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Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle
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Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle

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Mitochondrial ATPase and high-energy phosphates in failing hearts

J Liu1, C Wang, Y Murakami

  • 1Department of Medicine, University of Minnesota Health Sciences, Minneapolis, Minnesota 55455, USA.

American Journal of Physiology. Heart and Circulatory Physiology
|August 22, 2001
PubMed

Insights

In heart failure, high-energy phosphates decrease, impacting mitochondrial function. This study shows reduced mitochondrial ATPase protein expression in failing hearts, linked to increased ADP levels.

Area of Science:

  • Cardiology
  • Biochemistry
  • Physiology

Background:

  • Myocardial infarction can lead to left ventricular remodeling (LVR) or congestive heart failure (CHF).
  • High-energy phosphates (HEP) are crucial for cardiac function.
  • Mitochondrial ATPase is vital for cellular energy production.

Purpose of the Study:

  • To investigate high-energy phosphates (HEP) and mitochondrial ATPase protein expression in pigs with LVR or CHF post-myocardial infarction.
  • To assess the cardiac response to increased workload in these conditions.

Main Methods:

  • Utilized (31)P magnetic resonance spectroscopy to measure HEP.
  • Administered dobutamine-dopamine infusion and pacing to increase cardiac workload.
  • Analyzed mitochondrial F(0)F(1)-ATPase subunit protein expression via Western blotting.
  • Compared pigs with LVR (n=9), CHF (n=8), and normal controls (n=7).

Main Results:

  • Hearts with LVR showed decreased phosphocreatine (PCr)-to-ATP ratio and increased ADP at baseline.
  • These changes were more pronounced in hearts with CHF.
  • HEP levels remained stable in normal and LVR hearts during dobutamine-dopamine infusion.
  • CHF hearts exhibited further decreases in PCr-to-ATP ratio and increases in ADP.
  • Failing hearts displayed significant reductions in mitochondrial F(0)F(1)-ATPase subunits (alpha: -36%, beta: -16%, oligomycin sensitivity-conferring protein: -40%, initiation factor 1: -41%).

Conclusions:

  • Reduced mitochondrial F(0)F(1)-ATPase protein expression in failing hearts is associated with elevated myocardial free ADP.
  • These molecular changes likely contribute to the impaired energy metabolism observed in heart failure.

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