| First Author | Chen G | Year | 2001 |
| Journal | Am J Physiol Cell Physiol | Volume | 281 |
| Issue | 1 | Pages | C114-22 |
| PubMed ID | 11401833 | Mgi Jnum | J:70289 |
| Mgi Id | MGI:2136722 | Doi | 10.1152/ajpcell.2001.281.1.C114 |
| Citation | Chen G, et al. (2001) Deficiency in parvalbumin increases fatigue resistance in fast-twitch muscle and upregulates mitochondria. Am J Physiol Cell Physiol 281(1):C114-22 |
| abstractText | 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. |
