A combined stimulus of acute fasting and exercise modulates hippocampal mitochondrial quality control in healthy mice.

This study tested the hypothesis that a single bout of combined fasting and exercise induces mitochondrial quality control and proteostatic adaptations in the hippocampus. Male and female C57BL/6J mice were exposed to sedentary, fasting, exercise, or combined fasting plus exercise (FEx) conditions. To assess autophagic flux in vivo, animals received unilateral intrahippocampal injections of chloroquine or vehicle prior to tissue collection.

The dataset includes western blot, enzymatic activity, quantitative PCR, and proteomic measurements used to evaluate autophagy, protein degradation pathways, mitochondrial metabolism, and respiratory function. Western blot analyses quantified markers of autophagic flux and protein turnover, enzyme assays assessed mitochondrial complex II and IV activity, and qPCR was used to estimate relative mitochondrial DNA content. Proteomic profiling was performed using data-independent acquisition mass spectrometry and analyzed using established bioinformatic pipelines.

The data demonstrate that acute fasting plus exercise induces a robust autophagic response and widespread mitochondrial remodeling in the hippocampus, with more pronounced adaptations observed in females. Pathway-level analyses indicate coordinated regulation of metabolic, redox, and protein quality control networks, suggesting engagement of both canonical and non-canonical mitochondrial surveillance mechanisms.

All raw and processed data files, along with associated metadata and analysis outputs, are provided to enable independent verification, reanalysis, and integration with future studies. These datasets may be useful for investigators studying brain metabolism, mitochondrial biology, sex-specific stress responses, and lifestyle interventions in neurological health and disease.