Performance during a strenuous swimming session is associated with high blood lactate: pyruvate ratio and hypoglycemia in fasted rats.

The aim of this study was to investigate the effect of lactatemia elevation and glycemia reduction on strenuous swimming performance in fasted rats. Three rats were placed in a swimming tank at the same time. The first rat was removed immediately (control group) and the remaining ones were submitted to a strenuous swimming session. After the second rat was exhausted (Exh group), the third one was immediately removed from the water (Exe group). According to the period of time required for exhaustion, the rats were divided into four groups: low performance (3-7 min), low-intermediary performance (8-12 min), high-intermediary performance (13-17 min), and high performance (18-22 min). All rats were removed from the swimming tanks and immediately killed by decapitation for blood collection or anesthetized for liver perfusion experiments. Blood glucose, lactate, and pyruvate concentrations, blood lactate/pyruvate ratio, and liver lactate uptake and its conversion to glucose were evaluated. Exhaustion in low and low-intermediary performance were better associated with higher lactate/pyruvate ratio. On the other hand, exhaustion in high-intermediary and high performance was better associated with hypoglycemia. Lactate uptake and glucose production from lactate in livers from the Exe and Exh groups were maintained. We concluded that there is a time sequence in the participation of lactate/pyruvate ratio and hypoglycemia in performance during an acute strenuous swimming section in fasted rats. The liver had an important participation in preventing hyperlactatemia and hypoglycemia during swimming through lactate uptake and its conversion to glucose.

Rat liver responsiveness to gluconeogenic substrates during insulin-induced hypoglycemia.

Hepatic responsiveness to gluconeogenic substrates during insulin-induced hypoglycemia was investigated. For this purpose, livers were perfused with a saturating concentration of 2 mM glycerol, 5 mM L-alanine or 5 mM L-glutamine as gluconeogenic substrates. All experiments were performed 1 h after an ip injection of saline (CN group) or 1 IU/kg of insulin (IN group). The IN group showed higher (P<0.05) hepatic glucose production from glycerol, L-alanine and L-glutamine and higher (P<0.05) production of L-lactate, pyruvate and urea from L-alanine and L-glutamine. In addition, ip injection of 100 mg/kg glycerol, L-alanine and L-glutamine promoted glucose recovery. The results indicate that the hepatic capacity to produce glucose from gluconeogenic precursors was increased during insulin-induced hypoglycemia.

Changes in glycemia induced by exercise in rats: contribution of hepatic glycogenolysis and gluconeogenesis.

The participation of hepatic glycogenolysis and gluconeogenesis to the glycemic changes promoted by exercise was investigated. For this purpose, we employed swimming rats (2.5% body weight extra load attached to the tail, at 24 degrees C) using a favorable condition to measure hepatic glycogenolysis (fed rats) and a favorable condition to measure hepatic gluconeogenesis (fasted rats). This experimental approach permits us to compare the contribution of hepatic glycogenolysis and gluconeogenesis to glucose changes for a specific schedule of exercise. The animals were investigated at rest, after 5 minutes of swimming and after swimming to exhaustion. Our results show that hepatic glycogen has a crucial role to determine hyperglycemia during exercise. In contrast, hypoglycemia developed during exercise when glycogen was depleted. However, the ability of the liver to produce glucose from L-lactate, glycerol and L-glutamine was increased during exercise. Taken together, these findings suggest that the hepatic capacity to produce glucose from gluconeogenic substrates (except for L-alanine) was increased when hepatic glycogen stores were depleted. Thus, the increased capacity to produce glucose shown by livers from exercising rats must to be an important metabolic adaptation to protect against severe hypoglycemia.

Electrophoretic variation in esterases in 3 wild-type and respective mutant strains of Aspergillus flavus.

Wild-type strains and auxotrophic mutants of Aspergillus flavus, differing regarding aflatoxin production, were tested for esterases isozymes. Esterases variation was found in all strains used, and a possible correlation between the pattern of esterase bands and aflatoxin production is suggested.