Journal of Muscle Research & Cell Motility

, Volume 21, Issue 7, pp 621–628

Frog skeletal muscle fibers recovering from fatigue have reduced charge movement

  • Joseph D. Bruton
  • Péter Szentesi
  • Jan Lännergren
  • Håkan Westerblad
  • László Kovács
  • László Csernoch
Article

DOI: 10.1023/A:1005609405435

Cite this article as:
Bruton, J.D., Szentesi, P., Lännergren, J. et al. J Muscle Res Cell Motil (2000) 21: 621. doi:10.1023/A:1005609405435

Abstract

Following prolonged exercise, muscle force production is often impaired. One possible cause of this force deficit is impaired intracellular activation. We have used single skeletal muscle fibers from the lumbrical muscle of Xenopus laevis to study the effects of fatigue on excitation–contraction coupling. Fatigue was induced in 13 intact fibers. Five fibers recovered in normal Ringer only (fatigued-only fibers). The remaining eight fibers were subjected to a brief hypotonic treatment (F-H fibers) that is known to prolong the effects of fatigue. Intramembrane charge movement, changes in intracellular calcium concentration ([Ca2+]i) and force transients were measured in a single Vaseline gap chamber under voltage clamp. In F-H fibers, membrane capacitance was reduced. Confocal microscopy showed that this was not due to closure of the transverse tubules. The amount of normalized intramembrane charge was reduced from 21.0 ± 2.8 nC/μF (n = 10) in rested fibers to 12.2 ± 1.1 nC/μF in F-H fibers. However, the voltage dependence of intramembrane charge movement was unchanged. In F-H fibers, force production was virtually abolished. This was the consequence of the greatly reduced [Ca2+]i accompanying a depolarizing pulse. In recovering fatigued-only fibers, while the maximal available charge was not significantly smaller (18.3 ± 1.1 nC/μF), both calcium and force were reduced, albeit to a lesser extent than in F-H fibers. The data are consistent with a model where fatigue reduces the number of voltage sensors in the t-tubules and, in addition, alters the coupling between the remaining functional voltage sensors and the calcium channels of the sarcoplasmic reticulum.

Copyright information

© Kluwer Academic Publishers 2000

Authors and Affiliations

  • Joseph D. Bruton
    • 1
  • Péter Szentesi
    • 2
  • Jan Lännergren
    • 1
  • Håkan Westerblad
    • 1
  • László Kovács
    • 1
  • László Csernoch
    • 1
  1. 1.Department of Physiology & PharmacologyKarolinska InstitutetStockholmSweden
  2. 2.Department of Physiology, Medical and Health Science CentreUniversity of Debrecen, Cell Physiology Research Group of the Hungarian Academy of SciencesHungary