loading

About Author

At BILM, we believe in the power of Educating, Accrediting and inspiring Excellence in Longevity Medicine for doctors in the UK.

Contact Info

0

Your Cart 0

No products in the basket.

1. Scope

What this covers. Objective, performance-based measures of physical function used to estimate biological age, stratify mortality/morbidity risk, and monitor response to longevity interventions in adults attending a private UK longevity clinic. Core assessments covered: gait (walking) speed, handgrip strength (dynamometry), Timed Up-and-Go (TUG), Short Physical Performance Battery (SPPB), Five-Times-Sit-to-Stand (FTSST), standing balance, and cardiorespiratory fitness (CRF/VO₂max/estimated METs). Composite tools covered: comprehensive geriatric assessment (CGA), deficit-accumulation frailty index, Clinical Frailty Scale (CFS), FRAIL and PRISMA-7 questionnaires, and WHO Intrinsic Capacity.

What this does NOT cover. Molecular/omic ageing biomarkers (epigenetic clocks, proteomic/metabolomic clocks) except where they contextualise functional measures; disease-specific rehabilitation protocols; paediatrics; formal sports-performance testing. Specific pharmacological or device longevity interventions are out of scope except as the target of monitoring.

Positioning. Functional assessment is adjunctive to, not a replacement for, conventional primary and secondary care. Abnormal findings frequently reflect reversible or treatable conditions requiring conventional pathways. Most functional measures are validated as prognostic markers; treating the measure itself (rather than the underlying modifiable driver) is not evidence-based.

2. Background and biological rationale

  • Chronological age is a weak proxy for an individual’s physiological reserve; biological age — the degree to which physiology deviates from chronological expectation — better captures risk and is potentially modifiable (Kritchevsky & Cummings, JAMA 2025; Tuminello et al., GeroScience 2026).
  • Functional decline is a downstream, integrative readout of multiple ageing hallmarks (sarcopenia/mitochondrial decline, neuromuscular ageing, cardiovascular and pulmonary reserve loss, inflammaging). Because it integrates across organ systems, physical performance predicts mortality and disability strongly and often independently of, or better than, individual disease diagnoses (Rosenberg et al., BMJ Open 2019).
  • An international Delphi consensus endorsed functional measures — muscle mass, muscle strength/handgrip, TUG, gait speed, standing balance, frailty index — as core biomarkers of ageing for intervention studies, alongside physiological, inflammatory and epigenetic domains (Perri et al., J Gerontol A 2025).
  • Geriatric-assessment tools that incorporate physical-function metrics (e.g. gait speed) show superior discrimination for institutionalisation, dementia, disability and mortality compared with tools that omit them (Abbadi et al., BMC Medicine 2026).

Preclinical / mechanistic-only (clearly separated — do not use for hard clinical claims). Cellular-level ageing hallmarks (telomere attrition, DNA-methylation drift, senescent-cell burden, mitochondrial dysfunction) provide mechanistic plausibility linking interventions to functional change, but the causal chain from a molecular marker to a hard functional/clinical outcome is not established by robust human data (Hamczyk et al., JACC 2020). Functional performance should not be inferred from molecular markers, nor vice versa.

3. Evidence base and GRADE-style grading

Functional assessments are supported chiefly by large prospective cohorts and meta-analyses of cohorts (Level: high-quality prognostic evidence). Almost all evidence is observational/prognostic; there is no RCT evidence that acting on a functional test score, in isolation, alters mortality. Interventional RCTs exist for the upstream drivers (exercise, CGA), not for the measurement act itself.

