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Exercise & afib
Posted by Rob Wilson
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Re: Exercise & afib January 01, 2022 01:33PM |
Exercise-Related Acute Cardiovascular Events and Potential Deleterious Adaptations Following Long-Term Exercise Training: Placing the Risks Into Perspective–An Update: A Scientific Statement From the American Heart Association
"Recent studies have also shown that large exercise volumes and vigorous intensities are both associated with potential cardiac maladaptations, including accelerated coronary artery calcification, exercise-induced cardiac biomarker release, myocardial fibrosis, and atrial fibrillation. The relationship between these maladaptive responses and physical activity often forms a U- or reverse J-shaped dose-response curve. "
[www.ahajournals.org]
Atrial Fibrillation
AF is characterized by chaotic electrical activity that replaces normal sinus rhythm and eliminates the contribution of atrial contraction to left ventricular filling. AF is the most common arrhythmia in the general population,168 and the risk of AF depends on subject characteristics (age, race, height), health status (weight, blood pressure, [para]sympathetic tone, diabetes mellitus, a history of MI or heart failure), lifestyle factors (alcohol use, smoking, PA), obstructive sleep apnea,169 and cardiac characteristics (left atrial size and pressure).170,171 AF is associated with an increased risk for stroke,172 MI,173 heart failure,174 and a multitude of adverse clinical consequences.175
The relation between exercise and incident AF is complicated. Low levels of CRFe (<6 METs) are associated with a higher risk for AF, and individuals with higher levels of CRFe (7.9±1.0 and 9.3±1.2 METs) have a dose-dependent decrease in AF risk.176,177 Similarly, fit AF patients have a lower risk for AF recurrences during follow-up than their unfit counterparts.178 AF burden and symptom severity decreased significantly in patients with AF who increased their fitness during an exercise training program versus those who failed to improve178 and among patients with AF randomized to aerobic interval training in a small clinical trial.179 Although these observations suggest that fitter individuals have the lowest AF risk, there is substantial evidence that the risk for AF is higher in athletes than in control subjects. High-intensity exercise training180 and faster finishing times181 were associated with an increase of AF in physically active older adults and long-distance cross-country skiers, respectively. In the US Physician’s Health Study, men who jogged 5 to 7 times per week had a 50% higher risk of AF than men who did not exercise vigorously, even after adjustment for multiple cardiovascular risk factors.182 Three meta-analyses found that AF risk was 2- to 10-fold higher in endurance athletes than in control participants.170,183,184 Furthermore, long-term volume of vigorous endurance exercise (ie, ≥2000 hours of training169 or ≥20 years of training185) was strongly associated with an increased risk for lone AF. These data suggest that both low and very high volumes of exercise training are associated with an increased risk for AF, whereas moderate exercise volumes appear to reduce risk. Indeed, a nonlinear meta-regression analysis including data from 19 studies and 29 855 AF cases found a J-shaped association between PA volumes and risk for AF.186 Individuals performing 5 to 20 MET-hours of PA per week had a significantly lower risk for AF, whereas physically inactive or highly active individuals (20−55 MET-h/wk) had similar relative risks for AF (Figure 6). A trend toward increased AF risk is apparent among individuals reporting >55 MET-h/wk, equaling >9.5 hours of vigorous exercise training per week.
Figure 6. Dose–response association between physical activity volume and AF risk.
Individuals performing physical activity for 5 to 20 MET-h/wk demonstrate a significant risk reduction for AF, whereas higher exercise volumes do not appear to attenuate AF risk. A trend toward increased AF risk is apparent among individuals reporting >55 MET-h/wk. AF indicates atrial fibrillation; and MET-hrs/week, metabolic equivalents of task hours per week. Adapted from Ricci et al186 by permission of SAGE Publications, Ltd. Copyright © 2018, by the European Society of Cardiology.
The underlying mechanisms responsible for the increased prevalence of AF among athletes are unknown, but several pathways have been proposed (Figure 7). A prolonged (2 year) training study incorporating high-intensity training sessions showed that although left ventricular remodeling appears to plateau when training load plateaus, left atrial remodeling continues, even when the training dose is stable.187 This finding suggests that the atria are especially prone to dilation and remodeling in individuals who have trained at a high level for many years. Interindividual genetic variability could also put some athletes at a higher risk of pathological remodeling leading to lone AF.188–190 Furthermore, increased parasympathetic tone191 in combination with left atrial enlargement192 is likely to contribute to the increased AF risk, but exercise-induced sympathetic stimulation,193 sustained hemodynamic stress,194 and inflammation and oxidative stress195 could also contribute to the development of AF in the most active exercisers.
Figure 7. Potential mechanisms and associated sequelae for atrial fibrillation induced by strenuous endurance exercise.
The combination of autonomic, structural, and hemodynamic effects of high-volume, high-intensity aerobic exercise, repeated over time, likely impart some of the increased risk for atrial fibrillation. Adapted from Eijsvogels et al.37 Copyright © 2018, The Authors. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
In summary, the reported negative impact of high-volume, high-intensity exercise on maladaptive responses, specifically AF, varies considerably, according to the quality of evidence available. Indeed, differences in study methodology have led to varying estimates regarding the magnitude of risk, ranging from an ≈20% increase to a >10-fold risk of incident AF.196 And, for obvious reasons, there may never be randomized, controlled quality evidence addressing the potential for an “alternative hypothesis” or U-shaped relation between exercise and AF.
Training for Longevity: The Reverse J-Curve for Exercise [www.ncbi.nlm.nih.gov]
Dose of jogging and long-term mortality: the Copenhagen City Heart Study [pubmed.ncbi.nlm.nih.gov] (not afib specific)
Edited 2 time(s). Last edit at 01/01/2022 01:42PM by GeorgeN.
