Longitudinal Study Examining the Relationship Between Structural and Electrical Changes Associated with Exercise

Editor's Note: Commentary based on McNamara DA, Aiad N, Howden E, et al. Left atrial electromechanical remodeling following 2 years of high-intensity exercise training in sedentary middle-aged adults. Circulation 2019;139:1507-16.

Background

  • Regular, moderate-intensity exercise has been associated with a reduced risk of atrial fibrillation (AF). However, epidemiological data suggests a U-shaped relationship between the amount of exercise and incident AF; increased risk of AF is seen in inactive individuals and also in those with long term exposure to high-intensity exercise.1
  • Potential mechanisms for the increased incidence of AF in an athletic cohort includes maladaptive left atrial (LA) remodeling with conduction system fibrosis, increased vagal tone, sympathetic surges with exercise, atrial ectopy and oxidative stress amongst others.2 The "dam wall" theory has been proposed to explain the hemodynamics of exercise and subsequent atrial remodeling. Increased cardiac output during exercise subject the heart valves, or dams, to a higher volume over a shorter period of time. Resultant flooding of the dam into the lower pressure atria chambers can occur, leading to remodeling seen with exercise.3
  • Electrical predictors of AF in athletes include the filtered P-wave duration, atrial late potentials, as well as presence of premature atrial contractions.
  • McNamara and colleagues designed a prospective randomized clinical trial to explore the theory that with high-intensity exercise, LA structural changes will lead to electrical changes and an increase in AF over time.

Methods

  • 262 previously sedentary, middle-aged subjects were screened, and after exclusion for known risk factors for AF and a brief screening period for AF, 61 subjects were randomized to either a 24-month exercise training program or a non-aerobic exercise, balance and flexibility control group. The exercise program consisted of 10 months of increasing exercise load, based on frequency, intensity and duration of exercise, until a peak exercise regimen was reached, followed by 14 months of a maintenance exercise program. Additionally, a competitive asters age-match group of 14 patients were studied to provide reference for comparison to the exercise group. 28 and 25 subjects from the exercise and control group were analyzed, respectively. There was an 88% compliance with the exercise intervention.

Results

  • Echocardiographic data: in the exercise group, LA and LV volumes increased proportionally after the 10 month training phase; however, after the maintenance phase, the LA volume continued to increase while LV volumes remained the same (increased LA:LV ratio). In comparison to the masters athletes, the absolute chamber volumes were lower but the LA:LV ratio was comparable. Minimal changes in chamber volumes were seen in the control group over time. The mean LA ejection fraction (EF) remained unchanged in the control group and increased in the exercise group. The mean LA EF observed in the exercise and Masters groups were similar. Active emptying percentage decreased in both the exercise and control groups.
  • Electrocardiographic data: there was no change in either group regarding filtered P-wave duration or atrial late potentials, and there was no difference in premature atrial contractions between the two groups. Neither group was found to develop AF based on their heart rate monitoring protocol.

Conclusion

  • 24 months of intense exercise training in a previously sedentary middle-aged population resulted in a disproportionate increase in LA volume compared to LV volume without evidence of significant electrical alterations in atrial activation.
  • Exercise induced morphological changes may proceed electrical remodeling suggesting that cumulative lifetime exposure to exercise rather than exercise intensity may be the more important predictor of AF in this cohort.

Perspective

  • LA enlargement is associated with an increased risk for AF, heart failure and death, and as we learn more, it continues to be implicated as a harbinger for other diseases. While increased exposure to exercise has been linked to both a higher incidence of AF and increased LA size, a causal relationship between LA size and subsequent AF will need to be further explored with longer-term prospective clinical exercise trials. It remains important to counsel our athletic patients about the risk of AF with exercise while the mechanistic connection is explored.

References

  1. Calvo N, Ramos P, Montserrat S, et al. Emerging risk factors and the dose-response relationship between physical activity and lone atrial fibrillation: a prospective case-control study. Europace 2016;18:57-63.
  2. Mont L. Arrhythmias and sport practice. Heart 2010;96:398-405.
  3. LaGerche A, Claessen G. Increased flow, dam walls, and upstream pressure: the physiological challenges and atrial consequences of intense exercise. JACC Cardiovasc Imaging 2016;9:1389-91.

Clinical Topics: Arrhythmias and Clinical EP, Diabetes and Cardiometabolic Disease, Heart Failure and Cardiomyopathies, Noninvasive Imaging, Prevention, Sports and Exercise Cardiology, Implantable Devices, Atrial Fibrillation/Supraventricular Arrhythmias, Acute Heart Failure, Echocardiography/Ultrasound, Exercise, Stress, Sports and Exercise and Imaging

Keywords: Atrial Fibrillation, Atrial Premature Complexes, Atrial Remodeling, Control Groups, Risk Factors, Longitudinal Studies, Athletes, Prospective Studies, Stroke Volume, Heart Rate, Heart Conduction System, Electrocardiography, Heart Atria, Cardiac Output, High, Sports, Heart Failure, Exercise, Heart Valves, Exercise Therapy, Echocardiography, Oxidative Stress


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