Temperature dependency of force loss and Ca homeostasis in mouse EDL muscle after eccentric contractions

Warren, Gordon L., Christopher P. Ingalls, and R. B. Armstrong. Temperature dependency of force loss and Ca2 homeostasis in mouse EDL muscle after eccentric contractions. Am J Physiol Regulatory Integrative Comp Physiol 282: R1122–R1132, 2002. First published December 21, 2001; 10.1152/ajpregu.00671.2001.—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 (EDL) 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 five eccentric or five 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. After 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 after eccentric contractions is temperature dependent, but the temperature dependency does not appear to be readily explainable by alterations in Ca2 homeostasis.