Outcome / measureEvidence statementGRADE certaintyKey limitationsStrength of recommendation
Cardiorespiratory fitness → all-cause mortalityMeta-analysis of 37 cohorts (n≈2.26M): top vs bottom CRF tertile RR 0.55; each +1-MET RR 0.89 (Laukkanen et al., 2022). Overview of 199 cohorts, >20.9M observations, consistent dose-response (Lang et al., 2024).High (prognostic)Residual confounding; reverse causation largely excluded by long follow-up (Clausen et al., 2018)Strong — measure and track CRF as a prognostic vital sign (AHA scientific statement, Ross et al. 2016)
Handgrip strength → all-cause & CV mortalityUK Biobank n≈500k: per 5-kg lower grip, all-cause mortality HR ~1.16–1.20 (Celis-Morales, BMJ 2018). PURE (n≈140k): stronger predictor of CV death than SBP (Leong, Lancet 2015). Dose-response meta-analysis, 48 studies, n>3.1M (López-Bueno, 2022).High (prognostic)Prognostic not causal; measurement standardisation variesStrong — measure and track; weak as a stand-alone therapeutic target
SPPB → mortality & incident disabilityMeta-analysis, 17 studies, n=16,534: vs score 10–12, score 0–3 OR 3.25, 4–6 OR 2.14, 7–9 OR 1.50 for mortality (Pavasini, BMC Med 2016); predicts incident ADL disability and mobility loss (Minneci, 2015; Western, ELSA 2022).High (prognostic, older adults)Population skews ≥65y; less validated in midlifeStrong in older adults; conditional in midlife (indirectness)
Gait speed → mortality/frailtyGait speed <0.8 m/s ~99% sensitive for Fried frailty phenotype (Kim & Rockwood, NEJM 2024); independent mortality/NHT predictor (Rosenberg, 2019). NICE frailty criterion.High (prognostic)Affected by acute illness; floor/ceiling in fit midlife adultsStrong
Comprehensive geriatric assessment (interventional)Cochrane: CGA in community-dwelling frail older people reduces hospital admission (low certainty); no clear mortality/NH-admission benefit (Briggs, 2022).Low–ModerateHeterogeneous “usual care”; sparse adverse-event dataConditional — offer in frail older adults
Composite “fitness-age”/physical-capacity batteries → biological ageCorrelate with validated CVD/mortality risk scores and Klemera-Doubal biological age (Manca, 2023; Tzemah-Shahar MAPS, 2026).Low–ModerateSmall samples; not yet calibrated/validated for individual predictionOnly in research for scoring; components usable clinically
Molecular ageing clocks as functional surrogatePredict mortality at population level (Kusters & Horvath, 2025; Yamada, 2025) but do not substitute for functional testing and lack RCT-proven responsiveness.Low–Very low for clinical useIndirectness, analytic variability, race/sex modulationOnly in research / experimental

Publication-bias note. CRF and grip-strength meta-analyses report broadly consistent effects with low heterogeneity by subgroup; small-study/positive-result bias cannot be excluded for composite “fitness-age” indices, which remain exploratory.

4. Patient selection and indications

Who may benefit (offer/consider).

  • Adults ≥50–60y, and any adult with elevated cardiometabolic risk, sedentariness, obesity, T2DM, or prior CVD — CRF and grip strength are prognostic across these groups (Ross 2016; Kim 2017).
  • Older adults (≥65y) with possible frailty, falls, unintentional weight loss, or multimorbidity — SPPB, gait speed, TUG, grip strength, and CGA are best validated here (Pavasini 2016; Briggs 2022).
  • Middle-aged adults seeking a modifiable, trackable healthspan target — CRF and strength offer actionable, reversible goals.
  • Athletic individuals — distinguish performance goals from longevity: extreme-fitness cohorts show continued (not reversed) mortality benefit with no evidence of harm at high METs (Kokkinos, 2022).

Inclusion thresholds worth flagging. Gait speed <0.8 m/s; TUG >12 s; grip strength <27 kg (men)/<16 kg (women); SPPB <10 (older adults) — each denotes elevated risk warranting evaluation (Clegg & Hassan-Smith, NICE-based, 2018; Kim & Rockwood 2024). Use age/sex-specific normative percentiles where available (ELSA reference values, Grgic 2026).

Exclusion / caution for performance testing.

  • Acute illness or recent hospitalisation — NICE advises against performance-based frailty testing when acutely unwell (cannot distinguish frailty from acute deconditioning); use report/judgement tools (CFS, FRAIL) instead (Clegg 2018).
  • Unstable cardiac disease, uncontrolled hypertension, acute MSK injury, severe balance impairment/high fall risk — defer maximal CRF and balance/TUG testing or perform with specialist input and supervision.
  • Maximal/symptom-limited exercise testing (VO₂max) requires appropriate screening, resuscitation capability, and — for higher-risk individuals — cardiology oversight.

Regulatory / ethical status.

  • Functional assessments are validated clinical measures, used on-label/within intended use (dynamometry, physical-performance batteries, exercise testing). Their use as biological-age estimators or as longevity intervention endpoints is expert-consensus/emerging, not guideline-endorsed for individual-level decision-making.
  • Composite biological-age scoring and molecular clocks should be positioned as adjunctive, with explicit informed consent, or restricted to research/registry contexts. Do not represent surrogate markers as proven determinants of lifespan.

