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This Article Full Text Full Text (PDF) All Versions of this Article: 292/6/R2249    most recent 00415.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Fredsted, A. Articles by Clausen, T. Search for Related Content PubMed PubMed Citation Articles by Fredsted, A. Articles by Clausen, T.

ENVIRONMENTAL, EXERCISE AND RESPIRATORY PHYSIOLOGY

Causes of excitation-induced muscle cell damage in isometric contractions: mechanical stress or calcium overload?

¹Department of Physiology and Biophysics, University of Aarhus, Denmark; and ²Institute of Sports Science and Clinical Biomechanics, University of Southern Denmark, Odense, Denmark

Submitted 14 June 2006 ; accepted in final form 16 February 2007

Prolonged or unaccustomed exercise leads to muscle cell membrane damage, detectable as release of the intracellular enzyme lactic acid dehydrogenase (LDH). This is correlated to excitation-induced influx of Ca²⁺, but it cannot be excluded that mechanical stress contributes to the damage. We here explore this question using N-benzyl-p-toluene sulfonamide (BTS), which specifically blocks muscle contraction. Extensor digitorum longus muscles were prepared from 4-wk-old rats and mounted on holders for isometric contractions. Muscles were stimulated intermittently at 40 Hz for 15–60 min or exposed to the Ca²⁺ ionophore A23187. [GenBank] Electrical stimulation increased ⁴⁵Ca influx 3–5 fold. This was followed by a progressive release of LDH, which was correlated to the influx of Ca²⁺. BTS (50 µM) caused a 90% inhibition of contractile force but had no effect on the excitation-induced ⁴⁵Ca influx. After stimulation, ATP and creatine phosphate levels were higher in BTS-treated muscles, most likely due to the cessation of ATP-utilization for cross-bridge cycling, indicating a better energy status of these muscles. No release of LDH was observed in BTS-treated muscles. However, when exposed to anoxia, electrical stimulation caused a marked increase in LDH release that was not suppressed by BTS but associated with a decrease in the content of ATP. Dynamic passive stretching caused no increase in muscle Ca²⁺ content and only a minor release of LDH, whereas treatment with A23187 [GenBank] markedly increased LDH release both in control and BTS-treated muscles. In conclusion, after isometric contractions, muscle cell membrane damage depends on Ca²⁺ influx and energy status and not on mechanical stress.

N-benzyl-p-toluene sulfonamide; Ca²⁺; muscle damage; passive stretch

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