All the data collected to date suggests that lactate should come flooding out of fish muscle after a bout of exhaustive execise. Typically, after exercise, muscle lactate levels are high, (~40-60 umol/g) about 10-15-fold higher than in the blood. Furthermore, at physiological pH, the majority of the lactate exists in the dissociated anionic form, that is, it is negatively charged. Together, both of these forces create a strong electrochemical gradient that should favour lactate leaving the muscle, yet it doesn't. In fact, there is considerable evidence indicating muscle can take up lactate from the blood into the muscle. To address this problem, we developed a muscle sarcolemmal vesicle preparation. which consist of vesicles made only from muscle plasma membrane. Using this preparation, Karen Laberee (Laberee & Milligan, 1999) demonstrated that the muscle is capable of carrier-mediated inward directed lactate transport. The carrier has a low affinity for lactate, suggesting it is operative when extracellular lactate levels are high (~15-25 mM). This is consistent with some of our previous work showing that in vivo trout muscle can take up and metabolize lactate when lblood evels are high, but not when blood levels are low.

More recently, in her M.Sc. research, Rainie Sharpe has shown that lactate efflux from within the sarcolemmal vesicles is a very slow process, apparently, which occurs via passive diffusion, most likely of the undissociated lactic acid. The efflux rates are in the pmol/mg protein/min range, whereas the lactate influx (uptake) rates are in the nmol/mg protein/min range. This suggests that the trout skeletal muscle membrane is "tight" with regards to lactate efflux; in otherwords, lactate does not readily leave the muscle. This observation fits well with the in vivo scenario, in which there is mounting evidence that lactate is retained within the muscle (we now know by virture of the muscle membrane's low permeability to lactate) for use as a glycogenic substrate.