PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Cardiomegaly, Exercise-Induced”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

83 records · Page 5Linked to original sources
PubMed1976

The effect of complete and partial deconditioning on exercise-induced cardiovascular changes in the rat.

Exercise conditioning of young male rats by swimming for 1 h, 5 times per week for 10 weeks results in a reduced gain in body weight, cardiac hypertrophy and hyperplasia, an increase in myocardial capillary density, and an increase in cross-sectional laminal areas of extracoronary collateral arteries. The effects of partial or complete deconditioning on these changes were studied by randomizing young male rats exercise-conditioned for 10 weeks to groups either kept sedentary or subjected to varying amounts of exercise for a second 10-week period. Their hearts were compared with those of unexercised controls using quantitative histologic measurements. During the second 10 weeks, exercise conditioning was found not to continue to suppress weight gain. However, frequent relative short-duration exercise sessions (as little as 15 min per session) frequently prevented an accelerated increase in body weight associated with deconditioning. A complete regression of exercise-induced cardiovascular adaptive changes occurred when wxercise was discontinued completely for 10 weeks or the duration of sessions was cut to 15 min. In order to maintain cardiac hypertrophy, exercise had to be continued for 1 h, 5 times per week while hyperplasia could be maintained with shorter duration, less frequent sessions (30 min, twice a week). The maintenance of increased myocardial capillary density required a similar amount of exercise, and at least 1 h of exercise once a week was necessary to maintain the enlargement of ECA.20

Adaptation, Physiological↗
PubMed2006

Upregulation of heat shock transcription factor 1 plays a critical role in adaptive cardiac hypertrophy.

Exercise-induced cardiac hypertrophy has been reported to have better prognosis than pressure overload-induced cardiac hypertrophy. Cardiac hypertrophy induced by exercise was associated with less cardiac fibrosis and better systolic function, suggesting that the adaptive mechanisms may exist in exercise-induced hypertrophy. Here, we showed a critical role of heat shock transcription factor 1 (HSF1), an important transcription factor for heat shock proteins, in the adaptive mechanism of cardiac hypertrophy. We examined expression of 8800 genes in the heart of exercise-induced hypertrophy model using DNA chip technique and compared with pressure overload-induced hypertrophy. Expression of HSF1 and its target molecule heat shock proteins was significantly upregulated in the heart by exercise but not by chronic pressure overload. Constitutive activation of HSF1 in the heart significantly ameliorated death of cardiomyocytes and cardiac fibrosis and thereby prevented cardiac dysfunction as well as hypertrophy induced by chronic pressure overload. Conversely, decreased activity of HSF1 in the heart promoted cardiac dysfunction in response to exercise, a load that normally leads to adaptive hypertrophy with preserved systolic function. Likewise, cardiac function was significantly impaired from the early phase of pressure overload, when HSF1 activation was inhibited. These results suggest that HSF1 plays a critical role in the transition between adaptive and maladaptive hypertrophy.

Adaptation, Physiological↗
PubMed1990

Exercise-induced subendocardial dysfunction in dogs with left ventricular hypertrophy.

The effects of treadmill exercise on regional myocardial blood flow and function were examined in 10 adult, conscious dogs with left ventricular hypertrophy (LVH) induced by aortic banding in puppies, which resulted in a left ventricular (LV) weight/body weight ratio of 8.5 +/- 0.3. Data were compared with results from eight control dogs with an LV weight/body weight ratio of 4.9 +/- 0.2. At rest, LV systolic and end-diastolic pressures were significantly greater (p less than 0.01), and mean arterial pressure was significantly less (p less than 0.05) in LVH dogs. Mean myocardial blood flow (control dogs, 0.98 +/- 0.11 ml/min/g; LVH dogs, 1.16 +/- 0.06 ml/min/g) and the transmural blood flow distribution at baseline, as assessed by endocardial/epicardial blood flow ratio (control, 1.35 +/- 0.12; LVH, 1.21 +/- 0.09), were similar in the two groups. During exercise to a target heart rate (240 beats/min), LVH dogs demonstrated greater (p less than 0.01) increases in LV systolic and end-diastolic pressures. In control dogs, as expected, exercise augmented velocity of circumferential fiber shortening (16 +/- 9%) and shortening fraction (15 +/- 5%), but in LVH dogs, exercise reduced the velocity of circumferential fiber shortening (-14 +/- 6%) and shortening fraction (-17 +/- 5%). Exercise also increased full wall thickening (35 +/- 5%), subendocardial wall thickening (66 +/- 10%), and subepicardial wall thickening (44 +/- 9%) in control dogs. In LVH dogs, exercise increased subepicardial wall thickening (31 +/- 9%) and reduced subendocardial wall thickening (-40 +/- 7%); full wall thickening did not change (-11 +/- 9%). This was associated with a fall in endocardial/epicardial flow ratio to 0.72 +/- 0.05 (p less than 0.01) in LVH dogs. The subendocardial dysfunction persisted late into recovery, at a time when the transmural blood flow distribution had returned to baseline; this occurrence suggested myocardial stunning. Thus, in dogs with LVH, selective subendocardial hypoperfusion and profound selective depression in subendocardial wall thickening are observed during exercise. The subendocardial dysfunction persisted into recovery despite resolution of the perfusion abnormality.

