Abstract
BackgroundAtrial fibrillation (AF) is the most common arrhythmia and is often associated with altered Ca2+ handling. Evidence points to low aerobic capacity as predictor of cardiovascular disease and AF. The hypothesis of the present study was that rats, genetically selected on the basis of low running capacity has impaired Ca2+ handling compared to rats selected for high running capacity.MethodLow capacity runners (LCR) (n=5) develop characteristics of the metabolic syndrome, and high capacity runners (n=5) develop a healthy and athletic phenotype. The exercise capacity was measured by VO2max. Ca2+ handling were measured in isolated Fura-2/AM loaded atrial cardiomyocytes.ResultsVO2max was 30% lower in LCR than HCR. Cardiomyocyte function was significantly depressed in LCR; fractional shortening was 52% lower and time to 50% relenghtening was 42% prolonged. We observed no differences in peak systolic and diastolic Ca2+, as well as no significant difference in amplitude of Ca2+ transient between the two groups. This indicate reduced Ca2+sensitivity in cardiomyocytes from LCR. SR Ca2+ load, assessed by caffeine-induced Ca2+ release, was not different between groups. Time to 50% Ca2+ transient decay was prolonged by 58% in LCR. We found no difference in Ca2+ decay between the two groups during caffeine induced Ca2+ transient, reflecting unaltered NCX function; neither did we find any changes in the plasma membrane Ca2+ exchanger (PMCA). The impaired diastolic Ca2+removal is therefore mainly attributed to reduced SERCA function in LCR (39%). Diastolic SR Ca2+ leak was increased in LCR compared to HCR.ConclusionOur data demonstrate differences in atrial Ca2+handling between rats selected for high and low aerobic capacity and we suggest that impaired Ca2+ handling in LCR may be an important factor in initiation of AF.
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