Resistance exercise shifts muscle progenitor cells to support growth in older adults
Blood flow restricted resistance training expands pro-myogenic fibro-adipogenic progenitors and inflammatory macrophages during muscle hypertrophy in older individuals.
bioRxiv · Wang J et al. · Paper published 28 Sep 2026
In a preprint studying healthy older individuals, researchers evaluated cellular adaptations in skeletal muscle following six weeks of blood flow restricted resistance exercise. Flow cytometry showed that the exercise enlarged both fibro-adipogenic progenitors (FAPs) and muscle stem cells. Total FAP abundance remained constant, but the population shifted toward a CD90-high phenotype. Transcriptional analysis revealed that CD90-high FAPs were enriched for matrix-related genes and pro-myogenic secretory factors. In culture experiments, conditioned media from CD90-high FAPs promoted myotube growth compared to media from CD90-low FAPs. Exercise training also increased the proportion of CD11c-positive pro-inflammatory macrophages in the muscle microenvironment. Further ex vivo testing showed that TNF-alpha suppressed human primary FAP proliferation, suggesting that macrophage signaling may limit excessive progenitor expansion during tissue remodeling.
Why it matters
Understanding how cellular niche components like FAPs and macrophages coordinate during exercise provides insight into how aging skeletal muscle retains the capacity for hypertrophy.
Caveats
This work is a preprint that has not yet undergone peer review, and functional cell interactions were tested using in vitro and ex vivo models.
Written from the paper’s abstract, and every claim checked against it before publishing. Read the paper for the full methods and data.
The paper
Fibro-adipogenic Progenitor and Macrophage Remodeling of the Aging Skeletal Muscle Niche During Exercise-Induced Hypertrophy
Wang J, Brorson J, Kuhdal S et al.
bioRxiv · 28 Sep 2026 · Preprint, not yet peer-reviewed
- Relevance
- Relevant
- News value
- Notable
- Evidence
- Human trial
- Status
- Preprint
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