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.

Endurance training in the rat. I. Myocardial mechanics and biochemistry

1981 ◽  
Vol 51 (4) ◽  
pp. 934-940 ◽  
Author(s):  
D. O. Nutter ◽  
R. E. Priest ◽  
E. O. Fuller
Keyword(s):  
Endurance Training ◽  
Myocardial Contractility ◽  
Left Ventricular ◽  
Isometric Tension ◽  
Treadmill Running ◽  
Male Rats ◽  
Heart Weight ◽  
Succinate Dehydrogenase Activity ◽  
Myocardial Mechanics ◽  
Muscle Contractile

The effects of physical training and detraining on cardiac structure and myocardial mechanics were studied in young and adult male rats trained by graded treadmill running for 12 wk and compared with sedentary controls. Detraining was produced by training for 12 wk followed by 6 sedentary wk. A training effect was demonstrated by increased succinate dehydrogenase activity in skeletal muscle (trained 10.0 +/- 1.2 mumol . g-1 . min-1; sedentary 6.4 +/- 0.8 mumol . g-1 . min-1; P less than 0.05). Although heart weight-to-body weight ratios were increased in trained rats of both ages, left ventricular fiber diameters and myocardial RNA, DNA, and collagen content were unchanged by training. Active and passive mechanics (myocardial contractility and stiffness) were studied in left ventricular papillary muscles and did not differ significantly between groups, with the exception of depressed contractility observed in young trained rats [(e.g., papillary peak developed isometric tension at Lmax (length at peak tension)] was 2.64 +/- 0.24 g/mm2 in trained vs. 3.59 +/- 0.22 g/mm2 in sedentary (P less than 0.01). This difference was abolished by detraining. Papillary muscle contractile responses to calcium, norepinephrine, and hypoxia were not altered by training or detraining. In conclusion, moderate endurance training did not result in significant cardiac hypertrophy, altered myocardial stiffness, or consistent changes in myocardial contractility.

Cardiac adaptations to endurance training in rats with a chronic myocardial infarction

1989 ◽  
Vol 66 (2) ◽  
pp. 712-719 ◽  
Author(s):  
T. I. Musch ◽  
R. L. Moore ◽  
P. G. Smaldone ◽  
M. Riedy ◽  
R. Zelis
Keyword(s):  
Myocardial Infarction ◽  
Endurance Training ◽  
Left Ventricular ◽  
Treadmill Running ◽  
Coronary Artery Ligation ◽  
Maximal Heart Rate ◽  
Chronic Myocardial Infarction ◽  
Artery Ligation ◽  
Training Paradigm ◽  
Myosin Isozyme

The hemodynamic response to maximal exercise was determined in sedentary and trained rats with a chronic myocardial infarction (MI) produced by coronary artery ligation and in rats that underwent sham operations (SHAM). Infarct size in the MI groups of rats comprised 28–29% of the total left ventricle and resulted in both metabolic and hemodynamic changes that suggested that these animals had moderate compensated heart failure. The training regimen used in the present study produced significant increases in maximal O2 uptake (VO2max) when expressed in absolute terms (ml/min) or when normalized for body weight (ml.min-1.kg-1) and consisted of treadmill running at work loads that were equivalent to 70–80% of the animal's VO2max for a period of 60 min/day, 5 days/wk over an 8- to 10-wk interval. This training paradigm produced two major cardiocirculatory adaptations in the MI rat that had not been elicited previously when using a training paradigm of a lower intensity. First, the decrement in the maximal heart rate response to exercise (known as “chronotropic incompetence”) found in the sedentary MI rat was completely reversed by endurance training. Second, the downregulation of cardiac myosin isozyme composition from the fast ATPase V1 isoform toward the slower ATPase (V2 and V3) isoforms in the MI rat was partially reversed by endurance training. These cardiac adaptations occurred without a significant increase in left ventricular pump function as an increase in maximal cardiac output (Qmax) and maximal stroke volume (SVmax) did not occur in the trained MI rat.(ABSTRACT TRUNCATED AT 250 WORDS)

Myocardial hypoperfusion/reperfusion tolerance with exercise training in hypertension

