High-intensity interval resistance training (HIIRT) improves liver gluconeogenesis from lactate in Swiss mice.

High-intensity physical exercise favors anaerobic glycolysis and increases lactatemia. Lactate is converted back to glucose in the liver, so that the lactate threshold, an indicator of physical performance, must be related to the gluconeogenic capacity of the liver. This research assessed the effect of a high-intensity interval resistance training (HIIRT) on liver gluconeogenesis from lactate. Swiss mice were trained (groups T) on vertical ladder with overload of 90% of their maximal load. Control animals remained untrained (groups C0 and C8). In situ liver perfusion with lactate and adrenaline was performed in rested mice after 6 hours of food deprivation. There were larger outputs of glucose (T6, 71.90%; T8, 54.53%) and pyruvate (T8, 129.28%) (representative values for 4 mM lactate) in the groups trained for 6 or 8 weeks (T6 and T8), and of glucose in the presence of adrenaline in group T8 (280%). The content of PEPCK, an important regulatory enzyme of the gluconeogenic pathway, was 69.13% higher in group T8 than in the age-matched untrained animals (C8). HIIRT augmented liver gluconeogenesis from lactate and this might improve the lactate threshold. Novelty: The liver metabolizes lactate from muscle into glucose. Physical training may enhance the gluconeogenic capacity of the liver. As lactate clearance by the liver improves, lactate threshold is displaced to higher exercise intensities.

Oral glutamine is superior than oral glucose to promote glycemia recovery in mice submitted to insulin-induced hypoglycemia.

The effect of the oral administration of blood glucose precursors on glycemia recovery and liver glucose production in fasted mice subjected to insulin-induced hypoglycemia (IIH) was investigated. IIH was obtained with increasing doses (from 0.5 to 2.0 U·kg(-1)) of intraperitoneal regular insulin where glycemia was evaluated from 0 to 300 min after insulin injection. The dose of 1.0 U·kg(-1) showed the best results, that is, a clear glycemia recovery phase without convulsions or deaths. Thus, this dose was used in all experiments. Afterwards, mice submitted to IIH received orally by gavage: saline (control group), glucose (100 mg·kg(-1)), glycerol (100 mg·kg(-1)), lactate (100 mg·kg(-1)), alanine (100 mg·kg(-1)), or glutamine (100 mg·kg(-1)). It was observed that glutamine was more effective in promoting glycemia recovery if compared with glucose, lactate, glycerol, or alanine. In agreement with these results, the best performance in terms of liver glucose production was obtained when glutamine was used as glucose precursors. These results open perspectives for clinical studies to investigate the impact of oral administration of gluconeogenic amino acids to promote glycemia recovery during hypoglycemia.