricular diastolic collapse as observed on two-dimensional echocardiography. In hypotensive cardiac tamponade (cardiac output diminished by 70%), the decreased transmural right atrial pressure that developed during ventricular systole was accompanied by diminished antegrade flow in the superior vena cava. In advanced and hypotensive tamponade, ventricular filling occurred mainly during atrial contraction.     

Effect of endurance training on cardiac morphology in Alaskan sled dogs

The cardiac morphology of 77 consciousAlaskan sled dogs before and after 5 mo of endurance training (20 km/day team pulling a sled and musher) was studied usingtwo-dimensional and M-mode echocardiography. Subgroups included dogswith at least one season of previous training ("veterans") anddogs undergoing their first season of training ("rookies").Training resulted in a significant (P < 0.05) decrease in resting heart rate (15%) and significant increases in interventricular septal thickness (systole, 15%; diastole, 13%), left ventricular (LV) internal dimension in diastole (LVIDd, 4%), LV free wall thickness in systole (9%) and diastole (LVWd, 9%), and left atrial diameter (5%) in all dogs, but the increase in LVWd was greater in rookies (16%) than in veterans (7%).Training increased end-diastolic volume index (8%), LV mass index(24%), and heart weight index (24%) and decreased the LVIDd-to-LVWd ratio (6%) but did not alter cardiac index. We conclude that increased LV mass attributable to LV dilation and hypertrophy isassociated with endurance training in Alaskan sled dogs.Disproportionate LV wall thickening accompanying LV dilation suggeststhat cardiac morphological changes are due to volume and pressureloading. These training-induced changes are similar to those documented in human athletes undergoing combined isometric and isotonic training and differ from studies of dogs trained on treadmills.

     

Concentric adaptation of the left ventricle in response to controlled upper body exercise training.

Upper body exercise has many applications to the rehabilitation and maintenance of cardiovascular health of individuals who are unable to exercise their lower body. The hemodynamic loads of upper body aerobic exercise are characterized by relatively high blood pressure and relatively low venous return. It is not clear how the left ventricle adapts to the specific hemodynamic loads associated with this form of exercise training. The purpose of this study was to measure left ventricular structure and function in previously sedentary men by using echocardiography before and after 12 wk of aerobic arm-crank exercise training (n = 22) or a time control period (n = 22). Arm-crank peak oxygen consumption (in ml x kg(-1) x min(-1)) increased by 16% (P < 0.05) after training, and significant differences (P < 0.05) were found in wall thickness (from 0.86 to 0.99 cm) but not in left ventricular internal dimension in diastole or systole. This suggested a concentric pattern of left ventricular hypertrophy that persisted after scaling to changes in anthropometric characteristics. No differences (P < 0.05) were found for any measurements of resting left ventricular function. We conclude that upper body aerobic exercise training results in a specific left ventricular adaptation that is characterized by increased left ventricular wall thickness but no change in chamber dimension.     

The role of displacement of the mitral annulus in left atrial filling and emptying in the intact dog

The variations in ventricular-atrial mitral annular position during the cardiac cycle and the simultaneous changes in left atrial silhouette area (obtained by angiography after injections of contrast material into the main pulmonary artery) were investigated in six experiments on intact dogs with chronically implanted intracardiac markers. Frame-by-frame measurements of the angiograms (120 frames/s) were used to determine, under various hemodynamic conditions, the duration, magnitude, and average rate of the mitral annular motion and of the simultaneous changes in left atrial area during atrial filling (ventricular systole) and atrial emptying (early in ventricular diastole). The mitral annulus was seen to move towards the ventricular apex during systole and towards the atrium early in diastole with the duration, average rate, and magnitude of displacement (although varying widely) showing good statistical correlations (P less than 0.0005-0.005) with the changes in projected left atrial area. These findings suggest that the duration, rate, and magnitude of atrial filling and emptying may be, in the intact heart, determined by the movements of the atrioventricular junction.     

