At our center there is a wide focus on increasing the knowledge of the mechanisms involved in heart disease, and developing methods aimed to prevent or treat disease. A recently published study by PhD student Anne Berit Johnsen and CERG colleagues provides a significant contribution to the field.
What we know from before, is that impaired cardiomyocyte contractility and Ca2+ handling is typically observed in patients with left ventricular contractile dysfunction. Further, previous studies have shown that exercise may improve the left ventricular function in patients suffering from heart failure after heart infarction. Exercise is also found to improve cardiomyocyte function and Ca2+ handling in rats with the same disease. But is there even beneficial effects of exercise on atrial myocyte function and Ca2+ handling?
To explore this, contractile function and Ca2+ handling in atrial myocytes of sham-operated rats and rats with post-infarction heart failure was compared. The effects of aerobic interval training was also investigated. The results were in line with what previous research: high intensity aerobic interval training restored atrial myocyte contractile function and reversed changes in atrial Ca2+ handling in heart failure rats.
This study increases our understanding of how atrial myocyte contractile dysfunction in post-infarction heart failure is associated with major impairment in Ca2+ handling, whereas aerobic interval training can restore the dysfunction via improved Ca2+ handling. As mentioned in a previous blog post, animal studies are important steps on the way to understanding the human heart. In future studies this model can help to highlight important mechanisms behind heart failure as a substrate that promotes atrial fibrillation, and also the effect of training as a treatment.
Maria Henningsen, CERG.