Don - Give your heart plenty of time to heal before doing anything too strenuous
You should be aware of the fact that the 'scarring' which is is the term EPs use for fibrosis is the result of magnesium deficiency and oxidative stress damage (ROS and inflammation) ... as discussed in several previous posts that mention the findings of William Rowe, MD, with long distance runners and the fibrosis resulting from free radical damage and continually elevated catecholamines. Cardiac fibrosis is a common finding in afibbers with a history of intense, prolonged endurance exercise. The ablation doesn't stop future formation of fibrosis.
If you haven't used supplemental magnesium prior to your ablation, it's excellent post-ablation support. Most people don't get enough magnesium from food to meet the requirements of the body… and magnesium is easily and quickly depleted by stress, (exercise is a form of stress), various drugs, alcohol and more. (many posts here on the function and importance of magnesium... use the advance search feature).
If you read through Conference Room 75 and also 24, both discuss causes of Cardiac Fibrosis.
Previous Posts – the first includes CR 75 and 24 hyperlinks
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From the William Rowe report:
Direct myocardial injury
The mechanism for catecholamine-induced myocardial scarring[11-13] is not limited to ischaemia.[28] Along with several other mechanisms,[11,13,29,30] formation of high concentrations of free fatty acids by catecholamine-induced lipolysis[19] can be very injurious.[30] However, emphasis has been placed on the ischaemic mechanism since the single case supporting this hypothesis showed evidence of exercise-induced ischaemia,[7] which could also explain the apparent recurrence of pulmonary oedema in the South African runners.[6] This mechanism also provides a teleological rationale[2] for ensuring adequate rest periods between endurance exercise for regression of ischaemia and endothelial repair. Furthermore, in the presence of an endothelial injury,[12] an ischaemic insult to the myocardium may occur at lower (ie, more plausible) catecholamine concentrations[10] than those possibly required for a direct myocardial injury.[29] Epidemiological studies to confirm this hypothesis would require necropsy examinations to establish the presence of focal fibrosis and to exclude confounding factors. One factor would be pathological ventricular hypertrophy since this process may itself cause myocardial necrosis.[31]
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I wish you well with your healing process and a long, afib free life!
Healthy regards,
Jackie