Deficiency in parvalbumin increases fatigue resistance in fast-twitch muscle and upregulates mitochondria
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Chen, Gaoping
Institute of Anatomy, University of Bern, CH-3012 Bern, and
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Carroll, Stefanie
National Institutes of Health, Bethesda, Maryland 20814;
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Racay, Peter
Program in Neuroscience, Institute of Histology and General Embryology, University of Fribourg, CH-1705 Fribourg, Switzerland;
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Dick, Jim
Deptartment of Anatomy, University College, London WC1E 6BT, United Kingdom; and
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Pette, Dirk
Faculty of Biology, University of Constance, D-78457 Constance, Germany
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Traub, Irmtrud
Faculty of Biology, University of Constance, D-78457 Constance, Germany
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Vrbova, Gerta
Deptartment of Anatomy, University College, London WC1E 6BT, United Kingdom; and
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Eggli, Peter
Institute of Anatomy, University of Bern, CH-3012 Bern, and
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Celio, Marco
Program in Neuroscience, Institute of Histology and General Embryology, University of Fribourg, CH-1705 Fribourg, Switzerland;
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Schwaller, Beat
Program in Neuroscience, Institute of Histology and General Embryology, University of Fribourg, CH-1705 Fribourg, Switzerland;
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Published in:
- American Journal of Physiology-Cell Physiology. - American Physiological Society. - 2001, vol. 281, no. 1, p. C114-C122
English
The soluble Ca2+-binding protein parvalbumin (PV) is expressed at high levels in fast-twitch muscles of mice. Deficiency of PV in knockout mice (PV −/−) slows down the speed of twitch relaxation, while maximum force generated during tetanic contraction is unaltered. We observed that PV-deficient fast-twitch muscles were significantly more resistant to fatigue than were the wild type. Thus components involved in Ca2+ homeostasis during the contraction-relaxation cycle were analyzed. No upregulation of another cytosolic Ca2+-binding protein was found. Mitochondria are thought to play a physiological role during muscle relaxation and were thus analyzed. The fractional volume of mitochondria in the fast-twitch muscle extensor digitorum longus (EDL) was almost doubled in PV −/− mice, and this was reflected in an increase of cytochrome coxidase. A faster removal of intracellular Ca2+concentration ([Ca2+]i) 200–700 ms after fast-twitch muscle stimulation observed in PV −/− muscles supports the role for mitochondria in late [Ca2+]iremoval. The present results also show a significant increase of the density of capillaries in EDL muscles of PV −/− mice. Thus alterations in the dynamics of Ca2+ transients detected in fast-twitch muscles of PV −/− mice might be linked to the increase in mitochondria volume and capillary density, which contribute to the greater fatigue resistance of these muscles.
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Open access status
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green
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https://sonar.ch/global/documents/139383
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