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Related Experiment Videos

Effect of exercise on cardiac cyclic AMP.

W K Palmer1

  • 1Department of Physical Education, University of Illinois, Chicago 60680.

Medicine and Science in Sports and Exercise
|December 1, 1988
PubMed
Summary

Intense exercise and cold exposure significantly increase cyclic AMP (adenosine monophosphate) levels in the heart. This elevation, sustained post-stress, appears to involve increased cardiac phosphodiesterase activity, suggesting a protein synthesis-mediated regulatory mechanism.

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Area of Science:

  • Physiology
  • Biochemistry
  • Molecular Biology

Background:

  • Physiological stress, such as intense exercise and cold exposure, can alter cellular signaling pathways.
  • Cyclic AMP (adenosine monophosphate) is a crucial second messenger involved in various cellular responses.
  • Understanding the regulation of cyclic AMP metabolism during stress is vital for comprehending cellular adaptation.

Purpose of the Study:

  • To investigate the impact of a single bout of intense swimming on cyclic AMP content in various tissues.
  • To examine the time course and intensity dependence of exercise-induced myocardial cyclic AMP elevation.
  • To explore the relationship between elevated cyclic AMP and cardiac phosphodiesterase (PDE) activity.

Main Methods:

  • Rats were subjected to intense swimming exercise and cold exposure (2 degrees C for 1-7 days).

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  • Cyclic AMP content and phosphodiesterase (PDE) activity were measured in skeletal muscle, liver, and heart tissue.
  • Dibutyryl cyclic AMP was administered to rats, and the effect on cardiac PDE activity was assessed in the presence of cycloheximide.

    • Main Results:

    • Intense swimming significantly increased cyclic AMP content in fast-twitch skeletal muscle, liver, and heart.
    • Myocardial cyclic AMP remained elevated for at least 24 hours post-exercise, showing a time-dependent increase during exercise.
    • Cardiac cyclic AMP elevation occurred with sufficient exercise duration (>30 min) but was independent of intensity, and also observed after cold exposure.
    • Both exercise and cold exposure increased cardiac PDE activity, which was further elevated by dibutyryl cyclic AMP administration.
    • The increase in cardiac PDE activity induced by dibutyryl cyclic AMP was inhibited by cycloheximide, indicating de novo protein synthesis.

    Conclusions:

    • Cyclic AMP plays a significant role in the metabolic regulation of the heart during physiological stress.
    • Prolonged elevations in cyclic AMP may lead to the induction or activation of specific PDE isozymes.
    • The observed increase in cardiac PDE activity appears to be mediated by the synthesis of new protein, suggesting a feedback mechanism for cyclic AMP homeostasis.