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Updated: Sep 2, 2026
Contractility Measurements on Isolated Papillary Muscles for the Investigation of Cardiac Inotropy in Mice
Published on: September 17, 2015
Functional properties and [Ca(2+)](i) metabolism of creatine kinase--KO mice myocardium
Andreas W Bonz1, Silke Kniesch, Ulrich Hofmann
1Department of Cardiology, University of Würzburg, Josef-Schneider-Strasse 2, 97080, Würzburg, Germany. a.bonz@medizin.uni-wuerzburg.de
Abstract:
One major function of the creatine kinase system is to maintain energy demand of myofibrillar contraction processes. Loss of the CK-system led to adaptations in skeletal muscle. To analyze the impact on myocardial function contractile parameters and intracellular calcium metabolism of transgenic mice lacking mitochondrial CK (ScCKmit(-/-)) alone or both mitochondrial and cytoplasmic ScCK (CK(-/-)) were investigated compared to wild type at various workload conditions using isolated intact muscle fibers. Force development at baseline conditions, force-frequency relationship (60-600/min), and rapid frequency switch (60-600/min) were unaltered in myocardium of transgenic mice compared to wild type. Intracellular calcium metabolism revealed unchanged amplitude of the intracellular calcium transients (ICT), refilling of the sarcoplasmic reticulum (calcium reuptake, post-rest behavior) in the ScCKmit(-/-) and CK(-/-) mice. The results demonstrate the effectiveness of myocardial energy-recruiting compensatory mechanisms at baseline as well as under stress conditions in CK depleted myocardium of transgenic mice.
Insights
Mice lacking creatine kinase (CK) showed no changes in heart muscle contraction or calcium handling. The heart effectively compensates for energy demands, even under stress, in these CK-depleted models.
Area of Science:
- Biochemistry
- Physiology
- Molecular Biology
Background:
- The creatine kinase (CK) system is crucial for maintaining energy balance in myofibrillar contraction.
- Skeletal muscle undergoes adaptations following the loss of the CK system.
Purpose of the Study:
- To investigate the impact of mitochondrial CK (ScCKmit(-/-)) or both mitochondrial and cytoplasmic CK (CK(-/-)) deficiency on myocardial function.
- To analyze contractile parameters and intracellular calcium metabolism in transgenic mice compared to wild type under various workload conditions.
Main Methods:
- Isolated intact muscle fibers from transgenic mice (ScCKmit(-/-), CK(-/-)) and wild type were used.
- Contractile parameters including force development, force-frequency relationship, and rapid frequency switch were measured.
- Intracellular calcium metabolism, including calcium transient amplitude and sarcoplasmic reticulum refilling, was assessed.
Main Results:
- Myocardial force development, force-frequency relationship, and rapid frequency switch were unaltered in ScCKmit(-/-) and CK(-/-) mice compared to wild type.
- Intracellular calcium metabolism, indicated by calcium transient amplitude and sarcoplasmic reticulum calcium reuptake, remained unchanged.
- No significant differences in post-rest behavior were observed between transgenic and wild-type mice.
Conclusions:
- The study demonstrates the effectiveness of compensatory energy-recruiting mechanisms in the myocardium of CK-depleted mice.
- The heart maintains normal contractile function and calcium handling despite deficiencies in the creatine kinase system.
- These findings highlight the heart's adaptability in meeting energy demands under both baseline and stress conditions.
