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Function and bioenergetics in isolated perfused trained rat hearts

R G Spencer1, P M Buttrick, J S Ingwall

  • 1National Institutes of Health, National Institute on Aging, Baltimore, Maryland 21224, USA.

The American Journal of Physiology
|January 1, 1997
PubMed
Summary

Physiologically hypertrophied hearts from swim-trained rats show improved function during hypoxia and reoxygenation. Adaptations in the creatine kinase (CrK) system, not high-energy phosphate (HEP) levels, likely explain this enhanced resistance to hypoxic insult.

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Area of Science:

  • Cardiovascular Physiology
  • Exercise Physiology
  • Metabolic Biochemistry

Background:

  • Physiological cardiac hypertrophy, induced by endurance training, may confer resistance to stress.
  • Understanding the mechanisms behind this protective effect is crucial for cardiovascular health.

Purpose of the Study:

  • To evaluate the resistance of physiologically hypertrophied rat hearts to hypoxic insult.
  • To correlate functional changes with high-energy phosphate (HEP) metabolites and enzymatic activity.

Main Methods:

  • Quantified functional deficits during hypoxia/reoxygenation in swim-trained vs. sedentary rat hearts.
  • Assessed HEP metabolites using 31P nuclear magnetic resonance (NMR) spectroscopy.
  • Performed in vivo saturation transfer NMR and in vitro enzymatic assays.

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Main Results:

  • Trained hearts exhibited improved systolic and diastolic function during hypoxia and faster recovery during reoxygenation.
  • No significant differences in baseline HEP levels or ATP/phosphocreatine (PCr) loss during hypoxia were observed.
  • Increased creatine kinase (CrK) forward rate constant and mitochondrial CrK to citrate synthase ratio in trained hearts.

Conclusions:

  • Enhanced cardiac function during hypoxia in trained rats is not explained by overall HEP levels.
  • Adaptations within the creatine kinase (CrK) system likely contribute to the improved resistance to hypoxic insult.