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J Appl Physiol 88: 91-101, 2000;
8750-7587/00 $5.00
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Vol. 88, Issue 1, 91-101, January 2000

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

Todd A. McBride1, Bradley W. Stockert2, Fredric A. Gorin3, and Richard C. Carlsen2

1 Department of Biology, California State University, Bakersfield 93311; and Departments of 2 Human Physiology and 3 Neurology, University of California, Davis, California 95616

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.

skeletal muscle; lengthening contraction; resting membrane potential


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