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Weaker, Not Just Lighter: Monitoring Strength and Function, Not Lean Mass, During GLP-1 Weight Loss

Submitted:

30 September 2026

Posted:

02 October 2026

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Abstract
Debate about weight loss on GLP-1-based medicines has centered on how much lean mass is lost. Lean mass alone is an insufficient gauge. In older adults strength declines about three times faster than lean mass, power declines earlier still, and strength rather than mass predicts mortality; in pooled cohorts DXA lean mass does not predict falls, mobility limitation, hip fracture or death. On these medicines functional results diverge: walking distance improves in several trials, and grip strength rose in one cohort and fell in another. Assessing strength before treatment has already been recommended. This Perspective, opened by a clinical case, adds a construct and a rule. Functional discordance is a within-person decline in strength or physical performance beyond measurement error in the absence of a corresponding adverse lean-mass signal. I propose a pragmatic schedule: grip strength, five-times chair-stand time and usual gait speed, with a timed stair climb where feasible, before treatment, at 3, 6 and 12 months, and around dose reduction or discontinuation; change called real only beyond the measurement error of the test; results judged against the patient's baseline and a fixed threshold; assistance recorded. A confirmed functional decline beyond error should prompt clinical review, whatever lean mass shows. The rationale is strongest in older and vulnerable patients. The proposal is falsifiable: if lean-mass change reliably identifies the patients whose function declines, surveillance adds little; if discordance is common, lean mass is an inadequate surrogate for preserved capacity.
Keywords: 
functional discordance
;  
dynapenia
;  
muscle power
;  
GLP-1 receptor agonists
;  
muscle strength
;  
sarcopenia
;  
obesity
;  
functional assessment
Subject: 
Medicine and Pharmacology  -   Clinical Medicine
A Patient
A man in his early sixties came to me nine months after starting a dual agonist. The referral said deconditioning after weight loss. The scan said success. He had lost what the field calls a good mix: most of it fat, lean mass mostly kept.
He dated the change to month six. Not pain. Stairs. One flight at home that had been automatic now needed the rail and a pause on the landing. He walked more on flat ground because that was the advice he had been given. No one had measured grip, a timed chair stand, or the stairs as a test. The scale was still falling. He took that as proof the legs would catch up.
At month nine he missed a step carrying a bag. He caught the first stumble. He did not catch the second. No stroke. No new foot drop. No fracture that needed hardware. He came in because he no longer trusted the flight.
Grip was already below the cut point I use. Five chair rises took more than fifteen seconds. Stair-climb performance was poor for a man who still looked well muscled on dual-energy X-ray absorptiometry (DXA). He had not become empty on the scan. He had become underpowered.
I told him the same thing I tell the room after thirty-two years. I watch the stairs more than the test tubes. The medicine did the weight. Nobody had measured whether he could still produce force quickly once the weight was gone. The landing had measured it for us.
The Wrong Question
Public and professional debate about GLP-1-based therapy has asked how much of the weight lost is muscle. The trials answer it. In the SURMOUNT-1 body-composition substudy, tirzepatide reduced lean mass by 10.9% and fat mass by 33.9% over 72 weeks, and about a quarter of the weight lost was lean mass in both the tirzepatide and placebo arms [1]. In the STEP 1 substudy, semaglutide reduced lean mass by 9.7% alongside a 15.0% loss of body weight [2]. Whatever interpretation is placed on the amount of lean mass lost, these measurements do not establish whether force-producing capacity has been preserved.
Whether strength is kept is a different question, and lean mass cannot answer it. The patient above had a good mix on the scan and could not trust his stairs. Mass is a stock. Strength is what the stock can do when it is asked. A framework that treats functional capacity as a regulated quantity, maintained by demand and read only under load, predicts exactly this gap between the tissue and its use [3].
Why Lean Mass Is the Wrong Gauge
The claim is not that lean mass is useless. It is that lean mass is an insufficient surrogate for the capacity it is assumed to represent. The dissociation between mass and strength is among the best-established findings in the biology of aging. In the Health, Aging and Body Composition (Health ABC) study, annualized leg strength declined by 2.6% to 4.1% depending on sex and race, about three times the rate of loss of leg lean mass, near 1% a year, and gaining lean mass was not accompanied by maintaining strength [4]. Over five years in the same cohort, loss of muscle torque was two to five times greater than loss of muscle cross-sectional area, and weight gain did not prevent it [5]. Strength, not muscle mass, was associated with mortality: low mass did not explain the association of strength with death [6].
The Sarcopenia Definitions and Outcomes Consortium, pooling cohort data, found that DXA lean mass was not associated with incident adverse outcomes, while weakness by grip strength combined with slow gait consistently predicted falls, hip fracture, mobility limitation and death [7,8]. Clark and Manini named the age-related loss of strength dynapenia, to separate it from sarcopenia as loss of mass, and later extended the term to the loss of strength and power [9,10]. The revised European consensus now makes low strength, not low mass, the first sign of probable sarcopenia [11].
