Muscle as a vital organ
Sarcopenia, imaging, and the case for measuring what we already see — in two parts
Click a labelled point on the scan ↑
Tap a tissue on the scan
From this one scan slice we can measure how much muscle there is, how good the muscle quality is, and how much fat is stored — usually from a scan the person already had for another reason.
Part I
The organ we forget to measure
For a century, radiology has treated skeletal muscle as scenery — the tissue the beam passes through on the way to the organ of interest. That framing is now scientifically and economically obsolete. Skeletal muscle is the largest metabolically active tissue in the body — roughly 40% of body mass — the principal site of insulin-mediated glucose disposal, an endocrine organ in its own right, and one of the most powerful population-level predictors of survival we can extract from imaging we have already acquired. Sarcopenia — its progressive loss — sits at the intersection of ageing, metabolic disease and preventive medicine. For a preventive-imaging practice, it is the clearest available example of value hiding in plain sight.
What sarcopenia actually is
The 2019 European consensus (EWGSOP2) redefined sarcopenia as a muscle disease — “muscle failure” — and made low muscle strength the primary criterion, with low muscle quantity or quality confirming the diagnosis and poor physical performance marking severity [S1]. The 2024 Global Leadership Initiative in Sarcopenia (GLIS) went further: sarcopenia is the concurrent combination of reduced muscle mass, reduced strength, and reduced muscle-specific strength — and, decisively, physical performance is an outcome of sarcopenia, not a defining component [S2]. Both agree it is a generalised muscle disease, increasingly prevalent with age, and at least partly reversible. Australia and New Zealand now have their own consensus guidance, which matters for any locally credible screening claim [S3].
The clinical stakes are not subtle. Low muscle mass — and, in particular, low muscle radiodensity on CT — independently predicts all-cause and one-year mortality, surgical complications, chemotherapy toxicity and loss of independence [S5][S6].
How radiology measures muscle
Click a modality to see what it measures — and where the honesty lives.
Read a single slice
Everything that matters on a body-composition CT lives on one axial image at the third lumbar vertebra (L3) — the scan at the top of this essay. Its labelled points are interactive: every tissue that drives the sarcopenia read — paraspinal and anterior abdominal wall muscle, visceral fat, subcutaneous fat and the vertebral (bone) landmark — can be measured off that single slice.
Why this is a cardiometabolic story, not a geriatric footnote
Skeletal muscle disposes of the majority of post-prandial glucose under insulin stimulation. Less functional muscle means less glucose sink — and worse glycaemic control. The relationship runs both ways: type 2 diabetes accelerates muscle loss through insulin resistance, inflammation, advanced glycation end-products, mitochondrial dysfunction and oxidative stress, while low muscle and intramuscular fat worsen insulin resistance [S8]. Sarcopenic obesity — low muscle wrapped in excess and infiltrating fat — is the most dangerous phenotype, because a normal BMI conceals it. Myosteatosis specifically tracks with metabolic derangement and predicts adverse cardiovascular outcomes, including after emergency PCI for myocardial infarction [S7].
Click a labelled point on this scan too ↑
Tap a tissue on this scan
The same tissues as the first scan, but a very different balance — more fat stored inside the belly, and less muscle around the spine.
For cardiometabolic rehabilitation this reframes muscle from cosmetic to prognostic: it is the tissue rehabilitation is trying to build, the endocrine organ (via myokines) through which exercise exerts systemic effects, and a measurable marker of whether a programme is working. A rehab pathway that never quantifies muscle is flying without its most informative instrument — one that, on any patient who has had a CT, is already in the archive.
The systems and economics view
The opportunistic-imaging argument is close to unanswerable on cost: no additional scan, no additional dose, marginal cost approaching the compute to segment the slice — increasingly automated by AI. The honest counterweights are reimbursement (often no item number for a muscle metric), workflow integration, medico-legal handling of incidental findings, and false-positive risk from miscalibrated thresholds at scale. The opportunity is to be the credible party that measures muscle rigorously, reports it with humility, links it to a cardiometabolic action pathway, and does so within Australian accreditation and radiologist-governance standards. Measuring the organ we have spent a century looking straight through is one of the highest-yield, lowest-cost moves available in preventive imaging.
Continue to Part II — Treatments & the evidence →
Part II
Treatments & the evidence
The reassuring headline is that sarcopenia is modifiable, and the most effective interventions are not pharmaceutical. The uncomfortable one is that no drug is yet approved specifically to treat it, so any pharmacological claim must be framed carefully.
1 · Resistance exercise — the cornerstone
The single most consistently effective intervention across randomised trials and meta-analyses, improving muscle mass, strength and physical performance. Progressive resistance training is first-line, first-priority, and the benchmark every other treatment is measured against. Aerobic and combined training add cardiometabolic benefit, but resistance work drives the muscle adaptation.