2006 ◽  
Vol 100 (2) ◽  
pp. 541-547 ◽  
Author(s):  
Patricia O. Reger ◽  
Mary F. Barbe ◽  
Mamta Amin ◽  
Brian F. Renna ◽  
Leigh Ann Hewston ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heat Shock ◽  
Exercise Training ◽  
Heat Shock Protein ◽  
Endurance Training ◽  
Left Ventricular ◽  
Treadmill Running ◽  
Rate Pressure Product ◽  
Protein Abundance ◽  
Myocardial Hypoperfusion

The purpose of this study was to examine whether exercise training, superimposed on compensated-concentric hypertrophy, could increase myocardial hypoperfusion-reperfusion (H/R) tolerance. Female Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) (age: 4 mo; N = 40) were placed into a sedentary (SED) or exercise training (TRD) group (treadmill running; 25 m/min, 1 h/day, 5 days/wk for 16 wk). Four groups were studied: WKY-SED ( n = 10), WKY-TRD ( n = 10), SHR-SED ( n = 10), and SHR-TRD ( n = 10). Blood pressure and heart rate were determined, and in vitro isolated heart performance was measured with a retrogradely perfused, Langendorff isovolumic preparation. The H/R protocol consisted of a 75% reduction in coronary flow for 17 min followed by 30 min of reperfusion. Although the rate-pressure product was significantly elevated in SHR relative to WKY, training-induced bradycardia reduced the rate-pressure product in SHR-TRD ( P < 0.05) without an attenuation in systolic blood pressure. Heart-to-body weight ratio was greater in both groups of SHR vs. WKY-SED ( P < 0.001). Absolute and relative myocardial tolerance to H/R was greater in WKY-TRD and both groups of SHR relative to WKY-SED ( P < 0.05). Endurance training superimposed on hypertension-induced compensated hypertrophy conferred no further cardioprotection to H/R. Postreperfusion 72-kDa heat shock protein abundance was enhanced in WKY-TRD and both groups of SHR relative to WKY-SED ( P < 0.05) and was highly correlated with absolute left ventricular functional recovery during reperfusion ( R2= 0.86, P < 0.0001). These data suggest that both compensated hypertrophy associated with short-term hypertension and endurance training individually improved H/R and that increased postreperfusion 72-kDa heat shock protein abundance was, in part, associated with the cardioprotective phenotype observed in this study.

Muscle metabolism and cardiac function of the myopathic hamster following training

1977 ◽  
Vol 43 (6) ◽  
pp. 936-941 ◽  
Author(s):  
W. L. Sembrowich ◽  
M. B. Knudson ◽  
P. D. Gollnick
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Function ◽  
Myocardial Function ◽  
Cardiac Contractility ◽  
Muscle Metabolism ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Treadmill Running ◽  
Succinate Dehydrogenase Activity ◽  
Positive Effect

The effect of 18 wk of treadmill running on skeletal muscle metabolism and myocardial function of normal and myopathic hamsters was examined. BIO 14.6 hamsters could tolerate an exercise intensity of about 18 m/min for 40 min, 5 days/wk. Further increases in speed or number of bouts per day resulted in a falloff in performance. Normal hamsters could tolerate higher speeds and longer exercise bouts. Exercise did not change the severity of lesions of either the heart or skeletal muscle of the myopathic hamsters. A training effect was evidenced by increased succinate dehydrogenase activity in the soleus muscle. Cardiac function was evaluated as contractility measured from left ventricular pressure curves and expressed as (dP/dt)/kP. The results suggested that cardiac contractility was not as severely depressed in the trained BIO 14.6 strain of hamsters as in nontrained controls. However, (dP/dt)/kP was lower in the trained myopathic animals than in normal hamsters. ATP, CP, and glycogen levels were lower in myopathic hamsters with the lowest values occurring in the trained group. These data demonstrate that the BIO 14.6 strain of hamster can tolerate exercise training and that such training may have a positive effect on cardiac function.