The arterial circulation of the heart

Blood flows into the aorta and its branches during left ventricular systole. Most of the arterial walls in the body stretch during systole in accordance with their elastic properties (Roston, 1962a, b). During diastole, the rebound of the distended walls supplies an additional propulsive force pushing the blood forward. Since the metabolic exchange between most of the tissues in the body and their blood vessels is ordinarily the same throughout the cardiac cycle, it makes little difference whether or not the blood flow occurs during systole or diastole. The circulation in the coronary arteries behaves in a quite different way. Because the muscle fibers of the heart contract during systole and relax during diastole, different conditions for blood flow and metabolic exchange exist during the phases of the cardiac cycle. As a result, specification of whether blood flows in the coronary arteries during systole or diastole may be important. Such specification complicates the study of the coronary artery circulation. For example, because of the arterial elasticity, some of the blood which enters the coronary arteries during diastole comes in contact with the muscle fibers during systole. The present work contains a theoretical study of the coronary artery circulation.     

Direct and series transmission of left atrial pressure perturbations to the pulmonary artery: a study using wave-intensity analysis

Pressure waves are thought to travel from the left atrium (LA) to the pulmonary artery (PA) only retrogradely, via the vasculature. In seven anesthetized open-chest dogs, a balloon was placed in the LA, which was rapidly inflated and deflated during diastole, early systole, and late systole. High-fidelity pressures were measured within and around the heart. Measurements were made at low volume [LoV; left ventricular end-diastolic pressure (LVEDP) = 5-9 mmHg], high volume (HiV; LVEDP = 16-19 mmHg), and HiV with the pericardium removed. Wave-intensity analysis demonstrated that, except during late systole, balloon inflation created forward-going PA compression waves that were transmitted directly through the heart without measurable delay; backward PA compression waves were transmitted in-series through the pulmonary vasculature and arrived after delays of 90 +/- 3 ms (HiV) and 103 +/- 5 ms (LoV; P < 0.05). Direct transmission was greater during diastole, and both direct and series transmission increased with volume loading. Pressure waves from the LA arrive in the PA by two distinct routes: rapidly and directly through the heart and delayed and in-series through the pulmonary vasculature.     

Regional left ventricular performance during normal and obstructed spontaneous respiration

To clarify the effects of respiration on left ventricular (LV) dimensions and shortening, we studied chronically instrumented dogs with endocardial sonomicrometer crystals in the anterior-posterior (AP), septal to lateral (SL), and long axes (LA) following pericardiectomy. Ten anesthetized dogs were examined during spontaneous unobstructed respiration, partial inspiratory obstruction (PIO), and Mueller maneuvers (MM). During unobstructed inspiration, end-diastolic dimensions (EDD) demonstrated a significant increase in the AP and a similar decrease in the SL axis (i.e., noncongruent shape changes). During PIO only the SL EDD diminished significantly, while no significant changes occurred in any EDD during MM. Individual dogs also demonstrated noncongruent shape changes at end systole during inspiration. However, the end-systolic dimensions for the entire group demonstrated a significant increase in one dimension during each inspiratory mode with no significant changes in the other two axes suggesting an increased ventricular volume. Regional shortening declined only in the SL axis during both unobstructed respiration and PIO. Spontaneous sighs with large tidal volumes, yet smaller changes in pleural pressure than during the MM, were associated with marked noncongruent shape changes in both diastole and systole. We conclude that 1) estimates of LV volumes during respiration based on only one or two axes and assuming regional congruent shape changes may be misleading; and 2) lung volume changes can affect LV geometry independently of changes in pleural pressure.     

Coronary circulatory pressure gradients

The pressure gradients of the canine coronary circulation were measured in 37 dogs during control and following eight interventions: left stellate ganglion or left vagosympathetic trunk stimulation, as well as isoproterenol, acetylcholine, noradrenaline, adenosine, phenylephrine, or adrenaline infusions. During control, pressure gradients in the epicardial coronary arteries (measured from the aorta to coronary artery branch) were 15.2 +/- 1 mmHg (1 mmHg (1 mmHg = 133.32 Pa) during systole and 10.6 +/- 1.5 mmHg during diastole. Adrenaline increased this systolic gradient, while acetylcholine and phenylephrine decreased it. In contrast, the pressure gradients in the small coronary arteries (from the branch of an epicardial artery to the pressure in an obstructed coronary artery) were 56 +/- 1.3 mmHg during systole and 63.7 +/- 1.3 mmHg during diastole. These gradients were increased by phenylephrine during both systole and diastole, noradrenaline and adrenaline during diastole and decreased by isoproterenol (systolic), left vagosympathetic trunk stimulation (diastolic), acetylcholine (systolic and diastolic), and adenosine (diastolic). The microcirculation and small vein gradients during control were 16.4 +/- 1.2 mmHg during systole and 8.5 +/- 0.8 mmHg during diastole. Decreases in this gradient were produced by isoproterenol, acetylcholine, and adenosine during systole and adenosine during diastole. These observations are consistent with the concept that the coronary circulation has considerable regulatory capacity in all of its component parts. Specifically, epicardial arteries appear to function as both conduits and as resistance vessels, small arteries as major resistance vessels, and the microcirculation and small veins as both capacitors and resistors.     

