Effects of physical training by running or swimming on ventricular performance of rat hearts.
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Biomedical subjects
Publications and source records attributed to J Scheuer.
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Thirty patients with triple-vessel coronary artery disease proven by angiography, symptomatic angina and a positive ECG stress test were evaluated with thallium-201 (201TI) scintigraphy. Twenty patients also had aortocoronary saphenous vein bypass surgery; 15 of them had repeat noninvasive evaluation. Seventy percent of these patients showed ischemia by 201TI scintigraphy, of which one-half returned to normal after surgery. Postoperative reversion of the ECG stress test together with 201TI stress/reperfusion imaging correlated well with the completeness of surgical revascularization. We could not explain the prevalence (80%) of infarcts detected by 201TI in this group, of which 76% could be anatomically correlated to epicardial scars. The positivity of infarcts by 201TI exceeded that predicted by previous history of infarction, Q waves on resting ECG or ventriculographic akinesis. These observations suggest that 201TI scintigraphy is a useful noninvasive tool in the follow-up and understanding of patients with coronary heart disease. These conclusions also support the concept that 201TI stress imaging need not have the identical connotation as the ECG stress test.
This review has pointed out the good correlation frequently observed between ATPase activity of various contractile protein preparations and contractile function of various muscles including the myocardium. Some of the variables in the measurement of the various ATPases and the relationship of these measurements to physiological ATPase in the intact myofibril have been mentioned. The possible roles of changes in the light chains of sulfhydryl groups in the control of ATPase activity have been outlined. The possibility that phosphorylating reactions might exert control over physiological activity remains to be clarified. It is evident that, despite the large amount of research that has been done, our understanding of how the biochemistry of contractile proteins relates to physiological function is in its infancy, and only with a more complete elucidation of the underlying biochemistry of the components of contractile proteins of physiological and pathophysiological adaptations become evident.
Cardiac function was determined non-invasively in 7 patients (average age 24 years) with chronic uremia. Each was on maintenance hemodialysis. Echocardiograms and carotid pulse tracings were recorded 30 minutes prior to dialysis, and again 30 minutes, 24 and 48 hours following hemodialysis. End-diastolic and end-systolic diameters averaged 5.4 +/- 0.2 and 3.4 +/- 0.1 cm, respectively before and 5.0 +/- 0.2 and 3.2 +/- 0.1 cm immediately after hemodialysis (P less than 0.05 for both). Calculated stroke volume fell from 92.1 +/- 8.8 to 76.7 +/- 10.5 ml (P less than 0.025). Heart rate increased minimally, and average cardiac output was not significantly increased. Following dialysis, body weight and systolic and diastolic blood pressures fell significantly. Thus preload as well as afterload declined. Because of the fall in both stroke volume and end-diastolic volume, a shift along the ventricular function curve downwards and to the left occurred implying diminished cardiac pumping function. Nonetheless the indices of myocardial contractility were normal and showed no change from pre-dialysis value. During the 48 hour interval following hemodialysis all measured and calculated values returned to pre-dialysis levels. Thus organic heart disease as evaluated by non-invasive techniques does not appear to be a necessary sequel to kidney failure, at least in young patients in a hemodialysis program. Gross abnormalities of myocardial function may be absent for at least seven years after the onset of chronic uremia.
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To determine the effects of chronic exercise on the coronary collateral circulation of dogs with normal coronary arteries, 1-yr-old purebred beagles were divided into sedentary control and exercising groups. The latter were trained to run on a treadmill. A lower maximal heart rate during a standardized exercise test protocol after a 10- to 12-week training period and a higher gastrocnemius cytochrome oxidase activity in the runners attested to the presence of cardiovascular and skeletal muscle training effects. However, left ventricular weights, left ventricle/body weight ratios, myocardial myofibrillar and myosin ATPases, and hemodynamics were similar in sedentary and exercising dogs except for a significantly higher resting cardiac output in the runners. After occlusion of the left anterior descending coronary artery, both collateral conductance (retrograde flow/aortic pressure) and collateral flow measured with microspheres tended to be lower in the trained dogs, but differences were not significant. The endocardial/epicardial flow ratio in the ischemic area after coronary occlusion did not distinguish between exercisers and controls. Thus treadmill running in the dog with normal coronary arteries produced a training effect, but had no effect on coronary collateral vessels.