Cardiac function in fetal sheep during two weeks of hypoxemia

1994 ◽  
Vol 266 (6) ◽  
pp. R1778-R1785 ◽  
Author(s):  
M. Kamitomo ◽  
L. D. Longo ◽  
R. D. Gilbert
Keyword(s):  
Arterial Pressure ◽  
Cardiac Function ◽  
Ventricular Function ◽  
Left Ventricular ◽  
Pressure Sensitivity ◽  
Sensitivity Curve ◽  
Fetal Sheep ◽  
Cardiac Responses ◽  
Ovine Fetal

Although several studies have examined fetal cardiac responses to acute hypoxemia, relatively little is known of the response to prolonged hypoxemia. To determine the effects of long-term hypoxemia on ovine fetal cardiac function, we measured right (QRV) and left ventricular outputs (QLV) and determined the effects of increasing preload (ventricular function curve) and afterload (arterial pressure sensitivity curve) on the left ventricle. Six days after fetal surgical instrumentation with catheters and electromagnetic flow probes (approximately 123 days gestation), we administered N2 into the maternal trachea for 14 days to reduce maternal PO2 to approximately 55 Torr (hypoxemic group, Hyp, n = 6). Normoxic animals were used as controls (Cont, n = 6). With the onset of hypoxemia, fetal arterial PO2 was reduced from approximately 27 to approximately 18 Torr. Fetal heart rate in Hyp fetuses decreased approximately 22% on day 14 compared with Cont (P < 0.05). Mean arterial pressure in the Hyp group was higher than that of Cont but not significantly so. Right and left atrial pressures were not affected by hypoxemia. QRV in Hyp fetuses was maintained on day 1 but decreased significantly by day 3 (approximately 19%) and further decreased on days 7 (approximately 28%) and 14 (approximately 34%). QLV was not depressed until day 7 (approximately 20%), with a further decrease on day 14 (approximately 38%). In association with the decreased QLV the plateau of the ventricular function curve in Hyp fetuses was depressed significantly on days 7 and 14. In contrast, the slope of the arterial pressure sensitivity curve in the Hyp group did not differ from Cont.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Environmentally persistent free radicals decrease cardiac function and increase pulmonary artery pressure

2012 ◽  
Vol 303 (9) ◽  
pp. H1135-H1142 ◽  
Author(s):  
Sarah Mahne ◽  
Gin C. Chuang ◽  
Edward Pankey ◽  
Lucy Kiruri ◽  
Philip J. Kadowitz ◽  
...  
Keyword(s):  
Free Radicals ◽  
Left Ventricle ◽  
Cardiac Function ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Diastolic Pressure ◽  
Silica Particles ◽  
Left Ventricular ◽  
Heme Oxygenase 1 ◽  
Stroke Work

Epidemiological studies have consistently linked inhalation of particulate matter (PM) to increased cardiac morbidity and mortality, especially in at risk populations. However, few studies have examined the effect of PM on baseline cardiac function in otherwise healthy individuals. In addition, airborne PM contain environmentally persistent free radicals (EPFR) capable of redox cycling in biological systems. The purpose of this study was to determine whether nose-only inhalation of EPFRs (20 min/day for 7 days) could decrease baseline left ventricular function in healthy male Sprague-Dawley rats. The model EPFR tested was 1,2-dichlorobenzene chemisorbed to 0.2-μm-diameter silica/CuO particles at 230°C (DCB230). Inhalation of vehicle or silica particles served as controls. Twenty-four hours after the last exposure, rats were anesthetized (isoflurane) and ventilated (3 l/min), and left ventricular function was assessed using pressure-volume catheters. Compared with controls, inhalation of DCB230 significantly decreased baseline stroke volume, cardiac output, and stroke work. End-diastolic volume and end-diastolic pressure were also significantly reduced; however, ventricular contractility and relaxation were not changed. DCB230 also significantly increased pulmonary arterial pressure and produced hyperplasia in small pulmonary arteries. Plasma levels of C-reactive protein were significantly increased by exposure to DCB230, as were levels of heme oxygenase-1 and SOD2 in the left ventricle. Together, these data show that inhalation of EPFRs, but not silica particles, decreases baseline cardiac function in healthy rats by decreasing cardiac filling, secondary to increased pulmonary resistance. These EPFRs also produced systemic inflammation and increased oxidative stress markers in the left ventricle.

scholarly journals Use of the Isolated Perfused Heart for Evaluation of Cardiac Toxicity

