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Posted on Wednesday March 25, 2026 in Muscle, Protein and Metabolic Resilience
An article written by Dr Edward Leatham, Consultant Cardiologist © 2025 E.Leatham
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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.
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.
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:
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.
From a metabolic perspective, skeletal muscle matters because it:
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.
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:
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.
By anchoring diagnosis to muscle mass, we risk several clinically relevant errors:
The evidence is clear: strength is the variable that predicts outcomes.(1–6)
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:
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.
Language shapes practice.
If the disease is framed as loss of mass:
If the disease is framed as loss of strength:
This is not semantic pedantry — it directly influences patient outcomes.
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.
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