Power, the product of force and speed, is the capacity the case turned on. It “declines earlier and more precipitously with advancing age compared with muscle strength” [12], and in the InCHIANTI cohort leg power was “a more influential proximal determinant of physical performance than impairments in strength” [13]. Catching a second stumble is a test of power. Walking on flat ground, the usual advice, asks little of it.
None of this is new. What is new is the need to apply it during large, sustained pharmacological weight loss.
What Happens to Function on GLP-1 Therapy
The functional evidence does not support a simple story of harm. In STEP-HFpEF, semaglutide improved 6-minute walk distance by 20.3 m more than placebo [14]. In people with obesity and knee osteoarthritis (STEP 9), the difference was 42.6 m [15]. In symptomatic peripheral artery disease with type 2 diabetes (STRIDE), maximum walking distance improved more with semaglutide than placebo [16]. In the SEMALEAN cohort of adults with obesity, lean mass fell by about 3 kg in the first 7 months and then stabilized, while handgrip strength was about 4 kg higher at 12 months [17]. In SURPASS-3 MRI, tirzepatide reduced muscle fat infiltration more than population estimates predicted for the weight lost [18].
Other evidence runs the other way. In a 24-month retrospective cohort of older adults with type 2 diabetes, 220 treated with semaglutide and 212 controls, grip strength rose and then declined in men and fell in women, and gait speed declined in both [19]. Reviewing these studies, Prokopidis concluded that “lean soft tissue loss is not a reliable predictor of muscle strength change following GIP/GLP-1 agonists,” with shorter-term studies suggesting preservation and longer-term data in older adults pointing to possible decline [20]. Others have found hard data on sarcopenia risk in vulnerable groups to be scarce while calling for dedicated studies with proper measures [21], and have examined the causes of sarcopenia and frailty in people taking these drugs [22].
Monitoring has also been proposed. A joint advisory from four societies recommends a baseline examination that includes muscle strength, function and body composition, and notes that DXA every one to two years may be too slow to catch early muscle loss [23]. A 2026 review proposes a stepwise approach, with handgrip strength, body composition, and gait speed or the Short Physical Performance Battery at baseline, while acknowledging that no validated monitoring algorithm yet exists for this population [24].
Read together, the available studies do not show a uniform direction of functional change: several report improved walking performance, whereas strength or gait decline has been observed in some patients. Lean-mass change alone does not establish which trajectory an individual patient is following. By his own history, the patient above was in the second group; his scan said he was in the first. The question for the clinician is not what happens on average. It is what is happening to this patient.
Functional Discordance: A Rule for the Individual Patient
The central measurement problem is not lean-mass loss itself but discordance between tissue and function. I use tissue–function discordance, hereafter functional discordance, to mean a within-person decline in strength or physical performance that exceeds the measurement error of the test in the absence of a corresponding adverse lean-mass signal. What counts as an adverse lean-mass signal is defined in advance by the study or program, rather than assumed from a universal threshold. The converse, an adverse lean-mass signal with preserved or improving function, is also discordant, but in the reassuring direction. Discordance between muscle mass and handgrip strength has been described before: in a cross-sectional national survey of 4,130 Korean adults, it was present in a substantial subset and was greater with older age and higher body fat [25]. The construct here is different: change within one person over time, judged against measurement error, during pharmacological weight loss. The primary descriptive quantity is the prevalence of within-person functional discordance.
The distinction matters because lean mass and function answer different questions. DXA estimates tissue. Grip strength measures force production. Chair rise, gait speed and stair climbing measure performance under specified task conditions. One cannot be assumed to substitute for another within an individual patient.
What neither the advisory nor the review supplies is a longitudinal rule tied to the course of treatment and explicit criteria for deciding when an observed change is real. Three established measures, grip strength, five-times chair-stand time and usual gait speed, form the core panel and take about fifteen minutes with a dynamometer, a chair and a marked walkway; a timed stair climb, the task the case turned on, can be added where a flight of stairs is available (Table 1).
When. I propose a pragmatic schedule, not an evidence-established one: before treatment; at 3, 6 and 12 months; and around substantial treatment transitions such as dose reduction or discontinuation, which are additional informative measurement points. The purpose is not to establish that the drug caused a change, but to determine whether strength or physical performance has changed while weight is being lost. In the case above, a test at month three or six might have found the loss before the landing did.
How to read it. Four conditions keep a good-looking number from hiding a real loss [27,28]:
