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 O2 uptake (VO2) kinetics that increases VO2 above rather than toward the predicted value. This response arises predominantly from within the exercising limbs and is temporally correlated with that of blood lactate. Lactate exerts a disproportionate metabolic stimulatory effect on gluconeogenic tissues, and there is a strong indication that lactate infusions may increase VO2 of resting tissues. To investigate the potential role of lactate in the VO2 slow component, we infused lactate in 20-min square-wave pulses (change of 10 mM) into the arterial blood supply of an electrically stimulated and surgically isolated dog gastrocnemius preparation (2 x 60-min bouts, approximately 30-40% peak VO2; n = 5) under iso-pH conditions at constant muscle temperature. With lactate infusions, intramuscular lactate concentration ([La]) rose proportionally with inflowing [La] (muscle [La] = 6.34 + 0.38 blood [La]; r = 0.642, P < 0.05) to approximately 80% of arterial blood [La], and neither blood (control, 7.39 +/- 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. Notwithstanding the obvious differences between this preparation and the exercising human, this finding does not support a role for lactate per se in driving the VO2 slow component during intense exercise.