Critical care medicine
August 7, 2026 · via Europe PMC
Rethinking Muscle Wasting in Critical Illness: A Systematic Review and Meta-Analysis of Myofiber Size and Protein Turnover.
González-Seguel F, Robinson CM, Caceres-Parra C, +10 more, Dupont-Versteegden EE.
AI summary — for doctors, generated from the abstract only
Muscle wasting in critical illness reflects smaller myofibers and higher protein-degradation markers, with no clear pooled difference in muscle protein synthesis.
What was studied
Systematic review and meta-analysis of 75 studies of skeletal muscle biopsies in adults with critical illness (2,023 patients, 642 controls), pooling myofiber size and protein turnover.
Key findings
- Cross-sectional area was 22% lower in critical illness before and after ICU discharge (e.g. MD -689 µm2, 95% CI -1265 to -113)
- Protein synthesis did not differ significantly from controls (MD 0.007%/hr; 95% CI -0.010 to 0.027)
- Degradation pathway markers were higher (standardized MD 0.5-1.7) across 11 studies
Clinical relevance
Suggests muscle loss in the ICU may be driven more by breakdown than reduced synthesis, which could inform where future interventions focus.
Who should care
Limitations
Meta-analyses of size and synthesis were based on few studies (six and seven), biopsies were mostly from one muscle in the first ICU week, and control groups varied.
Degradation, not impaired synthesis, appears prominent in ICU muscle wasting, though evidence is limited.
This is an AI-generated summary of the published abstract, not a clinical recommendation. It may not reflect the full text or subsequent updates — verify against the original source before acting on it.
Abstract
Objectives
To identify biological findings underlying skeletal muscle dysfunction in adults with critical illness and meta-analyze myofiber cross-sectional area and protein turnover variables.
Data sources
Six databases were electronically searched from inception to January 2025.
Study selection
We included original studies reporting biological findings obtained from skeletal muscle biopsies of adults with critical illness.
Data extraction
Bibliometrics, characteristics of the patients/controls, and biological findings were extracted in duplicate. Descriptive statistics of biological findings were performed. Random-effects meta-analyses investigated mean differences (MDs) in myofiber cross-sectional area and protein turnover compared with controls.
Data synthesis
From 22,035 titles screened, 75 studies ( n = 2,023 patients; n = 642 controls) published between 1988 and 2024 were included, with 48 unique patient datasets. Biopsies were mainly collected from vastus lateralis (64 [85%] studies) during the first ICU week (50% of studies) and post-ICU (9%). Biological findings included predominant type II myofiber atrophy with necrosis and structural degeneration, mitochondrial dysfunction, inflammatory/fibrotic changes, and upregulated ubiquitin-proteasome/autophagy pathways. Data from six studies ( n = 100 patients; 193 controls) indicated that cross-sectional area was 22% lower in patients with critical illness before (MD, -689 µm 2 ; 95% CI, -1265 to -113 µm 2 ; p = 0.02) and after (MD, -775 µm 2 ; 95% CI, -1512 to -37 µm 2 ; p = 0.04) ICU discharge. Across seven studies ( n = 126 patients; 61 controls) protein synthesis was not significantly different in patients with critical illness compared with controls (MD, 0.007%/hr; 95% CI, -0.010 to 0.027; p = 0.36). Protein degradation pathway markers were significantly higher (standardized MD ranging, 0.5-1.7) in data from 11 studies ( n = 439 patients; 163 controls).
Conclusions
Muscle wasting during critical illness reflects multifaceted biological disturbances. While myofiber size is significantly lower in patients with critical illness, pooled analyses show no significant differences in muscle protein synthesis compared with non-ICU controls, whereas protein degradation markers are consistently higher.
DOI
10.1097/ccm.0000000000007288
PMID
42565658
PMCID
PMC13632814
Research metadata (titles, abstracts, authors, publication dates) is sourced from Europe PMC, which aggregates content from PubMed/MEDLINE, PubMed Central, and other providers under the U.S. National Library of Medicine (NLM/NCBI). NLM does not claim copyright on abstracts; the original journal publishers or authors may hold rights to the full articles. AI-generated summaries are derived only from the abstract, never the full text, and are always labeled as AI-generated.
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