Aerobic interval training partly reverse contractile dysfunction and impaired Ca2+ handling in atrial myocytes from rats with post infarction heart failure

PLoS One. 2013 Jun 14;8(6):e66288. doi: 10.1371/journal.pone.0066288. Print 2013.

Abstract

Background: There is limited knowledge about atrial myocyte Ca(2+) handling in the failing hearts. The aim of this study was to examine atrial myocyte contractile function and Ca(2+) handling in rats with post-infarction heart failure (HF) and to examine whether aerobic interval training could reverse a potential dysfunction.

Methods and results: Post-infarction HF was induced in Sprague Dawley rats by ligation of the left descending coronary artery. Atrial myocyte shortening was depressed (p<0.01) and time to relaxation was prolonged (p<0.01) in sedentary HF-rats compared to healthy controls. This was associated with decreased Ca(2+) amplitude, decreased SR Ca(2+) content, and slower Ca(2+) transient decay. Atrial myocytes from HF-rats had reduced sarcoplasmic reticulum Ca(2+) ATPase activity, increased Na(+)/Ca(2+)-exchanger activity and increased diastolic Ca(2+) leak through ryanodine receptors. High intensity aerobic interval training in HF-rats restored atrial myocyte contractile function and reversed changes in atrial Ca(2+) handling in HF.

Conclusion: Post infarction HF in rats causes profound impairment in atrial myocyte contractile function and Ca(2+) handling. The observed dysfunction in atrial myocytes was partly reversed after aerobic interval training.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Caffeine / pharmacology
  • Calcium / metabolism*
  • Calcium Signaling*
  • Cardiotonic Agents / pharmacology
  • Electric Stimulation
  • Exercise Therapy
  • Female
  • Heart Atria / pathology*
  • Muscle Cells / drug effects
  • Muscle Cells / physiology*
  • Myocardial Contraction
  • Myocardial Infarction / physiopathology
  • Myocardial Infarction / therapy*
  • Oxygen Consumption
  • Physical Conditioning, Animal
  • Rats
  • Rats, Sprague-Dawley
  • Sarcoplasmic Reticulum Calcium-Transporting ATPases / metabolism

Substances

  • Cardiotonic Agents
  • Caffeine
  • Sarcoplasmic Reticulum Calcium-Transporting ATPases
  • Calcium

Grants and funding

This work was supported by grants from K.G. Jebsen Foundation and the Norwegian Research Council Funding for Outstanding Young investigators (to Ulrik Wisløff). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.