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.

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.

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.

Effect of endurance training on cardiac morphology in Alaskan sled dogs

1998 ◽  
Vol 85 (4) ◽  
pp. 1368-1375 ◽  
Author(s):  
R. L. Stepien ◽  
K. W. Hinchcliff ◽  
P. D. Constable ◽  
J. Olson
Keyword(s):  
Endurance Training ◽  
Morphological Changes ◽  
Left Ventricular ◽  
Volume Index ◽  
Heart Weight ◽  
Wall Thickening ◽  
Cardiac Morphology ◽  
End Diastolic Volume ◽  
Sled Dogs ◽  
Lv Mass

The cardiac morphology of 77 conscious Alaskan sled dogs before and after 5 mo of endurance training (20 km/day team pulling a sled and musher) was studied using two-dimensional and M-mode echocardiography. Subgroups included dogs with at least one season of previous training (“veterans”) and dogs 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 is associated with endurance training in Alaskan sled dogs. Disproportionate LV wall thickening accompanying LV dilation suggests that cardiac morphological changes are due to volume and pressure loading. 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.

Heart functional responses to pressure overload in exercised and sedentary rats

1976 ◽  
Vol 230 (1) ◽  
pp. 199-204 ◽  
Author(s):  
RT Dowell ◽  
AF Cutilletta ◽  
MA Rudnik ◽  
PC Sodt
Keyword(s):  
Cardiac Output ◽  
Diastolic Pressure ◽  
Heart Function ◽  
Pressure Overload ◽  
Normal Growth ◽  
Left Ventricular ◽  
Treadmill Running ◽  
Female Rats ◽  
Heart Weight ◽  
Functional Responses

Female rats that had been subjected to a moderate treadmill running program were compared with sedentary animals on the basis of heart weight, selected biochemical measurements, and heart function. Exercised animals maintained normal growth rate, and cardiac hypertrophy was not present. Left ventricular RNA, DNA, and cytochrome c levels were unchanged. Heart functional measurements obtained in situ were similar in sedentary and exercised animals under control conditions. When subjected to sustained (1-3 days) aortic constriction pressure overload, exercised animals maintained or increased myocardial contractility. Contractility was depressed in sedentary animals. Both sedentary and exercised animals increased left ventricular end diastolic pressure without changing contractility during acute (1-3 min) pressure overload. However, exercised animals were able to fully regain normal cardiac output when the acute overload was relieved. Cardiac output remained approximately 10% below control in sedentary animals. The improved ability of previously exercised animals to withstand pressure overload appears to be due to alterations in adaptation rather than preliminary augmentation of metabolism or function.

Myocardial mechanics predict hemodynamic performance during normal function and alcohol-induced dysfunction in rats

1991 ◽  
Vol 261 (6) ◽  
pp. H1880-H1888
Author(s):  
J. M. Capasso ◽  
P. Li ◽  
P. Anversa
Keyword(s):  
Pressure Rise ◽  
Normal Function ◽  
Left Ventricular ◽  
Isometric Tension ◽  
Papillary Muscles ◽  
Least Squares Regression ◽  
Tension Development ◽  
Myocardial Mechanics

To determine whether mechanical evaluation of muscle tissue removed from the myocardium can be employed as a direct indicator of cardiac contractile performance in situ, isometric and isotonic parameters of muscle mechanics in vitro were correlated with in vivo global functional characteristics of the same heart. Twelve-month-old animals maintained on standard food and water were employed as representative of normal cardiac function. Animals of identical age with left ventricular (LV) dysfunction induced by oral alcohol (30%) ingestion from 4 to 12 mo were utilized to represent depressed cardiac performance. Accordingly, 24 h after the establishment of the hemodynamic profile for a control or experimental heart, the LV posterior papillary muscle was removed from the same heart and examined isometrically and isotonically. Least squares regression analysis was employed to establish a correlation coefficient and P values between various in vitro and in vivo parameters. Hemodynamic measurements were performed under chloral hydrate anesthesia and LV pump performance was evaluated with respect to aortic and ventricular pressures and the rates of rise and decay of the LV pressure trace. Papillary muscles were evaluated with respect to timing parameters of the isometric and isotonic twitch, the first derivative of isometric tension development, and the speed of muscle shortening at increasing physiologic loads. LV peak rate of pressure rise and decay were then correlated with the various isometric and isotonic properties. Myocardial mechanics and hemodynamics revealed depressed function in the papillary muscles and hearts from alcoholic rats. Moreover, significant correlations were found between the LV rate of pressure change (peak +dP/dt and -dP/dt) and both isometric and isotonic twitch measurements.(ABSTRACT TRUNCATED AT 250 WORDS)

Maternal protein restriction compromises myocardial contractility in the young adult rat by changing proteins involved in calcium handling

2016 ◽  
Vol 120 (3) ◽  
pp. 344-350 ◽  
Author(s):  
Aucelia C. S. de Belchior ◽  
David D. Freire ◽  
Carlos P. da Costa ◽  
Dalton V. Vassallo ◽  
Alessandra S. Padilha ◽  
...  
Keyword(s):  
Cardiovascular Risk ◽  
Young Adult ◽  
Left Ventricular ◽  
Protein Restriction ◽  
Female Rats ◽  
Male Rats ◽  
Calcium Handling ◽  
Myocardial Mechanics ◽  
Maternal Protein Restriction ◽  
Calcium Handling Proteins

