Resistance training boosts lactate transporters and synaptic proteins in insulin-resistance mice

This investigation delineates the influence of resistance training on the expression of synaptic plasticity-related proteins in the hippocampi of insulin-resistant mice and explores the underlying molecular mechanisms.

Resistance training mitigates insulin resistance and improves hippocampal synaptic plasticity by normalizing blood lactate levels and enhancing mTOR, MCTs, and synaptic plasticity-related proteins. It may also activate mTORC1 via the PI3K/Akt pathway, promote lactate utilization, and enhance synaptic plasticity proteins, potentially alleviating peripheral insulin resistance. Further research is needed to confirm these mechanisms.

Six-week-old male C57BL/6 J mice were stratified into a control group and a high-fat diet group to induce insulin resistance over a 12-week period. Subsequently, the mice were further divided into sedentary and resistance training cohorts, with the latter engaging in a 12-week ladder-climbing regimen. Post-intervention, blood, and hippocampal specimens were harvested for analytical evaluation.

In the insulin-resistant mice, elevated blood lactate levels were observed alongside diminished expression of synaptic plasticity-related proteins, monocarboxylate transporters (MCTs), and reduced phosphorylation of protein kinase B (Akt) and mechanistic target of rapamycin (mTOR). In contrast, the expression of eukaryotic translation initiation factor 4 E-binding protein 2 was significantly augmented. Resistance training mitigated insulin resistance, decreased blood lactate levels, and enhanced the expression and phosphorylation of mTOR, regulatory-associated protein of mTOR, MCTs, and synaptic plasticity-related proteins. Conclusions: Resistance training mitigates insulin resistance and improves hippocampal synaptic plasticity by normalizing blood lactate levels and enhancing mTOR, MCTs, and synaptic plasticity-related proteins. It may also activate mTORC1 via the PI3K/Akt pathway, promote lactate utilization, and enhance synaptic plasticity proteins, potentially alleviating peripheral insulin resistance. Further research is needed to confirm these mechanisms.