Endurance training prevents, while high intensity interval training exacerbates, molecular markers of heart failure in cardiac muscle of hypertensive rats

Abstract

In recent years there has been considerable interest focused on investigating the metabolic effects of high intensity interval training (HIIT). HIIT is a time efficient alternative to classic endurance training (ET) that elicits similar metabolic responses in skeletal muscle. However, there is a lack of information regarding the impact of HIIT on cardiac muscle in disease states. Therefore, in a rodent model of hypertension-induced heart failure (HF), before overt HF developed, we determined the efficacy of ET and HIIT in ameliorating pathological remodeling. ET decreased left ventricle (LV) fibrosis by ~40% (P < 0.05), and promoted a 20% (P<0.05) increase in the LV capillary/fibre ratio, an increase in endothelial nitric oxide synthase protein (P<0.05), and a decrease in hypoxia inducible factor 1 alpha protein content (P<0.05). In contrast, HIIT did not decrease existing fibrosis, and HIIT animals developed a 20% (P<0.05) increase in LV mass in the absence of concomitant angiogenesis. These factors, along with a 50% increase (P<0.05) in the content of brain natriuretic peptide, strongly suggested pathological remodeling in response to HIIT. The current data support the longstanding belief in the effectiveness of ET in primary and secondary prevention in individuals with cardiovascular diseases. In contrast, HIIT exacerbated LV pathological remodeling LV in hypertensive rats, suggesting more investigation is required prior to commonplace application of HIIT in cardiovascular disease conditions.