"Recent studies have also shown that large exercise volumes and vigorous intensities are both associated with potential cardiac maladaptations, including accelerated coronary artery calcification, exercise-induced cardiac biomarker release, myocardial fibrosis, and atrial fibrillation. The relationship between these maladaptive responses and physical activity often forms a U- or reverse J-shaped dose-response curve. "
[www.ahajournals.org]
Atrial Fibrillation
AF is characterized by chaotic electrical activity that replaces normal sinus rhythm and eliminates the contribution of atrial contraction to left ventricular filling. AF is the most common arrhythmia in the general population,168 and the risk of AF depends on subject characteristics (age, race, height), health status (weight, blood pressure, [para]sympathetic tone, diabetes mellitus, a history of MI or heart failure), lifestyle factors (alcohol use, smoking, PA), obstructive sleep apnea,169 and cardiac characteristics (left atrial size and pressure).170,171 AF is associated with an increased risk for stroke,172 MI,173 heart failure,174 and a multitude of adverse clinical consequences.175
The relation between exercise and incident AF is complicated. Low levels of CRFe (<6 METs) are associated with a higher risk for AF, and individuals with higher levels of CRFe (7.9±1.0 and 9.3±1.2 METs) have a dose-dependent decrease in AF risk.176,177 Similarly, fit AF patients have a lower risk for AF recurrences during follow-up than their unfit counterparts.178 AF burden and symptom severity decreased significantly in patients with AF who increased their fitness during an exercise training program versus those who failed to improve178 and among patients with AF randomized to aerobic interval training in a small clinical trial.179 Although these observations suggest that fitter individuals have the lowest AF risk, there is substantial evidence that the risk for AF is higher in athletes than in control subjects. High-intensity exercise training180 and faster finishing times181 were associated with an increase of AF in physically active older adults and long-distance cross-country skiers, respectively. In the US Physician’s Health Study, men who jogged 5 to 7 times per week had a 50% higher risk of AF than men who did not exercise vigorously, even after adjustment for multiple cardiovascular risk factors.182 Three meta-analyses found that AF risk was 2- to 10-fold higher in endurance athletes than in control participants.170,183,184 Furthermore, long-term volume of vigorous endurance exercise (ie, ≥2000 hours of training169 or ≥20 years of training185) was strongly associated with an increased risk for lone AF. These data suggest that both low and very high volumes of exercise training are associated with an increased risk for AF, whereas moderate exercise volumes appear to reduce risk. Indeed, a nonlinear meta-regression analysis including data from 19 studies and 29 855 AF cases found a J-shaped association between PA volumes and risk for AF.186 Individuals performing 5 to 20 MET-hours of PA per week had a significantly lower risk for AF, whereas physically inactive or highly active individuals (20−55 MET-h/wk) had similar relative risks for AF (Figure 6). A trend toward increased AF risk is apparent among individuals reporting >55 MET-h/wk, equaling >9.5 hours of vigorous exercise training per week.
Figure 6. Dose–response association between physical activity volume and AF risk.
Individuals performing physical activity for 5 to 20 MET-h/wk demonstrate a significant risk reduction for AF, whereas higher exercise volumes do not appear to attenuate AF risk. A trend toward increased AF risk is apparent among individuals reporting >55 MET-h/wk. AF indicates atrial fibrillation; and MET-hrs/week, metabolic equivalents of task hours per week. Adapted from Ricci et al186 by permission of SAGE Publications, Ltd. Copyright © 2018, by the European Society of Cardiology.
The underlying mechanisms responsible for the increased prevalence of AF among athletes are unknown, but several pathways have been proposed (Figure 7). A prolonged (2 year) training study incorporating high-intensity training sessions showed that although left ventricular remodeling appears to plateau when training load plateaus, left atrial remodeling continues, even when the training dose is stable.187 This finding suggests that the atria are especially prone to dilation and remodeling in individuals who have trained at a high level for many years. Interindividual genetic variability could also put some athletes at a higher risk of pathological remodeling leading to lone AF.188–190 Furthermore, increased parasympathetic tone191 in combination with left atrial enlargement192 is likely to contribute to the increased AF risk, but exercise-induced sympathetic stimulation,193 sustained hemodynamic stress,194 and inflammation and oxidative stress195 could also contribute to the development of AF in the most active exercisers.
Figure 7. Potential mechanisms and associated sequelae for atrial fibrillation induced by strenuous endurance exercise.
The combination of autonomic, structural, and hemodynamic effects of high-volume, high-intensity aerobic exercise, repeated over time, likely impart some of the increased risk for atrial fibrillation. Adapted from Eijsvogels et al.37 Copyright © 2018, The Authors. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
In summary, the reported negative impact of high-volume, high-intensity exercise on maladaptive responses, specifically AF, varies considerably, according to the quality of evidence available. Indeed, differences in study methodology have led to varying estimates regarding the magnitude of risk, ranging from an ≈20% increase to a >10-fold risk of incident AF.196 And, for obvious reasons, there may never be randomized, controlled quality evidence addressing the potential for an “alternative hypothesis” or U-shaped relation between exercise and AF.
Training for Longevity: The Reverse J-Curve for Exercise [www.ncbi.nlm.nih.gov]
Dose of jogging and long-term mortality: the Copenhagen City Heart Study [pubmed.ncbi.nlm.nih.gov] (not afib specific)
Edited 2 time(s). Last edit at 01/01/2022 01:42PM by GeorgeN.
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