title: Atrial remodeling, autonomic tone, and lifetime training hours in nonelite athletes.
abstract: Endurance athletes have an increased risk of developing atrial fibrillation (AF) at 40 to 50 years of age. Signal-averaged P-wave analysis has been used for identifying patients at risk for AF. We evaluated the impact of lifetime training hours on signal-averaged P-wave duration and modifying factors. Nonelite men athletes scheduled to participate in the 2010 Grand Prix of Bern, a 10-mile race, were invited. Four hundred ninety-two marathon and nonmarathon runners applied for participation, 70 were randomly selected, and 60 entered the final analysis. Subjects were stratified according to their lifetime training hours (average endurance and strength training hours per week × 52 × training years) in low (<1,500 hours), medium (1,500 to 4,500 hours), and high (>4,500 hours) training groups. Mean age was 42 ± 7 years. From low to high training groups signal-averaged P-wave duration increased from 131 ± 6 to 142 ± 13 ms (p = 0.026), and left atrial volume increased from 24.8 ± 4.6 to 33.1 ± 6.2 ml/m(2) (p = 0.001). Parasympathetic tone expressed as root of the mean squared differences of successive normal-to-normal intervals increased from 34 ± 13 to 47 ± 16 ms (p = 0.002), and premature atrial contractions increased from 6.1 ± 7.4 to 10.8 ± 7.7 per 24 hours (p = 0.026). Left ventricular mass increased from 100.7 ± 9.0 to 117.1 ± 18.2 g/m(2) (p = 0.002). Left ventricular systolic and diastolic function and blood pressure at rest were normal in all athletes and showed no differences among training groups. Four athletes (6.7%) had a history of paroxysmal AF, as did 1 athlete in the medium training group and 3 athletes in the high training group (p = 0.252). In conclusion, in nonelite men athletes lifetime training hours are associated with prolongation of signal-averaged P-wave duration and an increase in left atrial volume. The altered left atrial substrate may facilitate occurrence of AF. Increased vagal tone and atrial ectopy may serve as modifying and triggering factors.
authors.affiliation: Department of Cardiology, Division of Cardiovascular Prevention, Rehabilitation and Sports Cardiology, Inselspital, University Hospital and University of Bern, Bern, Switzerland. matthias.wilhelm@insel.ch
authors.forename: Matthias
authors.initials: M
authors.lastname: Wilhelm
authors.forename: Laurent
authors.initials: L
authors.lastname: Roten
authors.forename: Hildegard
authors.initials: H
authors.lastname: Tanner
authors.forename: Ilca
authors.initials: I
authors.lastname: Wilhelm
authors.forename: Jean-Paul
authors.initials: JP
authors.lastname: Schmid
authors.forename: Hugo
authors.initials: H
authors.lastname: Saner
mesh_terms: D000328:Adult; D056352:Athletes; D001281:Atrial Fibrillation / Q000175:diagnosis / Q000503:physiopathology*; D004562:Electrocardiography; D006325:Heart Atria / Q000294:innervation* / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D014630:Vagus Nerve