This investigation evaluated the key morphological and functional differences between the athlete’s heart and the failing heart. The athlete’s heart has minimally thickened LV walls and similar ventricular dilation. In contrast, during the initial stages of disease, hypertension causes thickening of LV walls with no dilation. As the disease progresses, the LV walls begin to thin and there is significant dilation. Exercise causes the release of IGF-1, which leads to cardiomyocyte growth via PI3K and Akt1. In the diseased myocardium, there is an increase in angiotensin II and ET-1. A better understanding of these different signaling pathways will lead to the development of better therapeutic intervention strategies for the treatment of heart disease.

Link to article: http://physiologyonline.physiology.org/content/26/2/97.long

Group Members:

Zoey Scharf

Stephen Shey

Lee Seymour

Jarod Shelton