Intramyocardial pressure and coronary extravascular resistance

Intramyocardial pressure is an indicator of coronary extravascular resistance. During systole, pressure in the subendocardium exceeds left ventricular intracavitary pressure; whereas pressure in the subepicardium is lower than left ventricular intracavitary pressure. Conversely, during diastole, subepicardial pressure exceeds both subendocardial pressure and left ventricular pressure. These observations suggest that coronary flow during systole is possible only in the subepicardial layers. During diastolic, however, a greater driving pressure is available for perfusion of the subendocardial layers relative to the subepicardial layers. On this basis, measurements of intramyocardial pressure contribute to an understanding of the mechanisms of regulation of the phasic and transmural distribution of coronary blow flow.     

The influence of body composition, fat distribution, and sustained weight loss on left ventricular mass and geometry in obesity

Alterations in left ventricular mass and geometry vary along with the degree of obesity, but mechanisms underlying such covariation are not clear. In a case–control study, we examined how body composition and fat distribution relate to left ventricular structure and examine how sustained weight loss affects left ventricular mass and geometry. At the 10‐year follow‐up of the Swedish obese subjects (SOS) study cohort, we identified 44 patients with sustained weight losses after bariatric surgery (surgery group) and 44 matched obese control patients who remained weight stable (obese group). We also recruited 44 matched normal weight subjects (lean group). Dual‐energy X‐ray absorptiometry, computed tomography, and echocardiography were performed to evaluate body composition, fat distribution, and left ventricular structure. BMI was 42.5 kg/m², 31.5 kg/m², and 24.4 kg/m² for the obese, surgery, and lean groups, respectively. Corresponding values for left ventricular mass were 201.4 g, 157.7 g, and 133.9 g (P < 0.001). In multivariate analyses, left ventricular diastolic dimension was predicted by lean body mass (β = 0.03, P < 0.001); left ventricular wall thickness by visceral adipose tissue (β = 0.11, P < 0.001) and systolic blood pressure (β = 0.02, P = 0.019); left ventricular mass by lean body mass (β = 1.23, P < 0.001), total body fat (β = 1.15, P < 0.001) and systolic blood pressure (β = 2.72, P = 0.047); and relative wall thickness by visceral adipose tissue (β = 0.02, P < 0.001). Left ventricular adjustment to body size is dependent on body composition and fat distribution, regardless of blood pressure levels. Obesity is associated with concentric left ventricular remodeling and sustained 10‐year weight loss results in lower cavity size, wall thickness and mass.     

Relationship of pulmonary vein flow to left ventricular short-axis epicardial displacement in diastole: model-based prediction with in vivo validation

Previous studies in healthy humans have established that the (approximately 850 ml) volume enclosed by the pericardial sac is nearly constant over the cardiac cycle, exhibiting a transient approximately 5% decrease (approximately 40 ml) from end diastole to end systole. This volume decrease manifests as a "crescent" at the ventricular free wall level when short-axis MRI images of the epicardial surface acquired at end systole and end diastole are superimposed. On the basis of the (near) constant-volume property of the four-chambered heart, the volume decrease ("crescent effect") must be restored during subsequent early diastolic filling via the left atrial conduit volume. Therefore, volume conservation-based modeling predicts that pulmonary venous (PV) Doppler D-wave volume must be causally related to the radial displacement of the epicardium (Delta) (i.e., magnitude of "crescent effect" in the radial direction). We measured Delta from M-mode echocardiographic images and measured D-wave velocity-time integral (VTI) from Doppler PV flow of the right superior PV in 11 subjects with catheterization-determined normal physiology. In accordance with model prediction, high correlation was observed between Delta and D-wave VTI (r=0.86) and early D-wave VTI measured to peak D-wave velocity (r=0.84). Furthermore, selected subjects with various pathological conditions had values of Delta that differed significantly. These observations demonstrate the volume conservation-based causal relationship between radial pericardial displacement of the left ventricle and the PV D-wave-generated filling volume in healthy subjects as well as the potential role of the M-mode echo-derived radial epicardial displacement index Delta as a regional (radial) parameter of diastolic function.     

