Sarcopenia: Are We Diagnosing the Wrong Muscle Problem?

An article written by Dr Edward Leatham, Consultant Cardiologist     © 2025 E.Leatham

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Why this matters in a cardiometabolic clinic

Modern cardiometabolic clinics increasingly manage conditions driven by insulin resistance, visceral adiposity, hypertension, atrial fibrillation, heart failure with preserved ejection fraction, and vascular cognitive decline. These are not simply diseases of arteries or rhythm — they are diseases of metabolism.

At the centre of metabolic health sits skeletal muscle. Muscle is the primary site of glucose disposal, a major determinant of insulin levels, and a critical buffer against visceral fat accumulation. When muscle function deteriorates, insulin levels rise, visceral fat expands, blood pressure drifts upward, and cardiovascular risk escalates.

Yet muscle is still often conceptualised structurally — how much muscle a patient has — rather than functionally — how well that muscle works. This distinction matters, because metabolic health tracks far more closely with muscle strength than with muscle mass.(1–6)

This brings us to a fundamental question of language and diagnosis.

Sarcopenia: a diagnosis focused on mass, not function

The term sarcopenia literally means “loss of flesh”. It defines ageing muscle primarily by loss of muscle mass. Historically, this framing reflected early research focused on imaging, cross-sectional area, and visible wasting.

However, modern epidemiological and physiological studies show that muscle mass and muscle function diverge with age. Strength declines much faster than muscle mass, and individuals may retain apparently normal muscle bulk while experiencing profound weakness and metabolic deterioration.(4–6)

In clinical practice, many older adults are not sarcopenic by mass-based criteria — but they are clearly weak.

Strength is the prognostic variable

Large prospective cohort studies consistently demonstrate that muscle strength, most commonly assessed using grip strength, is a powerful predictor of outcomes.

Low grip strength is independently associated with:

• Cardiovascular mortality
• All-cause mortality
• Cancer mortality
• Respiratory mortality

These associations persist after adjustment for BMI, body size, and physical activity.(1,2)

Crucially, strength outperforms muscle mass as a predictor of survival. In older adults, strength — but not muscle mass — is associated with mortality risk.(4,5)

If prognosis tracks with strength rather than bulk, then it is loss of strength that defines the clinically meaningful disease.

Metabolic health follows strength, not size

From a metabolic perspective, skeletal muscle matters because it:

• Clears glucose from the bloodstream
• Buffers insulin exposure
• Oxidises fatty acids
• Generates mitochondrial ATP

Lower muscle strength identifies individuals with higher risk of insulin resistance, metabolic syndrome, type 2 diabetes, and cardiovascular disease, even when muscle mass is preserved.(3,5)

This explains a common and important clinical observation: resistance training improves insulin sensitivity and cardiometabolic health without visible hypertrophy, particularly in older adults. Improvements in muscle function and mitochondrial capacity occur long before — and sometimes without — increases in muscle size.

Dynapenia: closer to the truth, but underused

To address the mismatch between mass and function, the term dynapenia was introduced to describe age-related loss of muscle strength(7). Conceptually, this represented a major advance.

Dynapenia acknowledges that:

• Weakness can occur without muscle wasting
• Neuromuscular and mitochondrial dysfunction are central
• Functional decline is not simply a problem of shrinking tissue

Yet dynapenia never achieved widespread clinical adoption, in part because strength is harder to medicalise than mass. Muscle mass can be scanned; strength must be measured.

Ironically, many modern consensus definitions of sarcopenia now require low strength as the primary diagnostic criterion, with low muscle mass relegated to a supportive role. In effect, the science has already shifted — the name has not.

The diagnostic problem we have created

By anchoring diagnosis to muscle mass, we risk several clinically relevant errors:

1. Underdiagnosis
   Patients with preserved muscle mass but poor strength are missed.
2. False reassurance
   “Your muscle mass is normal” obscures real risk.
3. Misguided targets
   Interventions focus on hypertrophy rather than function.
4. Diluted metabolic framing
   The central role of muscle in insulin resistance and cardiometabolic disease is minimised.

The evidence is clear: strength is the variable that predicts outcomes.(1–6)

A more accurate way to think about ageing muscle

What we are really describing is not loss of muscle tissue, but loss of muscle capacity — reduced force generation, reduced fatigue resistance, and reduced metabolic flexibility.

A biologically accurate framing would emphasise:

• Strength
• Muscle quality
• Mitochondrial capacity
• Functional performance

Terms such as age-related muscle dysfunction or metabolic muscle insufficiency may be inelegant, but they better reflect the pathology encountered daily in cardiometabolic clinics.

Why this matters clinically

Language shapes practice.

If the disease is framed as loss of mass:

• We measure scans
• We chase size
• We miss function

If the disease is framed as loss of strength:

• We measure grip and sit-to-stand
• We prescribe resistance training
• We track functional improvement
• We meaningfully modify cardiometabolic risk

This is not semantic pedantry — it directly influences patient outcomes.

Conclusion

Sarcopenia describes what ageing muscle may look like.
It does not describe what ageing muscle does.

In cardiometabolic medicine — where insulin resistance, visceral adiposity, and cardiovascular risk converge — the most relevant pathology is loss of strength, not loss of mass.¹⁻⁶

If weakness predicts prognosis, then weakness should define the diagnosis.

Perhaps it is time our terminology caught up with our physiology.

References 

1. Celis-Morales CA, Welsh P, Lyall DM, Steell L, Petermann F, Anderson J, et al. Associations of grip strength with cardiovascular, respiratory, and cancer outcomes and all cause mortality: prospective cohort study of half a million UK Biobank participants. 2018 May 8 [cited 2026 Jan 21]; Available from: https://www.bmj.com/content/361/bmj.k1651 
2. Ruiz JR, Sui X, Lobelo F, Morrow JR, Jackson AW, Sjöström M, et al. Association between muscular strength and mortality in men: prospective cohort study. 2008 July 1 [cited 2026 Jan 21]; Available from: https://www.bmj.com/content/337/bmj.a439 
3. Srikanthan P, Karlamangla AS. Relative Muscle Mass Is Inversely Associated with Insulin Resistance and Prediabetes. Findings from The Third National Health and Nutrition Examination Survey. J Clin Endocrinol Metab [Internet]. 2011 Sept 1 [cited 2026 Jan 21];96(9):2898–903. Available from: https://doi.org/10.1210/jc.2011-0435 
4. Newman AB, Kupelian V, Visser M, Simonsick EM, Goodpaster BH, Kritchevsky SB, et al. Strength, But Not Muscle Mass, Is Associated With Mortality in the Health, Aging and Body Composition Study Cohort. J Gerontol Ser A [Internet]. 2006 Jan 1 [cited 2026 Jan 21];61(1):72–7. Available from: https://doi.org/10.1093/gerona/61.1.72 
5. Li R, Xia J, Zhang XI, Gathirua-Mwangi WG, Guo J, Li Y, et al. Associations of Muscle Mass and Strength with All-Cause Mortality among US Older Adults. Med Sci Sports Exerc. 2018 Mar;50(3):458–67. 
6. Peterson MD, Zhang P, Saltarelli WA, Visich PS, Gordon PM. Low Muscle Strength Thresholds for the Detection of Cardiometabolic Risk in Adolescents. Am J Prev Med. 2016 May;50(5):593–9. 
7. Clark BC, Manini TM. What is dynapenia? Nutr Burbank Los Angel Cty Calif [Internet]. 2012 May [cited 2026 Jan 21];28(5):495–503. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC3571692/ 

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