  • • Change must exceed error. A difference smaller than the test’s measurement error for that population is noise, however it is labeled. The error boundary should be prespecified from reproducibility data obtained with the same test protocol and, where possible, in a population similar to the patient being assessed. For 4-m usual gait speed in community-dwelling older adults, for example, the 95% minimum detectable change was 0.108 m/s in intermediate-speed walkers and 0.144 m/s in fast walkers [29]; for the five-times chair stand in older women it was 2.5 s [30]. Published minimum detectable change estimates for grip strength vary widely across protocols and populations [31], which reinforces the need to prespecify an error boundary appropriate to the test method and the patient population.
  • • Judge against a fixed threshold, not only the last value. A patient compared only with their own previous result can decline in steps too small to flag, each one accepted as the new baseline. The fixed threshold does not move.
  • • Record help. A chair stand with a hand on the thigh, or a flight climbed with the rail, is a different measurement from one without. Device use and human help are recorded separately at every visit [28].
  • • Record every trial. How much a patient varies between trials is information, and discarding all but the best result discards it [27].
What to do with it. The functional result, not lean mass, sorts the patient; lean mass labels the result as concordant or discordant (Table 2). A confirmed functional decline beyond measurement error should prompt clinical review of potentially modifiable contributors, including loading, nutrition, rate of weight loss, comorbidity and the appropriateness of the treatment regimen.
The response is not new either. In older adults losing weight by diet, adding exercise improved physical performance and strength, and combined aerobic and resistance training slowed the loss of lean mass most [32,33]; in community weight-loss programs, resistance training preserved knee-extensor strength that weight loss alone lost [34,35]. The joint advisory recommends strength training at least three times a week with at least 150 minutes of moderate aerobic exercise, and notes that a protein intake of 1.5 g per kilogram of lean body mass a day is considered more accurate, with an absolute target of 80 to 120 g a day to help adherence [23]. For the patient above, what was missing was power: load moved quickly, not only more walking. The contribution here is to say when those responses are needed for a given patient, by measuring the thing they are meant to protect.
What This Paper Does Not Claim
  • • It does not claim that GLP-1-based medicines cause weakness. The trial evidence on function is largely reassuring.
  • • It does not claim that strength predicts outcomes better than mass. That is established [6,7,8,11].
  • • It is not the first to report that lean-mass change may not track strength change on these agents [20], nor the first to argue that muscle assessment during treatment should extend beyond lean mass to muscle quality and function [36], nor the first to propose assessing strength during treatment [23,24].
It adds a named, countable construct, functional discordance, and a longitudinal rule for detecting it: a schedule tied to the course of treatment, four conditions for reading change in one patient, and a way to read function and lean mass together.
What Would Establish Whether the Rule Is Useful
This proposal is not a validated monitoring algorithm. The suggested schedule has not been prospectively tested; measurement-error boundaries vary by test protocol and population; and thresholds developed for sarcopenia assessment have not been established as treatment-monitoring thresholds during GLP-1-based weight loss. The available functional evidence is also heterogeneous across age, disease state, treatment and outcome measure. The rationale for surveillance is therefore strongest in older adults and in patients already vulnerable to loss of strength or physical function; its value in younger and otherwise robust patients remains to be established.
Those limitations make the proposal testable rather than merely precautionary. A prospective cohort needs serial body-composition and functional measurements obtained under standardized conditions. The primary descriptive quantity is the prevalence of within-person functional discordance. If lean-mass change reliably identifies the same patients whose strength or performance declines beyond measurement error, direct functional surveillance adds little. If discordance is common, tissue measurement alone is an inadequate surrogate for preserved capacity. The patient above illustrates the clinical situation the construct is intended to detect.
Conclusions
The scale reports weight. DXA reports tissue. Neither reports what the patient can do. During GLP-1-based weight loss, the clinically important question is not simply how much lean mass was lost, but whether strength and physical function were preserved. That question can be measured directly.
I propose a pragmatic longitudinal rule: measure strength and function before treatment and during weight loss, interpret change only beyond measurement error, retain fixed thresholds, and record the assistance state under which each test was performed. Lean mass remains useful, but it should not substitute for the capacity it is assumed to represent. What the rule looks for is functional discordance: strength or performance falling beyond measurement error without a corresponding adverse lean-mass signal.
The proposal is testable. If serial lean-mass change reliably identifies the same patients whose strength and function decline, direct functional surveillance adds little. If the two measures frequently diverge, then monitoring tissue alone is insufficient. During profound pharmacological weight loss, the patient should not merely become lighter. We should know whether the patient has become weaker.

