Elevations in blood lactate by exogenous infusion blunts exercise-stimulated whole-body lipolysis in healthy individuals: a randomized controlled trial.

The purpose of this study is to determine in humans whether lactate inhibits exercise-stimulated lipolysis, fat oxidation, and plasma glucose turnover. Eight healthy active individuals (3 women) completed 4 trials in a semi-randomized order. In two trials, subjects exercised for 60 min at 65±11% (mean±SD) of VO2 MAX while receiving isovolumetric infusions of either sodium lactate (MOD+LACT trial) or saline (MOD trial). In another trial, exercise intensity was increased to 82±11% of VO2 MAX (INT trial) to match lactate concentrations to those in the MOD+LACT trial. A trial without exercise was included. Stable isotopes of glycerol and glucose were infused to assess whole-body lipolysis (Ra Glycerol) and glucose turnover rates (Ra Glucose). Fat and carbohydrate oxidation were measured using indirect calorimetry. Basal metabolic rate and plasma concentrations of lactate, glucose, insulin, FFA, and glycerol were similar across trials. Plasma lactate was clamped at 4.31±1.68 mM during the MOD+LACT trial, which tripled MOD concentrations (1.42±0.93 mM; p=0.001) and matched INT concentrations (4.39±1.25 mM; p=0.819). MOD+LACT blunted the exercise-induced elevation in Ra Glycerol of MOD (average during exercise, 7.9±2.0 vs 10.5±2.2 µmol·kg-1·min-1; p=0.014). However, fat oxidation rates were similar in MOD+LACT and MOD (7.70 ±2.02 vs 7.38±1.47 µmol·kg-1·min-1; p=0.612) but reduced during INT (5.30±2.93 µmol·kg-1·min-1; p=0.045). Ra Glucose, plasma glucose, and insulin were elevated during INT but not affected by lactate infusion. Raising circulating lactate concentrations to levels observed during high-intensity exercise blunts exercise-stimulated whole-body lipolysis. However, in these metabolically healthy individuals, that reduction was not sufficient to compromise fat oxidation during moderate intensity exercise.