Animals↗
PubMed1993

Effects of volume and pressure overloads and myocardial hypertrophy on exercise-induced changes in electrocardiographic QRS amplitude.

To investigate the effects of volume and pressure overloads and myocardial hypertrophy on exercise-induced changes in QRS amplitude, we reviewed treadmill exercise electrocardiograms. In 10 normal young men, Rv5 amplitude decreased and Sv1 amplitude increased at peak exercise, and returned to the resting value in the recovery period. In 10 patients with aortic regurgitation, Rv5 and Sv1 amplitudes increased after 5 min of recovery. In 12 patients with essential hypertension and 10 with idiopathic hypertrophic non-obstructive cardiomyopathy, Rv5 amplitude remained unchanged or higher at peak exercise compared with the resting value, but patterns of serial changes were similar to that of normal subjects. In 9 patients with atrial septal defect, R'v1 amplitude increased with exercise, whereas it remained unchanged in 12 with isolated complete right bundle branch block. In 5 patients with mitral stenosis, Sv1 amplitude decreased at peak exercise. In conclusion, changes in QRS amplitude with exercise are influenced by hemodynamic abnormality and myocardial hypertrophy, and a major determinant of these serial changes seems to be the change in ventricular volume.

Adult↗
PubMedDate not supplied

Influence of physical exercise and sodium intake on arterial pressure and cardiac hypertrophy in rats.

Evidence shows that cardiac hypertrophy (CH) is a risk factor for many cardiovascular diseases. Several stimuli may cause CH-like manifestations and promote volume or pressure overload. Exercise-induced cardiac hypertrophy is an expected adaptation to regular exercise training. Salt intake has been shown to be the most important determinant of blood pressure in different populations. The purpose of the present work was to verify the influence of physical exercise and sodium intake on the blood pressure and myocardium. The study was performed on 36 rats divided into six groups: Group I (diet without salt overload), Group II (diet without salt overload and swimming), Group III (diet with 2.5% NaCl solution and swimming), Group IV (diet with 5% NaCl solution and swimming), Group V (diet with 2.5% NaCl solution without exercise), Group VI (diet with 5% NaCl solution without exercise). The arterial pressure was significantly lower in Group I when compared with Group IV. The ratio of cardiac mass/body mass was increased in Groups III and IV. In conclusion, there was evidence that exercise training and NaCl intake promotes arterial hypertension and cardiac hypertrophy.

Animals↗
PubMed2003

Duration-controlled swimming exercise training induces cardiac hypertrophy in mice.

Exercise training associated with robust conditioning can be useful for the study of molecular mechanisms underlying exercise-induced cardiac hypertrophy. A swimming apparatus is described to control training regimens in terms of duration, load, and frequency of exercise. Mice were submitted to 60- vs 90-min session/day, once vs twice a day, with 2 or 4% of the weight of the mouse or no workload attached to the tail, for 4 vs 6 weeks of exercise training. Blood pressure was unchanged in all groups while resting heart rate decreased in the trained groups (8-18%). Skeletal muscle citrate synthase activity, measured spectrophotometrically, increased (45-58%) only as a result of duration and frequency-controlled exercise training, indicating that endurance conditioning was obtained. In groups which received duration and endurance conditioning, cardiac weight (14-25%) and myocyte dimension (13-20%) increased. The best conditioning protocol to promote physiological hypertrophy, our primary goal in the present study, was 90 min, twice a day, 5 days a week for 4 weeks with no overload attached to the body. Thus, duration- and frequency-controlled exercise training in mice induces a significant conditioning response qualitatively similar to that observed in humans.

Adaptation, Physiological↗
PubMed1994

Exercise-induced cardiac hypertrophy. Fact or fallacy?