Funding

This research received no external funding.

Data Availability Statement

No new data were generated.

Use of Artificial Intelligence

AI tools were used for background research, citation retrieval, and output formatting. All content and conclusions were created by the author, who is solely responsible for the work.

Conflicts of Interest

The author declare no conflict of interest.

References

  1. Look, M.; Dunn, J.P.; Kushner, R.F.; Cao, D.; Harris, C.; Gibble, T.H.; et al. Body composition changes during weight reduction with tirzepatide in the SURMOUNT-1 study of adults with obesity or overweight. Diabetes Obes. Metab. 2025, 27(5), 2720–2729. [Google Scholar] [CrossRef]
  2. Wilding, J.P.H.; Batterham, R.L.; Calanna, S.; Van Gaal, L.F.; McGowan, B.M.; Rosenstock, J.; et al. Impact of semaglutide on body composition in adults with overweight or obesity: exploratory analysis of the STEP 1 study. J. Endocr. Soc. 2021, 5 (Suppl 1), A16–A17. [Google Scholar] [CrossRef]
  3. O’Leary, R.T. The Preservation of Functional Reserve: A Control Systems Framework for Human Aging. Life 2026, 16(9), 1457. [Google Scholar] [CrossRef]
  4. Goodpaster, B.H.; Park, S.W.; Harris, T.B.; Kritchevsky, S.B.; Nevitt, M.; Schwartz, A.V.; et al. The loss of skeletal muscle strength, mass, and quality in older adults: the Health, Aging and Body Composition Study. J. Gerontol. A Biol. Sci. Med. Sci. 2006, 61(10), 1059–1064. [Google Scholar] [CrossRef]
  5. Delmonico, M.J.; Harris, T.B.; Visser, M.; Park, S.W.; Conroy, M.B.; Velasquez-Mieyer, P.; et al. Longitudinal study of muscle strength, quality, and adipose tissue infiltration. Am. J. Clin. Nutr. 2009, 90(6), 1579–1585. [Google Scholar] [CrossRef]
  6. Newman, A.B.; Kupelian, V.; Visser, M.; Simonsick, E.M.; Goodpaster, B.H.; Kritchevsky, S.B.; et al. Strength, but not muscle mass, is associated with mortality in the health, aging and body composition study cohort. J. Gerontol. A Biol. Sci. Med. Sci. 2006, 61(1), 72–77. [Google Scholar] [CrossRef]
  7. Bhasin, S.; Travison, T.G.; Manini, T.M.; Patel, S.; Pencina, K.M.; Fielding, R.A.; et al. Sarcopenia definition: the position statements of the Sarcopenia Definition and Outcomes Consortium. J. Am. Geriatr. Soc. 2020, 68(7), 1410–1418. [Google Scholar] [CrossRef]
  8. Cawthon, P.M.; Manini, T.; Patel, S.M.; Newman, A.; Travison, T.; Kiel, D.P.; et al. Putative cut-points in sarcopenia components and incident adverse health outcomes: an SDOC analysis. J. Am. Geriatr. Soc. 2020, 68(7), 1429–1437. [Google Scholar] [CrossRef]
  9. Clark, B.C.; Manini, T.M. Sarcopenia ≠ dynapenia. J. Gerontol. A Biol. Sci. Med. Sci. 2008, 63(8), 829–834. [Google Scholar] [CrossRef]
  10. Manini, T.M.; Clark, B.C. Dynapenia and aging: an update. J. Gerontol. A Biol. Sci. Med. Sci. 2012, 67(1), 28–40. [Google Scholar] [CrossRef]
  11. Cruz-Jentoft, A.J.; et al. Sarcopenia: revised European consensus on definition and diagnosis. Age Ageing 2019, 48(1), 16–31. [Google Scholar] [CrossRef]
  12. Reid, K.F.; Fielding, R.A. Skeletal muscle power: a critical determinant of physical functioning in older adults. Exerc Sport Sci. Rev. 2012, 40(1), 4–12. [Google Scholar] [CrossRef]
  13. Bean, J.F.; Leveille, S.G.; Kiely, D.K.; Bandinelli, S.; Guralnik, J.M.; Ferrucci, L. A comparison of leg power and leg strength within the InCHIANTI study: which influences mobility more? J. Gerontol. A Biol. Sci. Med. Sci. 2003, 58(8), M728–M733. [Google Scholar] [CrossRef]
  14. Kosiborod, M.N.; Abildstrom, S.Z.; Borlaug, B.A.; Butler, J.; Rasmussen, S.; Davies, M.; et al. Semaglutide in patients with heart failure with preserved ejection fraction and obesity. N Engl. J. Med. 2023, 389(12), 1069–1084. [Google Scholar] [CrossRef]
