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PubMed1985

Exercise-induced myocardial capillary growth in the spontaneously hypertensive rat.

Spontaneously hypertensive rats (SHR) were studied to test the hypothesis that endurance exercise training can stimulate capillary growth and offset the decrement associated with the development of myocardial hypertrophy. The exercise group (SHR-T) was trained on a treadmill for 10 weeks at 70-90% maximum VO2 and compared to nontrained SHR and normotensive Wistar-Kyoto (WKY) at 16 weeks of age. Thus, the training program coincided with the development of hypertension and hypertrophy in SHR. Image analysis was used to study capillaries in one micron thick left ventricular tissue samples from perfuse-fixed hearts. Training did not affect left ventricular mass or blood pressure, but reversed the characteristic decrements in capillary surface area (CSA), volume (CV), and numerical density (CD). CSA and CV were most markedly affected by exercise, as mean values for these parameters increased by 31 and 40%, respectively, compared to SHR. The magnitude of these changes approximated the magnitude of hypertrophy as evidenced by left ventricular weight/body weight ratios (42% in SHR and 37% in SHR-T). Anatomical intercapillary distance was also normalized by training (means +/- SEM): SHR-T, 11.65 +/- 0.31; SHR, 13.97 +/- 0.37; WKY, 11.19 +/- 0.37. These data indicate that exercise stimulates capillary growth in the face of developing hypertension and its related left ventricular hypertrophy.

Animals↗

PubMed1983

Changes in lysosomal enzyme activities in exercise-induced cardiac hypertrophy of mice.

The activities of several lysosomal enzymes were assayed in control and in exercise-hypertrophied cardiac muscle of mice (Mus musculus). The repeated running program increased the activity of beta-glucuronidase (16.1%) in mouse cardiac muscle. Decreased activities of beta-N-acetylglucosaminidase (10.8%), acid ribonuclease (10.7%), and arylsulphatase (14.2%) were observed in the hypertrophied myocardium. The activities of acid deoxyribonuclease, cathepsin C, cathepsin D, and p-nitrophenylphosphatase as well as the activities of citrate synthase and cytochrome c oxidase, mitochondrial enzymes, were unaffected in cardiac muscle. We suggest that lysosomal enzyme responses are selective and highly different in physiologically and pathologically induced cardiac hypertrophies.

Acetylglucosaminidase↗

PubMed1989

Pathophysiologic assessment of left ventricular hypertrophy and strain in asymptomatic patients with essential hypertension.

To investigate the significance of the electrocardiographic (ECG) pattern of left ventricular hypertrophy and strain, two groups of asymptomatic patients with essential hypertension were compared. The patients were similar in terms of age, smoking habit, serum cholesterol and blood pressure levels, but differed in the presence (Group I, n = 23) or absence (Group II, n = 23) of the ECG pattern of left ventricular hypertrophy and strain. Group I patients had significantly more episodes of exercise-induced ST segment depression (14 versus 4, p less than 0.05) and reversible thallium perfusion abnormalities (11 of 23 versus 3 of 23, p less than 0.05) despite similar exercise capacity and absence of chest pain. Nonsustained ventricular tachycardia was detected on 24 h ambulatory ECG monitoring in two patients in Group I, but no patient in Group II. Coronary arteriography performed in 20 Group I patients demonstrated significant coronary artery disease in 8 patients. This study has shown that there is a subgroup of hypertensive patients with ECG left ventricular hypertrophy and strain who have covert coronary artery disease. This can be detected by thallium perfusion scintigraphy, and may contribute to the increased risk known to be associated with this ECG abnormality.

Angiography↗

PubMed1983

Exercise-induced cardiac dysfunction in sickle cell anemia. A radionuclide study.

Cardiac performance was studied by radionuclide angiography at rest and during exercise in 22 adolescents with sickle cell (SC) anemia and the results were compared with those in 12 control subjects. At rest, cardiac contractility was normal; cardiac output and end-diastolic volume were increased. At maximal exercise, heart rate, cardiac output response, and work capacity were reduced; the reduction was related to the degree of anemia. Left ventricular end-diastolic volume decreased with exercise most markedly in patients with ischemic exercise electrocardiograms. An abnormal ejection fraction response to exercise occurred in 4 patients; electrocardiographic signs of ischemia developed in all 4, and wall motion abnormalities in 2. Those patients who had electrocardiographic signs of ischemia had a significantly lower heart rate, ejection fraction, and cardiac output response to exercise, and a lower hematocrit level than subjects with normal results on exercise electrocardiography. The increase in cardiac output was not sufficient to maintain a normal level of exercise. The decrease in end-diastolic volume suggests that diastolic function was abnormal during exercise. Cardiac dysfunction was manifested by an abnormal ejection fraction response, wall motion abnormalities, and incomplete left ventricular filling during exercise.

Adolescent↗

PubMed1987

Dissociation between regional myocardial dysfunction and subendocardial ST segment elevation during and after exercise-induced ischemia in dogs.

