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1 Institute of Anatomy, University of Bern, CH-3012 Bern, and 3 Program in Neuroscience, Institute of Histology and General Embryology, University of Fribourg, CH-1705 Fribourg, Switzerland; 2 National Institutes of Health, Bethesda, Maryland 20814; 4 Deptartment of Anatomy, University College, London WC1E 6BT, United Kingdom; and 5 Faculty of Biology, University of Constance, D-78457 Constance, Germany
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 c
oxidase. 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+]i
removal. 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.
muscle fatigue; calcium-binding protein; EF hand; compensation
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