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Life sciences · Journal article
Cellular Signalling · July 30, 2026
Early or partial results. Treat as a signal, not a conclusion.
This mechanistic study demonstrates that acute combined fasting and exercise enhances autophagic flux in the mouse hippocampus and triggers sex-specific mitochondrial remodeling, with females showing greater proteomic and functional mitochondrial adaptability. The findings are limited to surrogate endpoints in healthy animals and require confirmation in larger samples and human studies before clinical relevance can be established.
Controlled experimental study in mice with four assigned groups (Sed, F, Ex, FEx) and pharmacological autophagy flux inhibition. Healthy male and female mice. Intervention: Single bout of fasting and/or exercise. Compared with: Sedentary control; fasting alone; exercise alone.
LC3-II levels significantly increased in FEx group following CQ treatment, indicating enhanced autophagic flux Female mice exhibited upregulation of proteins involved in TCA cycle, glutathione metabolism, and oxidative phosphorylation post-FEx Sedentary males failed to mount robust proteomic response to FEx, whereas females did
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These findings are currently exploratory and do not support clinical recommendations. The sex-specific mitochondrial responses suggest that exercise and fasting interventions may have differential effects by sex, which warrants investigation in human studies.
Mechanistic study in healthy mice using a single acute intervention with surrogate endpoints (mitochondrial markers, proteomics, autophagy flux) and no clinical outcome, requiring confirmation in larger and human cohorts.
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These findings are currently exploratory and do not support clinical recommendations. The sex-specific mitochondrial responses suggest that exercise and fasting interventions may have differential effects by sex, which warrants investigation in human studies.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Background and aims. Exercise and fasting are recognized for their ability to improve brain health and mitigate neurodegeneration. However, little is known about how these interventions acutely impact mitochondrial quality control mechanisms including mitophagy.Methods. We examined the effects of a single bout of fasting and exercise (FEx) on hippocampal mitochondrial function and proteomic remodeling in male and female mice. To assess in vivo autophagy dynamics, we combined proteomics with chloroquine (CQ) inhibition of autophagic flux. Mice were assigned to sedentary (Sed), fasting (F), exercise (Ex), or combined FEx groups and received unilateral intrahippocampal injections of CQ or PBS following treatments. Four hours later, hippocampi were collected for analysis.Results. LC3-II levels significantly increased in the FEx group only following CQ treatment, indicating enhanced autophagic flux. Proteomic profiling showed sedentary males failed to mount a robust response to FEx however females exhibited upregulation of proteins involved in the TCA cycle, glutathione metabolism, and oxidative phosphorylation, suggesting greater mitochondrial adaptability. Functional assays supported these findings, females showed increased complex IV activity post-FEx. The mitochondrial DNA / nuclear DNA ratio increased after FEx regardless of sex, and upstream regulator analysis predicted activation of mitochondrial biogenesis.Conclusions. Together, these data reveal sex-specific mitochondrial remodeling in response to acute fasting and exercise. Defining these normative responses is critical for understanding how mitochondrial adaptability shapes resilience or vulnerability to neurological challenges.
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