The impact of endurance exercise training on the heart has received significant research and clinical attention for well over a century. Despite this, many issues remain controversial and clinical interpretation can be complex of biomarkers of cardiomyocyte insult. This review assesses the current state of knowledge related to two areas of research where problems with clinical decision making may arise: (1) the impact of chronic endurance exercise training on cardiac structure, function and electrical activity to the point where the athletic heart phenotype may be similar to the expression of some cardiac pathologies (a diagnostic dilemma referred to as the ‘grey-zone’) and (2) the impact of acute bouts of prolonged exercise on cardiac function and the presentation of biomarkers and cardiomyocyte insult in the circulatory system. The combination of acute endurance exercise stress on the heart and prolonged periods of training are considered together in the final section.

https://bjsm.bmj.com/content/bjsports/46/Suppl_1/i29.full.pdf

The endurance athletes heart: acute stress and chronic adaptation

Ventricular tachyarrhythmias commonly occur in trained athletes during ambulatory Holter electrocardiography and are usually associated with a benign course. Such arrhythmias have been demonstrated to be sensitive to short periods of athletic deconditioning; however, their response to retraining is not known. Twenty-four hour Holter electrocardiographic monitoring was performed at peak training and after 3 to 6 months of deconditioning and was repeated in the present study after 2, 6, and 12 months of retraining in 37 athletes with frequent and complex ventricular tachyarrhythmias and without cardiovascular abnormalities. These subjects showed partial (101 to 500 ventricular premature complexes [VPCs]/24 hours) or marked (<100 VPCs) reversibility of arrhythmias after deconditioning. Retraining initially resulted in a significant increase in arrhythmia frequency compared with deconditioning (from 280 ± 475 to 1,542 ± 2,186 VPCs; p = 0.005), couplets (0.14 ± 0.42 to 4.4 ± 8.2; p = 0.005), and nonsustained ventricular tachycardia (from 0 to 0.8 ± 1.8; p = 0.02). Subsequently, a progressive reduction was seen in the frequency of all ventricular arrhythmias during the 1 year of training to well below that at the peak training levels (VPCs 917 ± 1,630, couplets 1.8 ± 4.2, and nonsustained ventricular tachycardia 0.4 ± 1.2). Such annual arrhythmia reduction was significantly greater statistically in those athletes with marked reversibility after deconditioning than in the athletes with partial reversibility (69 ± 139 vs 1,496 ± 1,917 VPCs/24 hours, respectively; p = 0.007). No cardiac events or symptoms occurred during 1 year of follow-up. In conclusion, in elite athletes without cardiovascular disease, a resumption in intense training after deconditioning was associated with variable, but prolonged, suppression of ventricular ectopy. The absence of adverse clinical events or symptoms associated with the resumption of training supports the continued eligibility in competitive sports for such athletes and is also consistent with the benign nature of physiologic athlete's heart syndrome.

Patterns of Ventricular Tachyarrhythmias Associated With Training, Deconditioning and Retraining in Elite Athletes Without Cardiovascular Abnormalities

The parasympathetic nervous system innervates the heart through two cervical vagal branches. The right vagal branch mainly influences the heart rate by the modulation of the rhythmogenesis of the s...

AV blocking due to asynchronous vagal stimulation in rats

Aims: To evaluate cardiac arrhythmias and rhythm disturbances on 24 h ambulatory electrocardiographic monitoring in a cohort of asymptomatic healthy individuals with normal clinical

Cardiac Arrhythmias and Atrioventricular Block in a Cohort of Asymptomatic Individuals without Heart Disease

LV Dimension and Nonsustained Ventricular Arrhythmia. Introduction: To test the hypothesis that frequent nonsustained ventricular premature heats (VPBs) in patients without underlying heart disease are the first marker of mild systolic dysfunction of the left ventricle, we evaluated whether a subclinical abnormality of left ventricular function and/or an intraventricular conduction defect was present at the first clinical documentation of the arrhythmia.



Methods and Results: We compared 57 patients (mean age 46 ± 14 years) with > 30 VPBs/hour and no heart disease (A) to 32 healthy volunteers (mean age 42 ± 12 years) without arrhythmia (B). Left ventricular echocardiographic parameters and signal-averaged ECG were evaluated. Filtered QRS duration (98 ± 10 msec in A vs 98 ± 7 msec in B) was similar in the two groups. End-diastolic left ventricular diameter (EDLVD) was 50 ± 6 mm in A versus 47 ± 3 mm in B (P < 0.005); 15 patients (26%) and none of the controls had EDLVD & 55 mm (P < 0.005). Filtered QRS interval was longer in the subgroup of patients (n = 15) with increased EDLVD (≥ 55 mm) compared with the subgroup (n = 42) with EDLVD < 55 mm (106 ± 9 msec vs 95 ± 9 msec; P < 0.001) and was related to greater left ventricular mass.



Conclusion: We documented a subclinical but significant increase of left ventricular dimensions that suggests that frequent VPBs may he an initial marker of mild systolic dysfunction of the left ventricle. However, an effect of VPBs per se in modifying left ventricular dimensions cannot he excluded.

Increased left ventricular dimensions in patients with frequent nonsustained ventricular arrhythmia and no evidence of underlying heart disease

The aim of this study was to assess the prevalence and the prognostic value of ventricular late potentials in apparently healthy top-level athletes with ventricular arrhythmias, and the effect of physiological myocardial hypertrophy (athlete's heart) on the electrogenesis of the signal-averaged electrocardiogram (ECG). Two groups of asymptomatic athletes without underlying heart disease were studied: group A consisted of 35 athletes without arrhythmias and group B of 25 athletes with frequent and complex ventricu lar arrhythmias (ventricular ectopic beats >5000. 24 h−1 and ventricular couplets >15 . 24 h−1). Late potentials were present if athletes had significantly prolonged filtered QRS and low amplitude signal duration and low root mean square voltages at both 25–250 Hz and 40–250 Hz filters. While late potentials were absent in all normal athletes of group A, they were present in seven of 25 (28%) athletes with arrhythmias of group B ( P <0·003 Ten of 25 athletes (five with and five without late potentials) of group B underwent programmed ventricular stimulation using a protocol comprising up to three extrastimuli. No episode of sustained ventricular tachycardia was induced. In four of five athletes with late potentials and in one of five without them, unsustained ventricular responses were induced. Echocardiographically determined left ventricular mass found in both groups of athletes did not influence the pathological result of the signal-averaged ECG parameters.

This study shows the applicability of the signal-averaged ECG in identifying ventricular late potentials in a selected population of top-level athletes with frequent and complex ventricular arrhythmias and without overt heart disease; it also shows that the presence of late potentials is not influenced by left ventricular mass, even if extreme (>350 g), and it is correlated to a non-sustained ventricular response during an electrophysiological study.

L. Verdile

Papers

Ventricular arrhythmias and athlete's heart. Role of signal-averaged electrocardiography.