  15. Bliddal, H.; Bays, H.; Czernichow, S.; Udden Hemmingsson, J.; Hjelmesaeth, J.; Morville, T.H.; et al. Once-weekly semaglutide in persons with obesity and knee osteoarthritis. N Engl. J. Med. 2024, 391(17), 1573–1583. [Google Scholar] [CrossRef]
  16. Bonaca, M.P.; Catarig, A.M.; Houlind, K.; Ludvik, B.; Nordanstig, J.; Ramesh, C.K.; et al. Semaglutide and walking capacity in people with symptomatic peripheral artery disease and type 2 diabetes (STRIDE): a phase 3b, double-blind, randomised, placebo-controlled trial. Lancet 2025, 405(10489), 1580–1593. [Google Scholar] [CrossRef]
  17. Alissou, M.; Demangeat, T.; Folope, V.; et al. Impact of semaglutide on fat mass, lean mass and muscle function in patients with obesity: the SEMALEAN study. Diabetes Obes. Metab. 2026, 28(1), 112–121. [Google Scholar] [CrossRef]
  18. Sattar, N.; Neeland, I.J.; Dahlqvist Leinhard, O.; Fernandez Lando, L.; Bray, R.; Linge, J.; et al. Tirzepatide and muscle composition changes in people with type 2 diabetes (SURPASS-3 MRI). Lancet Diabetes Endocrinol. 2025, 13(6), 482–493. [Google Scholar] [CrossRef]
  19. Ren, Q.; Zhi, L.; Liu, H. Semaglutide therapy and accelerated sarcopenia in older adults with type 2 diabetes: a 24-month retrospective cohort study. Drug Des. Devel Ther. 2025, 19, 5645–5652. [Google Scholar] [CrossRef]
  20. Prokopidis, K. Glucagon-like peptide-1 receptor agonists and muscle strength changes in older adults: risks beyond muscle mass reductions. Br. J. Pharmacol. Published online. 2026. [Google Scholar] [CrossRef]
  21. Scheen, A.J. GLP-1-derived therapies and sarcopenia: plea for a specific focus on at risk special populations. Diabetes Metab. 2026, 52(1), 101708. [Google Scholar] [CrossRef]
  22. Langer, H.T.; Joshi, A.S.; Muller-Werdan, U.; Norman, K. Causes of sarcopenia and frailty in people taking GLP1RAs. Nat. Rev. Endocrinol. 2026, 22, 383–384. [Google Scholar] [CrossRef]
  23. Mozaffarian, D.; Agarwal, M.; Aggarwal, M.; Alexander, L.; Apovian, C.M.; Bindlish, S.; et al. Nutritional priorities to support GLP-1 therapy for obesity: a joint Advisory from the American College of Lifestyle Medicine, the American Society for Nutrition, the Obesity Medicine Association, and The Obesity Society. Obesity 2025, 33(8), 1475–1503. [Google Scholar] [CrossRef]
  24. Mollero, E.L.M.; Dozzani, I.; Biamonte, E.; Bendotti, G.; Marzullo, P.; Aimaretti, G.; et al. Beyond weight loss: skeletal muscle health during incretin-based therapy in patients with diabesity. Nutrients 2026, 18(16), 2654. [Google Scholar] [CrossRef]
  25. Nguyen, V.T.; Jeong, Y.; Lee, T. Identifying individuals at risk of functional decline despite preserved muscle mass: insights from appendicular skeletal muscle mass and handgrip strength discordance. J. Clin. Med. 2026, 15(7), 2650. [Google Scholar] [CrossRef]
  26. Bean, J.F.; Kiely, D.K.; LaRose, S.; Alian, J.; Frontera, W.R. Is stair climb power a clinically relevant measure of leg power impairments in at-risk older adults? Arch. Phys. Med. Rehabil. 2007, 88(5), 604–609. [Google Scholar] [CrossRef]
  27. O’Leary, R.T. The Reserve Protocol: A Measurement Specification for Functional Reserve. Preprints.org 2026. [Google Scholar] [CrossRef]
  28. O’Leary, R.T. Assistance State as a Condition of Functional Measurement. Preprints.org 2026. [Google Scholar] [CrossRef]
  29. Goldberg, A.; Schepens, S. Measurement error and minimum detectable change in 4-meter gait speed in older adults. Aging Clin. Exp. Res. 2011, 23(5-6), 406–412. [Google Scholar] [CrossRef]
  30. Goldberg, A.; Chavis, M.; Watkins, J.; Wilson, T. The five-times-sit-to-stand test: validity, reliability and detectable change in older females. Aging Clin. Exp. Res. 2012, 24(4), 339–344. [Google Scholar] [CrossRef]
