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1 Department of Rehabilitation Sciences, Hong Kong Polytechnic University, Hung Hom, Kowloon, Hong Kong
2 Department of Physiology, University of Hong Kong, 5 Sasson Road, Hong Kong
3 Department of Physiology, University of Sydney, Sydney, NSW, Australia
* To whom correspondence should be addressed. E-mail: davida{at}physiol.usyd.edu.au.
The effect of eccentric contractions on intracellular sodium ([Na+]i ) and its distribution were examined in isolated rat and mouse muscle fiber bundles. [Na+]i was measured with either sodium binding benzofuran isophthalate or sodium green. Ten isometric contractions had no significant effect on force (measured after 5 min 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 per 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.
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