Effects of lactate on force production by mouse EDL muscle: implications for the development of fatigue.

Abstract

Numerous studies suggest that the accumulation of lactate during exercise contributes to the fatigue process. This notion is based on close negative correlations between force and intracellular muscle lactate concentrations during fatigue and recovery. In this investigation, we attempted to determine if lactate directly affects muscle force output. This was accomplished by incubating mouse extensor digitorum longus muscles in extracellular concentrations of 10, 20, 30 and 50 mM L-(+)-lactate at 21 and 37 degrees C and monitoring force output. At 21 degrees C, 30 and 50 mM, extracellular lactate significantly reduced tetanic force (Po 250 ms, 100 Hz) to 95 and 93% of initial, respectively. In addition, the rate of force development (+dP/dt) was reduced to 93 and 89% of initial. At 37 degrees C, the effects of extracellular lactate were augmented as Po was reduced to 73 and 62% of initial and +dP/dt was reduced to 55 and 44% of initial at 30 and 50 mM, respectively. We next sought to determine if the reduction in Po was due to altered sarcoplasmic reticulum (SR) function using a muscle homogenate fraction. The rate of AgNO3-induced SR Ca2+ release was depressed by 31% in the presence of 25 mM lactate. These results suggest that elevated lactate depresses force production by whole muscle and may play some role in the fatigue process. In addition, it appears that lactate depresses force production, in part, by inhibiting Ca2+ release from the SR.