Aerobic Interval Training Partly Reverse Contractile Dysfunction and Impaired Ca2+ Handling in Atrial Myocytes from Rats with Post Infarction Heart Failure

Background: There is limited knowledge about atrial myocyte Ca2+ handling in the failing hearts. The aim of this study was to examine atrial myocyte contractile function and Ca2+ handling in rats with post-infarction heart failure (HF) and to examine whether aerobic interval training could reverse a potential dysfunction. Methods and results: Post-infarction HF was induced in Sprague Dawley rats by ligation of the left descending coronary artery. Atrial myocyte shortening was depressed (p<0.01) and time to relaxation was prolonged (p<0.01) in sedentary HF-rats compared to healthy controls. This was associated with decreased Ca2+ amplitude, decreased SR Ca2+ content, and slower Ca2+ transient decay. Atrial myocytes from HF-rats had reduced sarcoplasmic reticulum Ca2+ ATPase activity, increased Na+/Ca2+-exchanger activity and increased diastolic Ca2+ leak through ryanodine receptors. High intensity aerobic interval training in HF-rats restored atrial myocyte contractile function and reversed changes in atrial Ca2+ handling in HF. Conclusion: Post infarction HF in rats causes profound impairment in atrial myocyte contractile function and Ca2+ handling. The observed dysfunction in atrial myocytes was partly reversed after aerobic interval training.