2 · Protein and nutrition
Higher protein intake augments gains in lean mass and strength primarily when combined with resistance training; protein alone in healthy adults has modest effect [S9]. In sarcopenic older adults, whey-protein supplementation during resistance training improves muscle mass and strength versus training alone [S10]. Practical targets sit above the RDA — commonly ~1.0–1.2 g/kg/day, up to ~1.2–1.6 g/kg/day where intake and renal function allow — with attention to leucine and per-meal distribution. Vitamin D repletion is warranted where deficient, though it does not build muscle in replete individuals.
3 · Treat the metabolic driver
In type 2 diabetes and sarcopenic obesity, controlling glycaemia, inflammation and the underlying disease is part of muscle preservation, given the bidirectional loop [S8]. Weight loss must be quality weight loss — fat down, muscle protected.
4 · The GLP-1 caveat — the live debate
GLP-1 and dual GLP-1/GIP receptor agonists produce large weight loss, but a meaningful fraction is lean mass — reported from as little as ~15% up to 40–60% of total weight lost, with wide heterogeneity by drug, population and comorbidity [S11]. Two honest qualifications: some lean-mass loss is the expected physiological accompaniment of fat loss, and DXA “lean mass” is an imperfect stand-in for muscle function. The prudent position is to pair these agents with resistance exercise and adequate protein, and to be especially vigilant in older, frailer patients — precisely the population in which serial imaging-based body-composition tracking earns its keep.
5 · Emerging pharmacotherapy — promising surrogates, unproven function
The most watched agents target the activin/myostatin pathway. In the BELIEVE phase 2 trial (Nature Medicine, 2026; 507 adults, 72 weeks), bimagrumab — an anti-activin type II receptor antibody — plus semaglutide produced ~22% total weight loss of which ~92% was fat, while limiting lean-mass loss to ~2.9%, versus ~7.4% with semaglutide alone; bimagrumab alone actually increased lean mass (~2.5%) [S12].
← Back to Part I
References
- [S1] Cruz-Jentoft AJ, et al. Sarcopenia: revised European consensus on definition and diagnosis (EWGSOP2). Age and Ageing, 2019. doi:10.1093/ageing/afy169
- [S2] Kirk B, et al. The conceptual definition of sarcopenia: Delphi consensus from the Global Leadership Initiative in Sarcopenia (GLIS). Age and Ageing, 2024. (PMC10960072)
- [S3] ANZSSFR Task Force. Consensus guidelines for sarcopenia prevention, diagnosis and management in Australia and New Zealand. Journal of Cachexia, Sarcopenia and Muscle, 2022. doi:10.1002/jcsm.13115
- [S4] Defining reference values for skeletal muscle metrics on abdominal CT: systematic review and meta-analysis. AJR American Journal of Roentgenology, 2025. doi:10.2214/AJR.25.32781
- [S5] Opportunistic measurement of skeletal muscle size and attenuation on CT predicts 1-year mortality in Medicare patients. Journals of Gerontology Series A, 2019. doi:10.1093/gerona/gly183
- [S6] Clinical, functional and opportunistic CT metrics of sarcopenia and all-cause mortality. Skeletal Radiology, 2023. doi:10.1007/s00256-023-04438-w
- [S7] Myosteatosis in cardiometabolic health (review), Endocrinology and Metabolism (PMC8743592); and myosteatosis predicts prognosis after emergency PCI for STEMI, Frontiers in Endocrinology, 2025.
- [S8] Sarcopenia and type 2 diabetes mellitus: a bidirectional relationship. Diabetes, Metabolic Syndrome and Obesity. doi:10.2147/DMSO.S186600
- [S9] Systematic review and meta-analysis of protein intake to support muscle mass and function in healthy adults. Journal of Cachexia, Sarcopenia and Muscle. doi:10.1002/jcsm.12922
- [S10] Whey protein supplementation during resistance training in older people with sarcopenia: systematic review and meta-analysis. Nutrients, 2023. doi:10.3390/nu15153424
- [S11] Changes in lean body mass with GLP-1-based therapies and mitigation strategies. Diabetes, Obesity and Metabolism. doi:10.1111/dom.15728
- [S12] Bimagrumab plus semaglutide for the treatment of obesity (BELIEVE): a randomized phase 2 trial. Nature Medicine, 2026. doi:10.1038/s41591-026-04204-0
Literature identified via PubMed and web search, July 2026. DOIs and figures to be re-verified before publication.
All views expressed here are my own personal opinions and are not medical advice. General information only — not clinical or financial advice. myradiologist.ai · ABN 29 692 758 115 · ACN 692 758 115