5. Assessment and baseline work-up

History & examination. Cardiometabolic and cardiovascular risk; falls, mobility, weight change, fatigue, cognition, mood; medications (polypharmacy, anticholinergics, sedatives); physical-activity level; smoking/alcohol; occupational/functional demands. Examination: BMI, waist circumference, resting BP/HR, cardiorespiratory and MSK screen.

Core functional battery (baseline).

  • Gait speed (usual pace, 4 m) — record m/s.
  • Handgrip strength — standardised dynamometry, best of trials, dominant/non-dominant, kg; compare to age/sex norms.
  • Chair stands — FTSST (seconds) or 5-rep as part of SPPB.
  • Balance — side-by-side, semi-tandem, tandem (± single-leg eyes-closed).
  • SPPB (older adults) — composite 0–12.
  • TUG (mobility/falls) — seconds.
  • Cardiorespiratory fitness — symptom-limited CPET/VO₂max where appropriate and safe; otherwise validated submaximal estimate of METs. Treat CRF as a clinical vital sign (Ross 2016).

Frailty/composite screening (older or multimorbid). CFS, FRAIL or PRISMA-7 for screening; deficit-accumulation frailty index or CGA where multidomain evaluation is indicated (Kim & Rockwood 2024; Briggs 2022). Consider WHO Intrinsic Capacity domains.

Baseline investigations (tailored, not indiscriminate). FBC, renal/liver function, HbA1c, lipids, TSH, vitamin D, and — where sarcopenia/weight loss suspected — nutritional markers; body composition (e.g. DXA/BIA) if muscle mass relevant. Investigate abnormal functional findings for reversible causes (anaemia, thyroid, B12, depression, occult cardiorespiratory disease) rather than attributing to “ageing”.

Risk stratification.

  • Low risk: normal/above-norm performance across battery, high CRF → reassurance, lifestyle optimisation, periodic re-test.
  • Moderate: one or more sub-threshold measures without red flags → targeted intervention (exercise prescription) + review.
  • High: frailty (CFS ≥5, SPPB <7, gait <0.8 m/s), falls, low CRF with comorbidity → CGA, conventional-care referral, cautious individualised plan.

Baseline documentation. Record raw values (not just categories), test conditions, date, normative percentile, and any interventions initiated — to allow meaningful longitudinal comparison. Where used, molecular ageing markers should be documented as research/adjunctive with explicit interpretation caveats.

6. Practical implementation (protocols, not drug dosing)

Functional assessment is diagnostic/monitoring, not therapeutic; there is no “dose”. The evidence-based intervention triggered by abnormal findings is structured exercise and, where relevant, CGA-guided multidomain care.

Standardised testing protocols (robust human data).

  • Gait speed: 4-m course, usual pace, static start, average of 2 trials.
  • Grip strength: seated (or standardised standing), elbow 90°, best of 2–3 per hand; calibrated dynamometer.
  • SPPB: balance + 4-m gait + 5× chair stand, scored 0–12.
  • TUG: rise from chair, walk 3 m, turn, return, sit — time in seconds.
  • CRF: symptom-limited incremental protocol to VO₂peak, or validated submaximal estimate; express in METs for prognostic interpretation (each +1 MET ≈ 11–17% lower all-cause mortality — Lang 2024).

Intervention triggered (robust human data — the actionable output).

  • Aerobic + resistance exercise targeting CRF and strength: evidence-based and the principal lever, given dose-responsive mortality associations of CRF and grip strength. Frailty guidelines recommend exercise ± nutritional support and, where indicated, geriatric evaluation/management (Zheng et al., 2022).
  • CGA-guided multidomain intervention in frail older adults (Briggs, Cochrane 2022).

Extrapolated / caution (early or exploratory data).

  • Composite “fitness-age” indices to set or communicate intervention goals — mechanistically appealing and correlated with risk scores, but not validated for individual prediction; use as motivational/tracking adjuncts only, not as clinical endpoints (Manca 2023; Tzemah-Shahar 2026).
  • Using molecular ageing-clock change as a treatment target — experimental / research only; responsiveness to intervention and linkage to hard outcomes are unproven.

7. Monitoring, safety and follow-up

What to track. Re-measure the same battery under identical conditions. Prioritise CRF (METs/VO₂), grip strength, gait speed, and SPPB (older adults) — all have dose-responsive prognostic value and are responsive to exercise. Note the trajectory: worsening frailty/performance trajectories predict higher mortality and QoL decline (Kim & Rockwood 2024).

