Electrocardiographic Findings in Athletic Students and Sedentary Controls

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We have previously compared the electrocardiogram of 1,299 male and female students of physical education and sports with 151 age- and sex-matched sedentary controls and found that the former had lower heart rate, longer conduction times and increased voltages. The same material of 1,450 young adult subjects was split according to sex into 617 females and 833 males in order to analyze the influence of gender on the resting 12-lead electrocardiogram. We found that females had a significant higher heart rate, shortened conduction times (PQ, Q, ventricular activation time and QRS) and a prolonged repolarization time (QT_C), decreased P, Q and T amplitudes as well as indices of right, septal and left hypertrophy, and ST elevation in precordial leads were lower in females than in males. These differences were highly significant with p values < 0.0001 for almost all parameters. Sinus bradycardia was more common in men and sinus tachycardia in women. The prevalence of other rhythms and supraventricular and ventricular premature beats was low in both sexes. AV block grade I was found in 1 % of females and 3% of males (p < 0.02). Notching of R/S in V₁ – V₂ and incomplete right bundle branch block were less common in females (p < 0.0001). The differences in ECG parameters between the two sexes in the total material persisted also when the athletic and control groups were investigated separately. Gender seems to be highly important for most ECG parameters in the resting ECG. This points to the necessity of discussing different upper normal limits for ECG parameters according to gender.

Section: Sex Differences In Heart Size and Body Buildsupporting

confidence: 71%

“…The methods of recording are described in detail in a previous paper [25]. The following parameters were measured.…”

Section: Evaluation Of the Electrocardiogrammentioning

confidence: 99%

Electrocardiographic Findings according to Sex in Athletes and Controls

Storstein

Bjørnstad²,

Hals

et al. 1991

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“…Whereas most investigators have found complete regression of heart size in athletes on cessation of train ing [5], others have found increased heart size in former athletes [6], Many generations of doctors have been taught that the athlete's heart is a pathological state, and this view was maintained until 1970 in some cardiological textbooks. However, most studies indicate that the mortality of heart disease is un changed in former athletes who have stopped training, while it is decreased in those who have continued training [7], Hypertrophic cardiomyopathy is probably the most impor tant cause of death in young athletes, often with signs of left ventricular hypertrophy be ing present in the ECG [8], We have demon strated increased indices of septal, right and left ventricular hypertrophy in athletic stu dents compared to sedentary controls [9], The present investigation divides the material ac cording to common upper normal limits for hypertrophy with the aim of determining the prevalence of hypertrophy and the correlation to other ECG criteria.…”

Section: Introductionmentioning

confidence: 99%

Electrocardiographic Findings of Left, Right and Septal Hypertrophy in Athletic Students and Sedentary Controls

Bjørnstad¹,

Storstein²,

Meen³

et al. 1993

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We have previously demonstrated increased voltage of septal, right and left ventricular depolarization in 1,299 athletic students compared to 151 sedentary controls. In the present investigation we have studied the prevalence of hypertrophy and the correlation between hypertrophy and other ECG findings. An increase of Q waves of more than 0.2 mV was associated with increased indices of right and left ventricular hypertrophy. Right ventricular hypertrophy was associated with an increased prevalence of incomplete right bundle branch block and increased parameters of septal and left ventricular hypertrophy. Left ventricular hypertrophy was associated with increased indices of septal and right ventricular hypertrophy and with bradycardia. Furthermore, left ventricular hypertrophy was characterized by ST elevation and increased T wave amplitudes, but not by repolarization abnormalities. Thus, our data point to a harmonious hypertrophy. Based on our findings we suggest the following normal limits in young people (20-30 years) according to the 97.5 percentile regarding the Sokolow index: for athletic students 5.3 (males) and 3.6 mV (females), for sedentary controls 4.0 (males) and 3.6 mV (females). It remains to be clarified whether these values are also valid in top athletes.

“…ST elevation was measured in any precordial lead at J-point [4]. At baseline Del Mar Innovator Model 750 A [3], at follow-up Oxford Medilog FD4 was used for Holter monitoring.…”

Section: Methodsmentioning

confidence: 99%

“…Later there has been general agreement that these cardiac alterations are a physiological phenomenon [2]. The most characteristic ECG findings of athlete’s heart are bradycardia and sinus pauses, increased precordial ST elevations (in males), T wave and QRS amplitudes [3, 4]. The most characteristic echocardiographic findings are increased left ventricular volume and mass [5].…”

Section: Introductionmentioning

confidence: 99%

Long-Term Assessment of Electrocardiographic and Echocardiographic Findings in Norwegian Elite Endurance Athletes

Bjørnstad¹,

Bjørnstad²,

Urheim³

et al. 2008

Objectives: The long-term outcome and clinical significance of athlete’s heart has been debated and more longitudinal data are needed. We present a prospective 15 years’ follow-up study of ECG and echo findings in elite endurance athletes following the end of their competitive career. Methods: Clinical evaluation, ECG, ambulatory Holter recording and echocardiography were performed in 30 top-level endurance athletes with a mean age of 24 years with follow-up 15 years later. All had then ended their competitive career, but still performed recreational sports activities. Results: No clinical events were reported. Average resting heart rate was unchanged (53.5 ± 10 at baseline and 55.4 ± 11 at follow-up, p = n.s.), complex ventricular arrhythmias did not occur and the number of ventricular premature beats (VPBs) were 0.4 ± 0.8/h at baseline and 3.8 ± 10/h at follow-up (p = n.s.). In a subgroup of 4 subjects with >100 VPBs per hour at follow-up left ventricular mass was increased compared to the others (p < 0.03). Furthermore, regression of sino-atrial (SA) and atrioventricular (AV) blocks was shown. There were no cases of atrial flutter or fibrillation. There was a slight reduction in mean left ventricular wall thickness (9.9 ± 1.2 vs. 9.5 ± 1.4 mm, p < 0.05) and a highly significant reduction of relative wall thickness (0.38 vs. 0.35, p < 0.001). Left ventricular end-diastolic volume (68 ± 6 vs. 70 ± 7 ml ml/m², p = n.s.) and left ventricular mass (109 ± 19 vs. 107 ± 19 g/m², p = n.s.) were unchanged when corrected for body surface area and ejection fraction (EF) increased (60 ± 7 vs. 67 ± 6%, p < 0.01). Parameters of left ventricular diastolic function were normal both at baseline and follow-up. Conclusions: There was no evidence of deleterious cardiac effects of previous top-level endurance athletic activity at 15 years’ follow-up.