High intensity interval and endurance training have opposing effects on markers of heart failure and cardiac remodeling in hypertensive rats

PLoS One. 2015 Mar 24;10(3):e0121138. doi: 10.1371/journal.pone.0121138. eCollection 2015.

Abstract

There has been re-emerging interest and significant work dedicated to investigating the metabolic effects of high intensity interval training (HIIT) in recent years. HIIT is considered to be a time efficient alternative to classic endurance training (ET) that elicits similar metabolic responses in skeletal muscle. However, there is a lack of information on the impact of HIIT on cardiac muscle in disease. Therefore, we determined the efficacy of ET and HIIT to alter cardiac muscle characteristics involved in the development of diastolic dysfunction, such as ventricular hypertrophy, fibrosis and angiogenesis, in a well-established rodent model of hypertension-induced heart failure before the development of overt heart failure. ET decreased left ventricle fibrosis by ~40% (P < 0.05), and promoted a 20% (P<0.05) increase in the left ventricular 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 displayed a 20% increase in left ventricular mass (P<0.05) and a 20% decrease in cross sectional area (P<0.05). HIIT also increased brain natriuretic peptide by 50% (P<0.05), in the absence of concomitant angiogenesis, strongly suggesting pathological cardiac remodeling. The current data support the longstanding belief in the effectiveness of ET in hypertension. However, HIIT promoted a pathological adaptation in the left ventricle in the presence of hypertension, highlighting the need for further research on the widespread effects of HIIT in the presence of disease.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Biomarkers / blood
  • Heart Failure / metabolism
  • Heart Failure / physiopathology*
  • Hypertension / metabolism
  • Hypertension / physiopathology*
  • Hypertrophy, Left Ventricular / metabolism
  • Hypertrophy, Left Ventricular / physiopathology
  • Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • Male
  • Nitric Oxide Synthase Type III / metabolism
  • Physical Conditioning, Animal / physiology*
  • Physical Endurance
  • Random Allocation
  • Rats
  • Rats, Inbred Dahl
  • Sodium, Dietary / administration & dosage
  • Ventricular Remodeling*

Substances

  • Biomarkers
  • Hif1a protein, mouse
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Sodium, Dietary
  • Nitric Oxide Synthase Type III
  • Nos3 protein, mouse

Grant support

This work was supported by Natural Science and Engineering Research Council of Canada Grant Number 2320 (http://www.nserc-crsng.gc.ca/). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.