Echocardiographic evidence of concentric left ventricular enlargement in female weight lifters

In this study we investigated resting left ventricular structure and function in elite female weight-lifters. Fifteen National Squad members [mean age (SD) 25 (6) years] were compared to a recreationally active control group [n = 46, 23 (3) years]. Subjects were matched for body mass, body surface area and fat free mass, but the controls were slightly taller (P<0.01). Athletes and controls demonstrated similar resting heart rates and blood pressures. Septal wall (ST), posterior wall (PWT) and left ventricular internal dimension in diastole and systole (LVIDd and LVIDs, respectively) were measured from M-mode echocardiograms. Calculations were made for left ventricular mass (LVM), mass-volume ratio (m:V), wall-thickness-cavity dimension ratio (h:R) and systolic function. Left ventricular filling velocities were determined via Doppler echocardiography. ST [9.0 (1.1) v.s. 7.7 (1.0) mm] and PWT [8.7 (1.4) v.s. 7.5 (1.3) mm] were greater, whereas LVIDd [46.2 (2.8) v.s. 48.4 (3.4) mm] was smaller in the weight-lifters (P<0.05). After allometrically adjusting for differences in height, the weight-lifters had a greater ST, PWT and LVM (P<0.05) and similar LVIDd. Both m:V and h:R were increased in the weightlifters (P<0.05). All functional data were within normal limits and no group differences were observed. The female weight-lifters demonstrated a concentric left ventricular enlargement that was not detrimental to left ventricular performance at rest.     

Ventricular dimensions measured noninvasively by echocardiography in the awake dog.

A surface echocardiographic technique was employed in 37 mongrel dogs for measurement of left ventricular dimensions. Intracardiac bolus injections of dextran were used as an echo contrast material to visualize cardiac chambers, and the identification of intracardiac structures was further confirmed by postmortem examination. The left ventricle could be satisfactorily visualized from both the right and left chest, providing two transverse left ventricular diameters nearly perpendicular to each other. End-diastolic and end-systolic diameter measurements in the two separate transverse planes differed by an average of only 0.07 and 0.1 cm, respectively, and dimensional measurements were reproducible from day to day. Diastolic diameter ranged from 3.0 to 4.7 cm (mean 3.7 cm) and systolic diameter 1.9 to 3.3 cm (mean 2.6 cm). Diameter was directly related to animal weight. Stroke volume calculated from the dimension measurements correlated with stroke volume calculated from indicator-dilution curves in 16 dogs. Ejection fraction averaged 0.67 and 0.54, depending on the formula used to calculate volumes. These results indicate that surface echocardiography can be employed to evaluate left ventricular dimensions in the awake dog.     

Stress Distribution in the Canine Left Ventricle during Diastole and Systole

A model is proposed for stress analysis of the left ventricular wall (LV wall) based on the realistic assumption that the myocardium is essentially composed of fiber elements which carry only axial tension and vary in orientation through the wall. Stress analysis based on such a model requires an extensive study of muscle fiber orientation and curvature through the myocardium. Accordingly, the principal curvatures were studied at a local site near the equator in ten dog hearts rapidly fixed in situ at end diastole and end systole; the fiber orientation for these hearts had already been established in a previous study. The principal radii of curvature were (a) measured by fitting templates to the endocardial and epicardial wall surfaces in the circumferential and longitudinal directions and (b) computed from measured lengths of semiaxes of ellipsoids of revolution representing the LV wall (“ellipsoid” data). The wall was regarded as a tethered set of nested shells, each having a unique fiber orientation. Results indicate the following. (a) Fiber curvature, k, is maximum at midwall at end systole; this peak shifts towards endocardium at end diastole. (b) The pressure or radial stress through the wall decreases more rapidly near the endocardium than near the epicardium at end diastole and at end systole when a constant tension is assumed for each fiber through the wall. (c) At end diastole the curve for the circumferential stress vs. wall thickness is convex with a maximum at midwall. In the longitudinal direction the stress distribution curve is concave with a minimum at midwall. Similar distributions are obtained at end systole when a constant tension is assumed for each fiber through the wall. (d) The curvature and stress distributions obtained by direct measurements at a selected local site agree well with those computed from “ellipsoid” data.     

