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Related Experiment Videos

Sprint training normalizes Ca(2+) transients and SR function in postinfarction rat myocytes.

L Q Zhang1, X Q Zhang, Y C Ng

  • 1Department of Medicine, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey, Pennsylvania 17033, USA.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|July 25, 2000
PubMed
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High-intensity sprint training (HIST) improved cardiac function in rats after myocardial infarction (MI). HIST normalized intracellular calcium dynamics and contraction in MI myocytes by modulating phospholamban, not SR Ca2+-ATPase expression.

Area of Science:

  • Cardiology
  • Exercise Physiology
  • Molecular Biology

Background:

  • Myocardial infarction (MI) in rats leads to myocyte hypertrophy, altered intracellular calcium dynamics, and impaired sarcoplasmic reticulum (SR) function.
  • Sedentary conditions post-MI exacerbate these cardiac abnormalities, including prolonged calcium decline and reduced SR function.

Purpose of the Study:

  • To investigate the effects of high-intensity sprint training (HIST) on restoring intracellular calcium ([Ca(2+)](i)) dynamics and SR function in rat myocytes post-MI.
  • To determine if HIST can ameliorate myocyte hypertrophy and improve cardiac contractile function following myocardial infarction.

Main Methods:

  • Rats underwent myocardial infarction (MI) and were subsequently subjected to 6-8 weeks of high-intensity sprint training (HIST) or remained sedentary (Sed).

Related Experiment Videos

  • Myocyte hypertrophy was assessed by measuring whole cell capacitances.
  • Intracellular calcium ([Ca(2+)](i)) dynamics, including systolic [Ca(2+)](i) and the half-time of [Ca(2+)](i) decline, were measured.
  • Expression levels of SR Ca(2+)-ATPase and phospholamban were quantified using Western blotting.

    • Main Results:

    • HIST significantly reduced myocyte hypertrophy in MI rats, with cell capacitances returning to levels similar to sham-operated controls.
    • High-intensity sprint training restored systolic [Ca(2+)](i) and the half-time of [Ca(2+)](i) decline toward normal values in MI myocytes.
    • While SR Ca(2+)-ATPase expression decreased in MI-Sed and further in MI-HIST myocytes, phospholamban expression was significantly reduced in MI-HIST myocytes.

    Conclusions:

    • High-intensity sprint training instituted shortly after myocardial infarction improves intracellular calcium dynamics in surviving myocytes.
    • The beneficial effects of HIST on SR function post-MI are achieved through modulating phospholamban regulation of SR Ca(2+)-ATPase activity, rather than increasing SR Ca(2+)-ATPase expression.