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Related Experiment Videos

Cardiac adaptations to chronic exercise in mice

M L Kaplan1, Y Cheslow, K Vikstrom

  • 1Department of Medicine, Albert Einstein College of Medicine, Montefiore Medical Center, Bronx, New York 10467.

The American Journal of Physiology
|September 1, 1994
PubMed
Summary

This study shows that mice develop cardiac hypertrophy with swimming exercise, increasing heart weight but not cardiac myosin ATPase activity. These findings are crucial for understanding adaptive cardiac hypertrophy in mouse models.

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Area of Science:

  • Physiology
  • Cardiovascular Biology
  • Exercise Science

Background:

  • Transgenic mice are valuable models for human cardiac disease.
  • Limited data exists on normal mouse heart physiology, hindering model interpretation.
  • Understanding adaptive cardiac responses in mice is essential.

Purpose of the Study:

  • To characterize the physiological response of adult mice to chronic physical conditioning.
  • To establish a baseline for normal cardiac adaptation in mice.
  • To investigate molecular changes associated with exercise-induced cardiac hypertrophy in mice.

Main Methods:

  • Adult female C57/B16 mice underwent a 4-week swimming conditioning program (90 min twice daily).
  • Physiological parameters including heart weight, heart rate response, and succinate dehydrogenase activity were measured.

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  • Cardiac tissue analysis included norepinephrine content, myosin, and myofibrillar adenosinetriphosphatase (ATPase) activities, and myosin heavy chain mRNA profiles.

    • Main Results:

    • Conditioned mice showed a 10% increase in heart weight and a 16% increase in heart weight-to-body weight ratio.
    • Heart rate response to submaximal workload decreased by over 20%.
    • Soleus muscle succinate dehydrogenase activity increased significantly, but cardiac tissue showed no changes in norepinephrine, ATPase activity, or myosin profiles.

    Conclusions:

    • Mice can develop cardiac hypertrophy in response to chronic swimming conditioning.
    • This adaptive cardiac hypertrophy in mice is not associated with alterations in cardiac myosin ATPase activity.
    • The study provides essential data for researchers using mouse models to study adaptive cardiac hypertrophy.