Effect of timing and velocity of impact on ventricular myocardial rupture

The effects of impact timing during the cardiac cycle on the sensitivity of the heart to impact-induced rupture was investigated in an open-chest animal model. Direct mechanical impacts were applied to two adjacent sites on the exposed left ventricular surface at the end of systole or diastole. Impacts at 5 m/s and a contact stroke of 5 cm at the end of systole resulted in no cardiac rupture in seven animals, whereas similar impacts at the end of diastole resulted in six cardiac ruptures. Direct impact at 15 m/s and a contact stroke of 2 cm at the end of either systole or diastole resulted in perforationlike cardiac rupture in all attempts. At low-impact velocity the heart was observed in high-speed movie to bounce away from the impact interface during a systolic impact, but deform around the impactor during a diastolic impact. The heart generally remained motionless during the downward impact stroke at high-impact velocity in either a systolic or diastolic impact. The lower ventricular pressure, reduced muscle stiffness, thinner myocardial wall and larger mass of the filled ventricle probably contributed to a greater sensitivity of the heart to rupture in diastole at low-impact velocity. However, the same factors had no role at high-impact velocity.     

Substantial changes in epicardial fat thickness after weight loss in severely obese subjects

We sought to evaluate the effect of weight loss on echocardiographic epicardial fat thickness, as index of visceral adiposity, and whether epicardial fat change after the weight loss can be proportionally different from overall body weight changes and related to cardiac parameters changes in severely obese subjects. This was an interventional study in 20 severely obese subjects (12 women, 8 men, BMI 45+/-5 kg/m(2), 35+/-10 years) who underwent 6-month very low calorie diet weight loss program. Baseline and after 6-month weight loss anthropometrics, echocardiographic epicardial fat thickness, left ventricular mass (LVM), and diastolic function parameters were assessed. Subjects lost 20% of original body weight, BMI reduced by 19% of original BMI, waist circumference decreased by 23% of initial waist circumference. Epicardial fat thickness decreased from 12.3+/-1.8 to 8.3+/-1 mm P<0.001 after the 6-month very low calorie diet, as -32% of baseline epicardial fat thickness. LVM and diastolic function changes were better correlated with epicardial fat changes. We showed that significant weight loss can be associated with significant reduction in the epicardial fat thickness, marker of visceral adiposity in severely obese subjects. Epicardial fat decrease, therefore visceral fat decrease, can be proportionally higher than overall adiposity decrease. Epicardial fat changes are significantly associated with obesity-related cardiac morphological and functional changes during weight loss. Measurement of echocardiographic epicardial fat thickness may provide an additional tool in understanding the metabolic risk associated with variation in fat distribution.     

Cardiac adaptation to endurance exercise in rats

Endurance exercise is widely assumed to improve cardiac function in humans. This project has determined cardiac function following endurance exercise for 6 (n = 30) or 12 (n = 25) weeks in male Wistar rats (8 weeks old). The exercise protocol was 30 min/day at 0.8 km/h for 5 days/week with an endurance test on the 6th day by running at 1.2 km/h until exhaustion. Exercise endurance increased by 318% after 6 weeks and 609% after 12 weeks. Heart weight/kg body weight increased by 10.2% after 6 weeks and 24.1% after 12 weeks. Echocardiography after 12 weeks showed increases in left ventricular internal diameter in diastole (6.39 ± 0.32 to 7.90 ± 0.17 mm), systolic volume (49 ± 7 to 83 ± 11 μl) and cardiac output (75 ± 3 to 107 ± 8 ml/min) but not left wall thickness in diastole (1.74 ± 0.07 to 1.80 ± 0.06 mm). Isolated Langendorff hearts from trained rats displayed decreased left ventricular myocardial stiffness (22 ± 1.1 to 19.1 ± 0.3) and reduced purine efflux during pacing-induced workload increases. 31P-NMR spectroscopy in isolated hearts from trained rats showed decreased PCr and PCr/ATP ratios with increased creatine, AMP and ADP concentrations. Thus, this endurance exercise protocol resulted in physiological hypertrophy while maintaining or improving cardiac function. (Mol Cell Biochem 251: 51–59, 2003)