  31. Bohannon, R.W. Test-retest reliability of measurements of hand-grip strength obtained by dynamometry from older adults: a systematic review of research in the PubMed database. J. Frailty Aging 2017, 6(2), 83–87. [Google Scholar] [CrossRef]
  32. Villareal, D.T.; Chode, S.; Parimi, N.; Sinacore, D.R.; Hilton, T.; Armamento-Villareal, R.; et al. Weight loss, exercise, or both and physical function in obese older adults. N Engl. J. Med. 2011, 364(13), 1218–1229. [Google Scholar] [CrossRef]
  33. Villareal, D.T.; Aguirre, L.; Gurney, A.B.; Waters, D.L.; Sinacore, D.R.; Colombo, E.; et al. Aerobic or resistance exercise, or both, in dieting obese older adults. N Engl. J. Med. 2017, 376(20), 1943–1955. [Google Scholar] [CrossRef]
  34. Rejeski, W.J.; Ambrosius, W.T.; Burdette, J.H.; et al. Community weight loss to combat obesity and disability in at-risk older adults. J. Gerontol. A Biol. Sci. Med. Sci. 2017, 72(11), 1547–1555. [Google Scholar] [CrossRef]
  35. Beavers, K.M.; Ambrosius, W.T.; Rejeski, W.J.; Burdette, J.H.; Walkup, M.P.; Sheedy, J.L.; et al. Effect of exercise type during intentional weight loss on body composition in older adults with obesity. Obesity 2017, 25(11), 1823–1829. [Google Scholar] [CrossRef]
  36. Jensterle, M.; Janež, A. Rethinking muscle health assessment in GLP-1-based therapies for obesity: beyond lean mass. Diabetes Obes. Metab. 2026, 28(6), 4428–4431. [Google Scholar] [CrossRef]
Table 1. The minimum functional surveillance panel. Grip is strength; chair-stand time, gait speed and stair-climb time are performance measures. The two consensus threshold sets differ; choose one and keep it.
Table 1. The minimum functional surveillance panel. Grip is strength; chair-stand time, gait speed and stair-climb time are performance measures. The two consensus threshold sets differ; choose one and keep it.
Test How Fixed thresholds
Grip strength Hand dynamometer, same hand, posture and instructions each visit; every trial recorded EWGSOP2: below 27 kg (men), 16 kg (women) [11]. SDOC: below 35.5 kg (men), 20 kg (women) [8]
Five-times chair stand Timed, arms crossed, same chair height each visit EWGSOP2: longer than 15 s [11]
Usual gait speed Marked course, repeated trials, every trial recorded SDOC: slower than 0.8 m/s [8]
Timed stair climb (where feasible) One flight, same stairs each visit, rail use recorded. Power can be calculated from time, vertical height and body mass [26], but it falls with body mass alone during weight loss, so time is the measure followed and power is secondary No consensus threshold; read time against the patient’s own baseline and measurement error
Table 2. Reading function and lean mass together. Function decides whether to review; lean mass says whether the change is concordant. The adverse lean-mass signal is defined in advance by the study or program.
Table 2. Reading function and lean mass together. Function decides whether to review; lean mass says whether the change is concordant. The adverse lean-mass signal is defined in advance by the study or program.
Functional result (against error) Adverse lean-mass signal Interpretation
Stable or improved Absent No measured functional deterioration
Declined beyond error Absent Functional discordance: functional deterioration is present without a corresponding adverse lean-mass signal. The opening case illustrates this clinical pattern but was not measured serially
Stable or improved Present Discordant in the reassuring direction: do not escalate on lean mass alone
Declined beyond error Present Concordant deterioration of tissue and function
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