A short-term training model previously shown to result in a tighter me
tabolic control in working muscle in the absence of an increase in mit
ochondrial potential was used to examine changes in lactate turnover.
Lactate flux was studied before and after 10 days of cycle training [2
h/day at 59% maximal oxygen consumption (Vover dotO(2max))] in untrai
ned men [Vover dotO(2max) = max 45.5 +/- 2.4 (SE) ml . kg(-1). min(-1)
). A primed constant infusion of L-[1-C-13]lactate was used to examine
lactate kinetics during a prolonged exercise protocol (90 min at 59%
Vover dotO(2max)). Rate of appearance of lactate increased with exerci
se (P < 0.01), both pretraining (rest = 30.3 +/- 4.9 ml . kg(-1). min(
-1), exercise = 115 +/- 14 ml . kg(-1). min(-1)) and posttraining (res
t 28.4 +/- 4.7 ml . kg(-1). min(-1), exercise = 112 +/- 13 ml . kg(-1)
. min(-1)). Despite a lower blood lactate concentration (P < 0.05) dur
ing exercise after training, there was no difference in the rate of ap
pearance of lactate. Training increased (P < 0.05) the metabolic clear
ance rate of lactate during exercise from 36.8 +/- 4.8 to 51.4 +/- 6.8
ml . kg(-1). min(-1). These findings indicate that at least part of t
he lower exercising blood lactate observed after training is due to an
increase in metabolic clearance rate. In addition, the lower intramus
cular lactate levels suggest a decreased recruitment of glycolysis par
ticularly early in exercise.