The onset and resolution of electrical and functional measures of regional myocardial ischemia were examined in nine conscious dogs during control exercise and exercise after beta-receptor blockade. The dogs had been instrumented with an ameroid constrictor and were studied when no regional dysfunction was evident at rest, although severe coronary stenosis or coronary occlusion with collateral circulation development was present. ST segment elevation was measured on subendocardial electrograms, and regional wall motion was studied by sonomicrometry. During control exercise, subendocardial myocardial blood flow in the ischemic zone, normalized to blood flow in the nonischemic zone, decreased. Subendocardial ST elevation increased slowly, was significantly different from control standing values by 2.5 minutes of exercise and returned quickly to control values within 5 minutes after exercise. Percent systolic wall thickening decreased rapidly, was significantly depressed by 1 minute of exercise and did not return to control values until 30 minutes after exercise. A second, identical exercise stress was performed on the same day after a single oral dose (1 mg/kg body weight) of atenolol. In the ischemic zone during exercise after atenolol compared with control exercise, normalized subendocardial myocardial blood flow was improved and significantly less ST elevation occurred, but the onset and resolution of ST elevation were not altered. Systolic wall dysfunction during exercise was significantly less after atenolol, and function returned toward preexercise values by 1 minute after exercise, even more rapidly than ST segment resolution.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2002

Complexities in ETS-domain transcription factor function and regulation: lessons from the TCF (ternary complex factor) subfamily. The Colworth Medal Lecture.

The ETS-domain transcription factor family can be divided into a series of subfamilies. Elk-1 represents the founding member of the ternary complex factor (TCF) subfamily. By focusing on the TCF subfamily, we can demonstrate the complexities that exist in the function and regulation of ETS-domain transcription factors. This article focuses on Elk-1 in detail and summarizes the functions of other TCFs. The key themes covered include the domain structure of the TCFs, the mechanisms of complex formation with serum response factor, regulation of TCFs by mitogen-activated protein kinase cascades, and transcriptional regulatory properties of the TCFs. Finally, the emerging role of the TCFs in vivo is discussed. A picture is developing indicating that, while these proteins exhibit significant sequence and functional conservation, key differences in their structure and regulation are being identified which may relate to unique functions of these proteins in vivo.

Amino Acid Sequence↗

PubMed2000

Anabolic steroids impair the exercise-induced growth of the cardiac capillary bed.

BACKGROUND: Concomitant application of anabolic-androgenic steroids and physical exercise can induce cardiac hypertrophy. These experiments investigate the still unknown response of the cardiac myocytes and capillaries to the combined influence of various anabolic steroids and muscular exercise. METHODS: Female SPF-NMRI mice were divided into the following groups: a) sedentary control, b) exercise (treadmill running); c) sedentary receiving Dianabol; d) exercise + Dianabol; e) exercise + Oral-Turinabol. After 3 and 6 weeks the left ventricular papillary muscles were studied morphometrically. Evaluated variables: minimal myocyte diameter, number of capillaries around a single myocyte, capillary density and intercapillary distance. RESULTS: Only the anabolic steroids + exercise groups showed a mild myocyte hypertrophy. In contrast, only exercise alone caused a significant increase of the capillary density after both experimental periods; e.g. capillary density after 6 weeks (capillaries/mm2, mean values +/- standard deviation, p < 0.05): control (4,272 +/- 287), exercise (5411 +/- 755), dianabol (4,004 +/- 333), dianabol + exercise (4,076 +/- 403), oral-turinabol + exercise (4,053 +/- 306). Moreover, unlike all other regimens, only exercise alone shortened the intercapillary distance. Finally, exercise without drugs induced the greatest increase in the number of capillaries around a single myocyte. CONCLUSIONS: Anabolic steroids combined with exercise: 1) induce mild hypertrophy of the cardiac myocytes, 2) impair the cardiac microvascular adaptation to physical conditioning. The microvascular impairment may cause a detrimental alteration of the myocardial oxygen supply, especially during muscular exercise.

Anabolic Agents↗

PubMed2000

Testosterone-propionate impairs the response of the cardiac capillary bed to exercise.

OBJECTIVE: Experimental application of anabolic-androgenic steroids and exercise training induce cardiac hypertrophy. This study quantifies for the first time, on microscopical level, the adaptation of the cardiac capillaries and myocytes to the concomitant application of testosterone-propionate and exercise training. METHODS: Female SPF-NMRI mice were studied over 3 and 6 wk. Experimental groups: (i) sedentary control (C); (ii) exercise (treadmill running, E); (iii) testosterone-propionate (TP); and (iv) testosterone-propionate+exercise (TPE). Morphometric parameters: 1) papillary muscles: capillary density, intercapillary distance, number of capillaries around a myocyte, and minimal myocyte diameter; and 2) left ventricular wall: capillary density and intercapillary distance. RESULTS: Papillary muscle: A striking suppression of the exercise-induced improvement in capillary supply occurs in the testosterone-propionate+exercise groups over 3 and 6 wk. Exercise without drugs increases significantly (P < 0.05) the capillary density, shortens significantly (P < 0.05) the intercapillary distance, whereas it increases the number of capillaries around a myocyte. These alterations are not observed in the testosterone-propionate treated sedentary animals; e.g., capillary density after 6 wk (mean values +/- standard deviation, capillaries x mm(-2)): C: 4272 +/- 287, E: 5411 +/- 758, TP: 4221 +/- 364, and TPE: 3997 +/- 397. Moreover, only in the testosterone-propionate+exercise groups occurs a mild myocyte hypertrophy after both time periods: there is a trend toward hypertrophy (P < 0.1) in comparison with the C groups and a significant hypertrophy (P < 0.05) in comparison with the E groups. CONCLUSIONS: Testosterone-propionate profoundly inhibits the exercise-induced augmented capillarization, whereas (under training conditions) it leads to a mild myocyte hypertrophy. The microvascular impairment could trigger an imbalance between the myocardial oxygen supply and demand, especially during physical exercise.

