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J Appl Physiol 94: 2475-2482, 2003. First published February 14, 2003; doi:10.1152/japplphysiol.01128.2002
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Vol. 94, Issue 6, 2475-2482, June 2003

Intracellular sodium in mammalian muscle fibers after eccentric contractions

Ella W. Yeung1, Heather J. Ballard2, J.-P. Bourreau2, and David G. Allen3

1 Department of Rehabilitation Sciences, Hong Kong Polytechnic University, Hung Hom, Kowloon; 2 Department of Physiology, University of Hong Kong, Hong Kong, China; and 3 Institute for Biomedical Research and Department of Physiology, University of Sydney F13, Sydney NSW 2006, Australia

The effect of eccentric contractions on intracellular Na+ concentration ([Na+]i) and its distribution were examined in isolated rat and mouse muscle fiber bundles. [Na+]i was measured with either Na+-binding benzofuran isophthalate or sodium green. Ten isometric contractions had no significant effect on force (measured after 5 min of recovery) and caused no significant change in the resting [Na+]i (7.2 ± 0.5 mM). In contrast 10 eccentric contractions (40% stretch at 4 muscle lengths/s) reduced developed force at 100 Hz to 45 ± 3% of control and increased [Na+]i to 16.3 ± 1.6 mM (n = 6; P < 0.001). The rise of [Na+]i occurred over 1-2 min and showed only minimal recovery after 30 min. Confocal images of the distribution of [Na+]i showed a spatially uniform distribution both at rest and after eccentric contractions. Gd3+ (20 µM) had no effect on resting [Na+]i or control tetanic force but prevented the rise of [Na+]i and reduced the force deficit after eccentric damage. These data suggest that Na+ entry after eccentric contractions may occur principally through stretch-sensitive channels.

muscle; eccentric damage; intracellular sodium; gadolinium; stretch-sensitive channels


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