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Left ventricular (LV) performance was studied in 30 rats conditioned by swimming and in 27 sedentary controls. Hearts were studied in the open chest both during sinus rhythm and during atrial pacing. Afterload was increased by occlusion of the aorta. Sinus rates were 328 beats/min in sedentary and 300 in conditioned animals (P less than 0.01). During ejection (E), peak left ventricular systolic pressure (PLVSP) and maximum LV dP/dt were significantly higher in conditioned than in sedentary animals. When data from hearts matched for similar heart rates were compared, increased LV performance was still seen during aortic obstruction in conditioned animals. Performance at pacing rates up to 400 beats/min was similar in hearts from conditioned and sedentary animals. At pacing rates above 400 beats/min cardiac performance was less in sedentary than in the conditioned animals. These data illustrate that although base-line cardiac performance may be the same in rats conditioned by a moderate swimming program and in sedentary animals, cardiac reserve is improved by the swimming program.
Cardiac microsomes enriched in fragmented sarcoplasmic reticulum (SR) were isolated from hearts of physically trained rats and were compared to those from sedentary rats. Preparations from conditioned rats were found to transport calcium to a greater extent than those from sedentary rats both in the absence and in the presence of 1 mM oxalate. Higher oxalate concentrations abolished the differences in calcium accumulation by cardiac microsomes from conditioned and sedentary rats and indicated a qualitative change in SR from conditioned hearts. We conclude that the increased transport by SR from hearts of conditioned rats may provide one mechanism for enhanced contractile reserve in these hearts.
We studied the performance of ventricular muscle and cardiac function of hearts from rats conditioned by swimming (CH) and from sedentary rats (SH) in an isolated working heart apparatus modified to measure end-diastolic volume by dye dilution. Instantaneous aortic flow, left ventricular (LV) pressure and oxygen consumption were measured. Heart rate and mean aortic pressure were kept constant, and atrial filling pressure was varied from 5 to 20 cm H2O. Heart weights of SH and CH were equal and end-diastolic pressures and volumes were similar at all atrial pressures. However, ejection fraction, calculated circumferential fiber velocity, peak systolic pressure, peak aortic flow, cardiac output, and stroke work were all greater in CH than in SH, and the differences increased as atrial pressure was increased. Maximal negative dP/dt was greater in CH than SH at all preloads (P less than 0.001). Oxygen consumption of CH was increased in proportion to the increase in work. These results indicate that the improved pumping performance of CH is due to a change in ventricular muscle function. Faster relaxation is a prominent effect of physical training on the rat heart and may foster more complete filling at high heart rates.
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Cardiac actomyosin ATPase was increased by making rats swim 150 min/day, 5 days/wk for 8 wk. Changes in Ca2+ -stimulated ATPase activity were then studied in these conditioned rats and in similarly conditioned animals in which swimming was subsequently discontinued (group A), reduced to 45 min/day (group B), or continued at the original level for an additional 8 wk (group C). After the 8-wk initial program actomyosin ATPase activity averaged 22% higher in hearts of conditioned rats than in hearts of sedentary controls (P is less than 0.001). In group A, actomyosin ATPase activity declined rapidly and reached the level found in sedentary controls by the 13th day. In group B, actomyosin ATPase activity declined to the control level by the 30th day. At the end of 16 wk the percent increase in actomyosin ATPase activity in group C over that in hearts of sedentary animals was approximately the same as after 8 wk. These results demonstrate that elevation in cardiac actomyosin ATPase caused by moderate physical training in rats is not maintained if the training program is decreased or discontinued. The training program must be continued at or near the initial level if the increases in cardiac actomyosin ATPase are to be sustained.