Rise In Blood Lactate Concentration Research Articles

Metabolic Studies on the Pathogenesis of Hangover

Abstract. A variety of metabolic parameters were evaluated in 23 healthy male volunteers, after ethanol administration (1.5 g/kg) and correlated to the symptoms of hangover. The degree of intoxication and hangover were estimated using a simple test program according to which 11 subjects had severe and 12 mild hangover. Sequential determinations of blood ethanol, acetaldehyde, glucose, lactate, free fatty acids (FFA), triglycerides (TG) and ketone bodies were made during the 21 hours after administration. Each subject served as his own control by taking part in an identical experimental session but receiving no ethanol.The maximal hangover occurred 12 to 14 hours after the initiation of drinking. At this time almost all of the ethanol and acetaldehyde had been eliminated from the blood. The intensity of the hangover did not correlate with the peak concentrations of ethanol or acetaldehyde in the blood. Marked hypoglycaemia regularly followed the administration of ethanol, but the nadir blood glucose values had no correlation with the intensity of hangover. Ethanol induced a significant rise in blood lactate concentration, the extent of which was similar in subjects with mild or severe hangover.During the most intensive hangover plasma FFA level increased when compared to the values observed during the control period. These concentrations were significantly higher in subjects with severe hangover than in those whose hangover was mild. An increase in plasma TG concentration regularly followed ethanol administration but the extent of the rise did not correlate with the degree of intoxication or hangover. Ethanol had a marked antiketogenic effect during the first 8 hours of the experiment after which the concentration of ketone bodies rose rapidly above the control level. Again the changes showed no correlation with the intensity of hangover.The results indicate that the intensity of hangover bears little relation to the changes in the metabolite concentrations measured. This suggests that the symptoms of hangover can not be accounted for by the ethanol‐induced alterations of the major blood metabolite concentrations.

Glucose tolerance and blood metabolite changes in galactosamine hepatitis and obstructive jaundice in the rat.

Abstract. Glucose tolerance and blood metabolite changes have been measured in starved rats either 24 h after D (+)‐galactosamine treatment or 9 days after bile duct ligation. In galactosamine‐treated rats (0.5 g/kg) there was enhanced glucose removal after intravenous glucose (1 g/kg) and hyper‐insulinism in the early part of the test. Fasting blood lactate and pyruvate concentrations were elevated in galactosamine‐treated rats (1 g/kg) and there was a greatly accentuated rise in blood lactate concentration after intravenous glucose (2.20 ±0.16 compared to 0.90 ± 0.23 mM), suggesting decreased gluconeogeneaia. Nine days after bile duct ligation there was enhanced glucose removal after intravenous glucose when compared to controls. Lactate and pyruvate concentrations were transiently elevated after intravenous glucose in the ligated rats consistent with the increased rate of glucose removal. Fasting ketone bodies were decreased in the ligated rats (2.87 ± 0.40 compared to 6.50 ± 0.87 mM) due to diminished fat stores and this decreased ketosis probably results in glucose removal comparable to that seen in fed rats.

The effect of hyperventilation on the lactacidaemia of muscular exercise.

1. Six men exercised at 600 kp m/min on a cycle ergometer. After a control period they hyperventilated at about twice the control level of ventilation. Capillary blood samples were taken for lactate estimations at the end of both 6 min periods. 2. Hyperventilation resulting in a fall in end-tidal Pco2 of 12·0 mmHg was associated with rise in blood lactate concentration of 1·07 mm/l. 3. It is concluded that the increase in blood lactate concentration attributable to hyperventilation is comparatively small in exercise tests involving short periods of moderately severe exertion. 4. In an additional subject exercising similarly, hyperventilation without a fall in Pco2 (‘normocapnic’ hyperventilation) was achieved by adding 3·8% CO2 to the inspired air. Subsequent hyperventilation while breathing air resulted in a fall in end-tidal Pco2 of 19·5 mmHg (‘hypocapnic’ hyperventilation) and a rise in blood lactate concentration of 1·21 mm/l. Parallel changes in pyruvate concentration occurred suggesting that lactate production had increased. Neither the origin nor the mechanism of this increase could be ascertained; however, it appeared unlikely to be due to increased anaerobic metabolism of the respiratory muscles as normocapnic hyperventilation was associated with virtually no change in blood lactate and pyruvate concentrations.