Temperature dependency of force loss and Ca2+homeostasis in mouse EDL muscle after eccentric contractions

Gordon L. Warren, Christopher P. Ingalls, R. B. Armstrong
2002 American Journal of Physiology. Regulatory Integrative and Comparative Physiology  
Warren, Gordon L., Christopher P. Ingalls, and R. B. Armstrong. Temperature dependency of force loss and Ca 2ϩ homeostasis in mouse EDL muscle after eccentric contractions. 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 Ca 2ϩ homeostasis explaining the greater isometric force loss observed at the higher
more » ... es. 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 45 Ca 2ϩ from the bathing medium, sarcoplasmic reticulum (SR) Ca 2ϩ uptake, and resting muscle fiber free cytosolic Ca 2ϩ concentration ([Ca 2ϩ ]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 Ca 2ϩ as indicated by LDH release and muscle 45 Ca 2ϩ 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 Ca 2ϩ uptake showed no impairment as temperature increased, and the eccentric contraction-induced rise in resting fiber [Ca 2ϩ ]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 Ca 2ϩ homeostasis.
doi:10.1152/ajpregu.00671.2001 pmid:11893617 fatcat:6iivr2lrdnbbzklnsyetq57vv4