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Articles in PresS, published online ahead of print December 21, 2001
Am J Physiol Regu Physiol, 10.1152/ajpregu.00671.2001
Submitted on November 9, 2001
Accepted on December 18, 2001
1 Physical Therapy, Georgia State University, Atlanta, GA, USA; Health & Kinesiology, Texas A&M University, College Station, TX, USA
2 Health & Kinesiology, Texas A&M University, College Station, TX, USA
* To whom correspondence should be addressed. E-mail: phtglw{at}langate.gsu.edu.
The goals of this study were first to determine the effect of temperature on the force loss that results from eccentric contractions in mouse extensor digitorum longus muscles and then to evaluate a potential role for altered Ca2+ homeostasis explaining the greater isometric force loss observed at the higher temperatures. Isolated muscles performed 5 eccentric or 5 isometric contractions at either 15, 20, 25, 30, 33.5, or 37 °C. Isometric force loss, caffeine-induced force, lactate dehydrogenase (LDH) release, muscle accumulation of 45Ca2+ from the bathing medium, sarcoplasmic reticulum (SR) Ca2+ uptake, and resting muscle fiber free cytosolic Ca2+ concentration ([Ca2+]i) were measured. The isometric force loss after eccentric contractions increased progressively as temperature rose; at 15 °C, there was no significant loss of force, but at 37 °C, there was a 30-39% loss of force. Following eccentric contractions, caffeine-induced force was not affected by temperature nor was it different from that of control muscles at any temperature. Loss of cell membrane integrity and subsequent influx of extracellular Ca2+ as indicated by LDH release and muscle 45Ca2+ accumulation, respectively, were minimal over the 15-25 °C range, but both increased as an exponential function of temperature between 30 and 37 °C. SR Ca2+ uptake showed no impairment as temperature increased, and the eccentric contraction-induced rise in resting fiber [Ca2+]i was unaffected by temperature over the 15-25 °C range. In conclusion, the isometric force loss following eccentric contractions is temperature dependent but the temperature dependency does not appear to be readily explainable by alterations in Ca2+ homeostasis.
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