Essay 05 · Writing · Muscle & Programmatics series

Muscle as a vital organ

Sarcopenia, imaging, and the case for measuring what we already see — in two parts

Axial CT at the third lumbar vertebra (L3): skeletal muscle, subcutaneous and visceral fat surrounding the vertebral body
A real CT scan slice through the belly at the L3 level — where muscle and fat are measured. Tap the gold points to see what each one is.

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

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.

The weak point, stated plainly: there is no universal muscle-mass cut-point. Widely used L3 thresholds derive from specific (often oncology) cohorts; a 2025 AJR systematic review confirmed that broadly applicable healthy-population reference values are still lacking, varying by sex, BMI and ethnicity [S4]. DXA “lean mass” is not muscle; muscle quantity is not quality; neither is strength — the very distinction GLIS insists on. Much muscle–mortality data is also observational (reverse causation). Any screening product must be calibrated to a defensible local reference and must not overclaim one number as a diagnosis. Stating these caveats is what makes the case credible.

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].

A second axial CT slice at L3 showing much more visceral fat and much less muscle
Compare with the scan at the top of this essay — here the dark visceral fat around the bowel is much greater and the muscle is noticeably thinner. This is the sarcopenic-obesity pattern, where a normal body weight can hide low muscle and high internal fat.

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].

Lead with the caveat: these are body-composition surrogate endpoints. There is not yet evidence that preserved lean mass translates into better strength, physical function, falls reduction or cardiovascular outcomes, and muscle spasms were a notable adverse effect in bimagrumab monotherapy arms. “Preserves muscle mass” is not the same claim as “keeps patients stronger and alive longer.”
Bottom line. Progressive resistance exercise plus adequate protein remains the evidence-based core, with vitamin D repletion where indicated and management of the underlying metabolic disease. Pharmacotherapy is advancing quickly on body-composition endpoints — the muscle-preserving-weight-loss story is real and commercially significant — but functional and hard-outcome evidence has not yet caught up, and the responsible position is to say so.

← Back to Part I

References

Literature identified via PubMed and web search, July 2026. DOIs and figures to be re-verified before publication.

Dr Lisa Sorger is a consultant radiologist, healthcare executive, medical administrator, company director and founder of myradiologist.ai. She writes on the economics and ethics of preventative imaging and diagnostic radiology.

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