Animals↗

PubMed1979

Development and regression of exercise-induced cardiac hypertrophy in rats.

Adult female rats were exercised by daily swimming. All the increase in heart weight induced by the exercise occurred within 14 days and averaged 30%. The half times of the increases in heart weight and total protein content were about 4.5 days, whereas that of cytochrome c, which was used as a mitochondrial marker, was 6.5 days. The total amounts of DNA and of hydroxyproline in the heart, which were used to evaluate the degree of connective tissue hyperplasia, increased only slightly (8% and 10%, respectively). Other animals were subjected to the same swimming program for 21 days. Groups of rats were killed at various time intervals after stopping exercise. Heart weight, total protein content, and total cytochrome c content decreased rapidly initially, with 60% of the total regression of hypertrophy occurring during the first week. Thereafter, heart weight fell more gradually toward the sedentary control value. The hydroxyproline content of the heart, which was increased 10%, did not decrease during the regression of the hypertrophy.

Animals↗

PubMed1986

Exercise-induced cardiac hypertrophy: a correlation of blood flow and microvasculature.

The effects of exercise conditioning on the myocardium were studied in seven instrumented pigs strenuously exercised for 12 wk by treadmill running. Data were compared with eight instrumented untrained pigs. O2 consumption measured during maximum exercise effort was significantly elevated in the trained pigs (71.7 +/- 4.0 vs. 56.3 +/- 3.0 ml X ml-1 X kg-1). Absolute right and left ventricular mass increased by 20 and 13%, respectively, in response to exercise. Myocyte cross-sectional area increased by 21% in the trained hearts compared with the untrained hearts. Transmural left ventricular myocardial blood flow (ml X min-1 X g-1) was not significantly different at rest, during maximum exercise, or during exercise with adenosine infusion. However, training caused an elevation of the regional epicardial blood flow noted during exercise and exercise with adenosine. In the trained pigs mean aortic pressure during maximum exercise with adenosine infusion was not significantly different compared with untrained pigs. Coronary resistance during exercise with adenosine infusion was the same in both animal groups. In the trained group capillary numerical (no./mm2) and length (mm/mm3) densities were reduced, whereas arteriolar numerical and length densities were significantly increased compared with the untrained group. Measurements of capillary luminal surface density (mm2/mm3) in the trained group were unchanged compared with the untrained group. These results suggest that strenuous exercise does not stimulate the production of new capillaries, but this is modified by the ability of existing capillaries to increase their luminal surface area to parallel increases in myocyte growth. The arteriolar data suggest that exercise promotes the formation of new arterioles.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Exercise training-induced alterations of cardiac morphology.

The data to date are ambivalent regarding exercise-induced cardiac enlargement in previously sedentary individuals. The training regimens used in previous longitudinal studies probably did not provide an optimum training stimulus. Accordingly we studied echocardiograms of the left ventricle of 11 relatively inactive individuals pre and post an intense endurance training program, when intensity was increased relative to improvement, thereby providing an optimum training stimulus. Subjects trained 6 days/wk for 7 wk, alternating days of continuous cycling (40 min) and interval running (5 5-min bouts). Exercise intensity was maintained at 85-90% of peak cycle ergometer O2 uptake (VO2) for cycle training by increasing power output approximately 11 W/wk and at approximately 100% of VO2max for run training by increased (P less than 0.01) approximately 950 ml/min (approximately 32%) and was correlated with training duration (r = 0.91; P less than 0.01). Training-induced increases (P less than 0.05) in interventricular septal thickness (IVS, mm) during both systole (13.4 +/- 0.9 to 14.9 +/- 0.8) and diastole (10.4 +/- 0.6 to 11.5 +/- 0.7) and in left ventricular end-diastolic dimension (4.96 +/- 0.16 to 5.13 +/- 0.19 cm). The absolute values of left ventricular end diastolic volume (LVEDV), stroke volume, ejection fraction, and left ventricular mass (LVM) increased (P less than 0.05) after training. Increases (P less than 0.05) in LVEDV index (64.3 +/- 3.3 to 69.0 +/- 3.4 ml/m2) and LVM index (114.1 +/- 6.5 to 124.5 +/- 7.3 g/m2) were also evident.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

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↗

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↗

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↗