After a century of research reports, the notion of exercise-induced cardiac hypertrophy is still an expected adaptation to regular exercise training. Experimental evidence reported both in animals and in humans over the past 3 decades suggests, however, that this conclusion may not be totally warranted. Data from 20 years of echocardiographic investigations of athletes and nonathletes indicate that differences in cardiac dimensions are not very large. Cross-sectional comparisons of over 1000 athletes and roughly 800 control individuals indicate an average difference of 1.6 mm in left ventricular (LV) wall thickness and of 5.3 mm in end-diastolic diameter. Differences reported after training programmes lasting 4 to 52 weeks are even smaller, with average increases of 0.3 mm in LV wall thickness and only 2.1mm in end-diastolic diameter. This article reviews data from animal and human studies concerning cardiac morphology and exercise training to show that the traditional interpretation of the literature has failed to take into account several methodological considerations or factors that may act as confounders in the interpretation of data. Results from animal studies indicate that the observation of cardiac hypertrophy is equivocal at best. In many reports the reported changes in heart size are not significant, and in instances where significant changes are reported these may be seen to be confounded by a number of factors. For example, in rats the reported training-induced hypertrophy may be related to gender differences in the responsiveness of cardiac dimensions or body and/or organ growth rather than to true heart hypertrophy. Furthermore, the interpretation of results from training studies in rats has often been based on the assumption that the metabolic, haemodynamic and thermoregulatory requirements of swimming and running exercise in rats are similar, which may in fact not be the case. In addition, the use of the heart weight/body weight ratio as an index of cardiac hypertrophy, although widespread in animal studies, is open to criticism owing to failure to control for concurrent changes in body weight. Several methodological considerations and factors confounding the outcome of exercise training in humans have also been omitted when interpreting echocardiographic cross-sectional and longitudinal findings. For example, in adult echocardiography the practical resolution of the echocardiographic technique amounts to roughly 2.2mm. It follows, therefore, that unless differences of changes in cardiac dimensions exceed the limit of resolution they are meaningless although statistically significant.(ABSTRACT TRUNCATED AT 400 WORDS)

Adaptation, Physiological↗
PubMed2000

Lack of effect of running training at two intensities on cardiac myosin isozyme composition in rats.

Little information is available regarding the influence of the intensity of endurance training over biochemical profiles in cardiac muscle. We assessed the effect of running training at two different intensities on cardiac myosin isozyme composition in rats. Male Sprague-Dawley rats (4 weeks old) were divided into four groups: sedentary control (SC), trained at 20 m/min (T20), trained at 40 m/min (T40), and weight-matched sedentary control (WMSC) groups. The T20 and T40 group rats were trained by treadmill running for 60 min/d, 5 d/week at 20 or 40 m/min, respectively, for 11 to 12 weeks. In both groups the left ventricle was significantly heavier than in WMSC animals. The ratio of left ventricle weight to body weight was significantly greater in T40 rats than in either the untrained (SC and WMSC) or trained T20 rats. Thus the extent of exercise-induced cardiac hypertrophy appears to be influenced by the intensity of running training. However, neither of the training programs (1) induced a change in cardiac myosin isozyme composition or (2) had any effect on myocardial succinate dehydrogenase or citrate synthase activity. These results suggest that although the intensity of running training may play an important role in cardiac morphological adaptation, it does not modulate the cardiac biochemical adaptation to running training.

Animals↗
PubMed1992

[Cardiac and humoral mechanisms of the preventive effect of physical activity on cardiovascular diseases].

Many recent studies on the effects of regular exercise on the heart, coronary arteries and the balance between haemostasis and fibrinolysis suggest several mechanisms that are able to explain the epidemiologically well-documented association of habitual physical activity with a reduced risk of cardiovascular disease. Based on a review of current evidence, it is proposed that i) the haemodynamic adaptation of an aerobically-trained heart is an important cardioprotective mechanism, ii) the importance of exercise-induced effects on the coronary vessels may currently be somewhat underestimated, and iii) the importance of training-related changes in the haemostatic-fibrinolytic balance is equivocal at present, since the relative intensity of exercise seems to be a modifying factor that has not been taken into account appropriately so far. Further biomedical research into the cardiac and humoral effect of physical training is, thus, needed to corroborate the recent epidemiological observation that moderate-intensity exercise is just as--or even more--cardioprotective than high-intensity sports activity.

Cardiomegaly↗
PubMed1984

Modifiers of exercise-induced S-T segment changes.

Myocardial ischemia due to coronary atherosclerosis is the usual cause of exercise-induced S-T segment changes. A number of drugs, electrolyte alterations, and hemodynamic factors may accentuate or mask these changes. The clinician should keep this in mind during the electrocardiographic interpretation of exercise tests.

Adrenergic beta-Antagonists↗