Glucose metabolism in the perfused liver did not improve with resistance training in male Swiss mice under caloric restriction.

CONTEXT: Energy homeostasis is a primary factor for the survival of mammals. Many tissues and organs, among which is the liver, keep this homeostasis in varied circumstances, including caloric restriction (CR) and physical activity. OBJECTIVE: This study investigated glucose metabolism using the following groups of eight-week-old male Swiss mice: CS, sedentary and fed freely; RS, sedentary and RT, trained, both under 30% CR (n = 20-23 per group). RESULTS: Organs and fat depots of groups RS and RT were similar to CS, although body weight was lower. CR did not impair training performance nor affected systemic or hepatic glucose metabolism. Training combined with CR (group RT) improved in vivo glucose tolerance and did not affect liver gluconeogenesis. CONCLUSIONS: The mice tolerated the prolonged moderate CR without impairment of their well-being, glucose homeostasis, and resistance training performance. But the higher liver gluconeogenic efficiency previously demonstrated using this training protocol in mice was not evidenced under CR.

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.