Stretch-activated ion channels contribute to membrane depolarization after eccentric contractions

Todd A. McBride, Bradley W. Stockert, Fredric A Gorin, Richard C. Carlsen

Research output: Contribution to journalArticlepeer-review

87 Scopus citations


We tested the hypothesis that eccentric contractions activate mechanosensitive or stretch-activated ion channels (SAC) in skeletal muscles, producing increased cation conductance. Resting membrane potentials and contractile function were measured in rat tibialis anterior muscles after single or multiple exposures to a series of eccentric contractions. Each exposure produced a significant and prolonged (>24 h) membrane depolarization in exercised muscle fibers. The magnitude and duration of the depolarization were related to the number of contractions. Membrane depolarization was due primarily to an increase in Na+ influx, because the estimated Na+-to-K+ permeability ratio was increased in exercised muscles and resting membrane potentials could be partially repolarized by substituting an impermeant cation for extracellular Na+ concentration. Neither the Na+/H+ antiport inhibitor amiloride nor the fast Na+ channel blocker TTX had a significant effect on the depolarization. In contrast, addition of either of two nonselective SAC inhibitors, streptomycin or Gd3+, produced significant membrane repolarization. The results suggest that muscle fibers experience prolonged depolarization after eccentric contractions due, principally, to the activation of Na+-selective SAC.

Original languageEnglish (US)
Pages (from-to)91-101
Number of pages11
JournalJournal of Applied Physiology
Issue number1
StatePublished - Jan 2000


  • Lengthening contraction
  • Resting membrane potential
  • Skeletal muscle

ASJC Scopus subject areas

  • Physiology
  • Endocrinology
  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation


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