Narrative review: autophagy, muscle–fat crosstalk and exercise in sarcopenic obesity
This narrative review describes how impaired autophagy may relate to sarcopenic obesity and suggests that exercise may support autophagic homeostasis, with long-term progressive moderate-intensity resistance plus aerobic exercise proposed as promising but still needing confirmation in SO-specific randomized controlled trials. [1]
Automatic summary · not editorially reviewed
The key findings
The review describes sarcopenic obesity as an age-related phenotype combining reduced skeletal muscle mass, impaired muscle function and excessive adiposity, linked to metabolic dysfunction, physical decline and increased mortality. [1]
Aging, obesity, chronic low-grade inflammation and insulin resistance may impair autophagic flux, which the review says could worsen muscle degeneration, ectopic lipid deposition and metabolic imbalance. [1]
The review suggests long-term, progressive, moderate-intensity resistance exercise combined with aerobic exercise may be promising for sarcopenic obesity, but confirmation in SO-specific randomized controlled trials is warranted. [1]
The source at a glance
- Study type / format
- Narrative review (abstract only)
- Population / context
- People with sarcopenic obesity, as described in a narrative review
- Summary based on
- Study abstract
- Original publication
- September 24, 2026
Age-related sarcopenic obesity and autophagy
The review describes sarcopenic obesity as a complex age-related phenotype in which reduced skeletal muscle mass, impaired muscle function and excessive adiposity occur together. The authors link this combination to metabolic dysfunction, physical decline and increased mortality. Autophagy, they write, maintains cellular homeostasis by regulating protein turnover, mitochondrial quality control, lipid metabolism and muscle–adipose crosstalk. Aging, obesity, chronic low-grade inflammation and insulin resistance may impair autophagic flux, which the review says could worsen muscle degeneration, ectopic lipid deposition and metabolic imbalance.
Supporting source [1]
Exercise modalities and proposed autophagy pathways
The review reports that exercise may support autophagic homeostasis through several mechanisms, including AMPK/mTOR/ULK1, TFEB/FoxO, PGC-1α-related, sirtuin-dependent and mitophagy-associated pathways. It states that different exercise modalities appear to confer distinct benefits: resistance exercise primarily promotes muscle anabolism and selective autophagy-related processes; aerobic exercise modulates mitophagy- and lipophagy-related processes; high-intensity interval training may induce rapid but recovery-dependent autophagy-related responses; and combined exercise may offer broader metabolic benefit by reducing adiposity while preserving muscle.
Supporting source [1]
Proposed strategy and need for SO-specific trials
Based on available direct and indirect evidence, the review suggests that long-term, progressive, moderate-intensity resistance exercise combined with aerobic exercise may be a promising strategy for managing sarcopenic obesity. The authors explicitly state that confirmation in sarcopenic-obesity-specific randomized controlled trials is warranted. They also call for future studies that integrate dynamic monitoring of autophagic flux, functional outcomes and phenotype-stratified exercise prescriptions to translate mechanistic insights into individualized interventions.
Supporting source [1]
How to interpret this
This is a narrative review; the abstract reports no study design details, sample sizes, follow-up or outcome data. The exercise strategy is based on direct and indirect evidence and is explicitly described as needing confirmation in sarcopenic-obesity-specific randomized controlled trials. Only the abstract was reviewed; the full text was not reviewed.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Jiang T, Wang X, Yao X, Xia J, Liang J. · europepmc.org · September 24, 2026