Maternal protein restriction (MPR) during pregnancy is associated with increased cardiovascular risk in the offspring in adulthood. In this study we evaluated the cardiac function of young male rats born from mothers subjected to MPR during pregnancy, focusing on the myocardial mechanics and calcium-handling proteins. After weaning, rats received normal diet until 3 mo old, when the following parameters were assessed: arterial and left ventricular hemodynamics and in vitro cardiac contractility in isolated papillary muscles. The body weight was lower and arterial pressure higher in the MPR group compared with young adult offspring of female rats that received standard diet (controls); and left ventricle time derivatives increased in the MPR group. The force developed by the cardiac muscle was similar; but time to peak and relaxation time were longer, and the derivatives of force were depressed in the MPR. In addition, MPR group exhibited decreased post-pause potentiation of force, suggesting reduced reuptake function of the sarcoplasmic reticulum. Corroborating, the myocardial content of SERCA-2a and phosphorylated PLB-Ser16/total PLB ratio was decreased and sodium-calcium exchanger was increased in the MPR group. The contraction dependent on transsarcolemmal influx of calcium was higher in MPR if compared with the control group. In summary, young rats born from mothers subjected to protein restriction during pregnancy exhibit changes in the myocardial mechanics with altered expression of calcium-handling proteins, reinforcing the hypothesis that maternal malnutrition is related to increased cardiovascular risk in the offspring, not only for hypertension, but also cardiac dysfunction.

Exercise- and hypertension-induced collagen changes are related to left ventricular function in rat hearts

1996 ◽  
Vol 270 (1) ◽  
pp. H151-H159 ◽  
Author(s):  
M. L. Burgess ◽  
J. Buggy ◽  
R. L. Price ◽  
F. L. Abel ◽  
L. Terracio ◽  
...  
Keyword(s):  
Heart Function ◽  
Left Ventricular ◽  
Male Rats ◽  
Heart Weight ◽  
Experimental Hypertension ◽  
Chronic Hypertension ◽  
Rat Hearts ◽  
Important Relationship ◽  
Collagen Iii ◽  
Left Ventricular Collagen

Chronic hypertension, known to affect the collagen profile of the heart, and exercise result in impaired or improved heart function, respectively. Collagen types I [alpha 1(I)2 and alpha 2(I)] and III [alpha 1(III)3] are the predominant interstitial collagens thought to influence cardiac function, and the ratio of type III to I (collagen III/I) is thought to be a significant factor in the altered relaxation observed in hypertrophy. The present study tested the hypothesis that the myocardial structure and function are different in chronically exercise-trained vs. hypertensive rat hearts. Male rats were either chronically exercised (XTr) or submitted to experimental hypertension by coarctation of the abdominal aorta (Hyp) for 10 wks. Heart rate, blood pressure, and maximal rate of fall of the left ventricular pressure (-dp/dt) were recorded during isoproterenol stimulation. Results showed that both Hyp and XTr had higher heart weight and left ventricular weight-to-body weight ratios (P < 0.05). Mean arterial pressure (MAP) was higher in Hyp and lower in XTr (P < 0.05), whereas (-dP/dt)/MAP was diminished in Hyp but enhanced in XTr. Left ventricular collagen was higher in Hyp than XTr, whereas collagen III/I was reduced in Hyp compared with XTr (P < 0.05). Scanning and transmission electron microscopy also supported an accumulation of left ventricular collagen in Hyp compared with XTr. A negative correlation was observed between collagen III/I and (-dP/dt)/ MAP (r = -0.91; P < 0.05). These results suggest an important relationship between adaptations in left ventricular collagen and the changes in diastolic function observed in both chronic hypertension and exercise cardiac stress.

scholarly journals Left ventricular remodeling with exercise in hypertension

2009 ◽  
Vol 297 (4) ◽  
pp. H1361-H1368 ◽  
Author(s):  
Stephen C. Kolwicz ◽  
Scott M. MacDonnell ◽  
Brian F. Renna ◽  
Patricia O. Reger ◽  
Rachid Seqqat ◽  
...  
Keyword(s):  
Exercise Training ◽  
Progenitor Cells ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular ◽  
Treadmill Running ◽  
Heart Weight ◽  
Cardiomyocyte Hypertrophy ◽  
Chronic Hypertension ◽  
Cardiac Progenitor Cells

We investigated how exercise training superimposed on chronic hypertension impacted left ventricular remodeling. Cardiomyocyte hypertrophy, apoptosis, and proliferation in hearts from female spontaneously hypertensive rats (SHRs) were examined. Four-month-old SHR animals were placed into a sedentary group (SHR-SED; n = 18) or a treadmill running group (SHR-TRD, 20 m/min, 1 h/day, 5 days/wk, 12 wk; n = 18). Age-matched, sedentary Wistar Kyoto (WKY) rats were controls ( n = 18). Heart weight was greater in SHR-TRD vs. both WKY ( P < 0.01) and SHR-SED ( P < 0.05). Morphometric-derived left ventricular anterior, posterior, and septal wall thickness were increased in SHR-SED relative to WKY and augmented in SHR-TRD. Cardiomyocyte surface area, length, and width were increased in SHR-SED relative to WKY and further increased in SHR-TRD. Calcineurin abundance was increased in SHR-SED vs. WKY ( P < 0.001) and attenuated in SHR-TRD relative to SHR-SED ( P < 0.05). Protein abundance and mRNA of Akt was not different among groups. The rate of apoptosis was increased in SHR-SED relative to WKY and mitigated in SHR-TRD. The abundance of Ki-67+ cells across groups was not statistically different across groups. The abundance of cardiac progenitor cells (c-Kit+ cells) was increased in SHR-TRD relative to WKY. These data suggest that exercise training superimposed on hypertension augmented cardiomyocyte hypertrophy, despite attenuating calcineurin abundance. Exercise training also mitigated apoptosis in hypertension and showed a tendency to enhance the abundance of cardiac progenitor cells, resulting in a more favorable cardiomyocyte number in the exercise-trained hypertensive heart.

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