1990 ◽  
Vol 18 (4a) ◽  
pp. 497-510 ◽  
Author(s):  
Peter G. Anderson ◽  
Stanley B. Digerness ◽  
Jerald L. Sklar ◽  
Paul J. Boor
Keyword(s):  
Rat Heart ◽  
Coronary Flow ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Heart Weight ◽  
Isolated Perfused Heart ◽  
Heart Model ◽  
Perfused Heart ◽  
Perfused Rat Heart ◽  
Isolated Perfused Rat Heart

The isolated perfused rat heart model can be used to evaluate cardiotoxicity, and is especially useful in distinguishing direct vs indirect cardiac injury. Various perfusion systems can be used to characterize the pathophysiologic as well as morphologic changes induced by drugs or chemicals of interest. The isolated perfused heart was used in the studies described herein to characterize the mechanism of allylamine cardiotoxicity. Rat hearts were perfused with Krebs-Henseleit buffer containing 10 mm allylamine and a latex balloon was inserted into the left ventricle to monitor pressure. Coronary flow in hearts perfused with 10 mm allylamine was similar to control hearts at 5, 10, and 30 min, but was reduced by 1 hr (11.5 ± 0.6 ml/min/g wet heart weight vs 16.0 ± 0.7, p < 0.01). Peak left ventricular systolic pressure increased in hearts perfused with allylamine for 5 min (156 ± 8 mm Hg vs 103 ± 9, p < 0.01), but by 2 hr was decreased compared to controls (89 ± 6 vs 105 ± 5, p < 0.05). End diastolic pressure was markedly increased at 2 hr (58 ± 3 vs 4 ± 0.8, p < 0.01). Morphologically, allylamine perfused hearts exhibited significant contraction band changes as well as numerous cells with marked swelling of the sarcoplasmic reticulum. The findings in this study suggest that allylamine produces direct myocardial damage that appears to be independent of coronary flow. These studies demonstrate that the isolated perfused rat heart model can be used to evaluate mechanisms of acute cardiotoxicity.

Cardiac microdialysis in isolated rat hearts: interstitial purine metabolites during ischemia

1992 ◽  
Vol 262 (6) ◽  
pp. H1934-H1938 ◽  
Author(s):  
D. G. Van Wylen ◽  
T. J. Schmit ◽  
R. D. Lasley ◽  
R. L. Gingell ◽  
R. M. Mentzer
Keyword(s):  
Uric Acid ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Isolated Perfused Heart ◽  
Perfused Heart ◽  
Purine Metabolites ◽  
Valuable Adjunct ◽  
Rat Hearts

Cardiac microdialysis is a recently developed technique that allows intramyocardial interstitial fluid (ISF) to be sampled via the implantation and perfusion of a small, hollow dialysis fiber within the myocardium. The purpose of this paper is to describe initial studies using cardiac microdialysis in the isolated perfused heart. Microdialysis probes, constructed in the laboratory, were implanted in the left ventricular myocardium of isolated perfused rat hearts and perfused at 0.5 microliter/min with Krebs-Henseleit buffer. The effluent dialysate, assayed for adenosine, inosine, hypoxanthine, xanthine, and uric acid, was used as an index of intramyocardial levels of these purine metabolites. All metabolites were elevated initially after implantation, declined rapidly in the first 45 min, and were then stable for the next 90 min. Based on in vitro percent recovery data, baseline dialysate concentrations were extrapolated to yield estimates of intramyocardial ISF (in microM) 0.47 adenosine, 0.85 inosine, 0.29 hypoxanthine, 0.49 xanthine, and 8.6 uric acid. During global zero-flow ischemia (37 degrees C), dialysate levels of all purine metabolites were elevated, with inosine being the predominant compound. Pretreatment of the hearts with 50 microM erythro-9-(2-hydroxy-3-nonyl)adenine, an adenosine deaminase inhibitor, markedly enhanced ISF adenosine accumulation and attenuated the accumulation of inosine, hypoxanthine, and xanthine. The simplicity and versatility of cardiac microdialysis in the isolated perfused heart suggest that this technique may be a valuable adjunct to the many studies performed using this preparation.

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