L-(-LACTATE INFUSION INTO WORKING DOG GASTROCNEMIUS - NO EVIDENCE LACTATE PER SE MEDIATES VO2 SLOW COMPONENT())

Constant-load exercise that engenders a sustained lactic acidosis (i.e ., above the lactate threshold) is accompanied by a slow component of O-2 uptake (VO2) kinetics that increases VO2 above rather than toward the predicted value. This response arises predominantly from within th e exercising limbs and is temporally correlated with that of blood lac tate. Lactate exerts a disproportionate metabolic stimulatory effect o n gluconeogenic tissues, and there is a strong indication that lactate infusions may increase VO2 Of resting tissues. To investigate the pot ential role of lactate in the VO2 slow component, we infused lactate i n 20-min square-wave pulses (change of 10 mM) into the arterial blood supply of an electrically stimulated and surgically isolated dog gastr ocnemius preparation (2 X 60-min bouts, similar to 30-40% peak VO2; n = 5) under iso-pH conditions at constant muscle temperature. With lact ate infusions, intramuscular lactate concentration ([La]) rose proport ionally with inflowing [La] (muscle [La] = 6.34 + 0.38 blood [La]; r = 0.642, P < 0.05) to similar to 80% of arterial blood [La], and neithe r blood (control, 1.39 +/- 0.01; high lactate, 7.40 +/- 0.01; P > 0.05 ) nor muscle (control, 7.02 +/- 0.03; high lactate, 7.00 +/- 0.04; P > 0.05) pH was changed. Compared with control values, lactate infusion decreased muscle VO2 from 5.1 +/- 0.3 to 4.1 +/- 0.2 ml min(-1) 100 g( -1) (P < 0.05). However, VO2 relative to tension remained constant. No twithstanding the obvious differences between this preparation and the exercising human, this finding does not support a role for lactate pe r se in driving the VO2 slow component during intense exercise.