Prolongation of the half-life of lactate after maximal exercise in patients with hepatic dysfunction.

Decreased hepatic clearance of exogenous sodium lactate has previously been demonstrated in patients with hepatic dysfunction. The purpose of this study was to obtain a more precise understanding of the rate of metabolic normalization or decrease of endogenously produced lactate in patients with hepatic cirrhosis. The differential kinetics of lactate metabolism are of clinical interest. Male volunteer patients with hepatic cirrhosis (n = 7), who had survived acute hospitalization, were compared to healthy age-matched males with normal liver function (n = 7). After arterial cannulation, bicycle ergometry was performed at a workload of 25 watts (W); the load was increased by increments of 25 W at 2-min intervals to maximum aerobic capacity. Lactate was measured in arterial blood before, at 4-min intervals during, and on a minimum of 11 occasions in the 30 to 70 min after exercise. The time interval during which lactate declined linearly to half its maximal concentration (Lt50) was graphically computed. The Lt50 was 34.8 +/- 4.5 min (mean +/- SEM) in the experimental group and 14.1 +/- 1.3 min in the control subjects (p less than .005). Lactate disappears from the bloodstream almost three times more slowly in patients with hepatic cirrhosis. The implication for interpretation of changes in lactate during circulatory shock in the presence of liver dysfunction is addressed.