Timepoints (pragmatic; expert-consensus intervals).

  • Short-term (6–12 weeks): after starting an exercise/rehab programme — confirm adherence, safety, early functional response.
  • Medium-term (3–6 months): reassess CRF and strength for meaningful change.
  • Long-term (annually): full battery; frailty re-screen forms basis of an annual review in older adults.

Safety of the assessments. Testing is generally low-risk. Principal hazards are falls during balance/TUG/gait testing and cardiac events during maximal CRF testing. Mitigate with screening, supervision, spotting, and appropriate emergency provision. Balance and maximal exercise testing are the highest-risk components.

  • Common (test-related): transient fatigue, breathlessness, musculoskeletal soreness.
  • Serious but rare: falls with injury; arrhythmia/ischaemia/rarely MI or sudden death during maximal exertion in susceptible individuals.
  • Action on abnormal findings: investigate reversible causes; refer to conventional care for red flags (exertional chest pain, syncope, significant new arrhythmia, rapid unexplained functional decline, unexplained weight loss); do not attribute decline to ageing without evaluation.

Interactions / comorbidity. Beta-blockers blunt HR and limit VO₂max interpretation; sedatives/anticholinergics and orthostatic hypotension worsen balance/gait performance; osteoarthritis and neuropathy confound MSK measures. Interpret in clinical context.

Special populations.

  • Pregnancy/breastfeeding: avoid maximal exercise testing; submaximal and non-exertional measures per obstetric guidance.
  • Renal/hepatic impairment, frailty, extremes of age: favour low-burden, non-maximal, report-based tools (CFS, FRAIL); performance testing may be impractical or unsafe (Kim & Rockwood 2024).
  • Acute illness: defer performance-based testing (NICE caution).

8. Contraindications and cautions

Absolute (to maximal CRF/exercise testing): acute MI/unstable coronary syndrome, decompensated heart failure, uncontrolled arrhythmia, severe symptomatic aortic stenosis, acute PE/DVT, acute myopericarditis, acute aortic dissection — refer, do not test.

Relative / specialist input advised: uncontrolled hypertension, significant but stable valvular/structural disease, high fall risk or severe balance impairment (defer/adapt balance and TUG), acute MSK injury, acute intercurrent illness, advanced frailty where testing burden outweighs value.

Harm likely to outweigh benefit with current evidence:

  • Using functional or molecular ageing scores to initiate off-label pharmacological “anti-ageing” therapy on the basis of surrogate change alone — not supported.
  • Over-testing the low-risk worried-well with expensive/invasive assessments of low incremental yield.
  • Attributing abnormal performance to “ageing” and omitting workup for treatable disease.

9. Practical management scenarios (CKS-style)

Scenario A — Middle-aged adult with multiple cardiometabolic risk factors

Recommendation: OFFER core functional assessment (Strong). CRF and grip strength are strong, dose-responsive, independent mortality predictors in exactly this group.

  1. Assessment: CRF (CPET or validated submaximal), grip strength, gait speed; standard cardiometabolic bloods and CV risk score. Screen for occult CVD before maximal testing.
  2. Shared decision-making/consent: frame CRF/strength as modifiable prognostic vital signs; be explicit that composite “biological-age” scores are adjunctive/emerging.
  3. Initiation: individualised aerobic + resistance exercise prescription; treat conventional risk factors per NICE.
  4. Monitoring: CRF and strength at 3–6 months; annual battery.
  5. Escalate/refer: exertional symptoms, ischaemia on testing, or failure to progress → cardiology/conventional care.

Scenario B — Older, frail patient with multimorbidity

Recommendation: OFFER frailty-appropriate assessment; CONSIDER CGA (Conditional). SPPB/gait speed/grip strength are well validated here; CGA reduces hospital admission (low certainty).

  1. Assessment: screen with CFS/FRAIL; if not acutely unwell, SPPB, gait speed, grip strength, TUG; proceed to CGA/deficit-accumulation index where multidomain needs exist. Avoid performance testing if acutely unwell.
  2. Consent: emphasise falls safety and reversible-cause evaluation over “anti-ageing” framing.
  3. Initiation: supervised, progressive exercise ± nutritional support; medication review/deprescribing; address reversible deficits.
  4. Monitoring: annual (or more frequent) review tracking frailty trajectory.
  5. Escalate/refer: falls, rapid decline, weight loss, or new red flags → geriatric medicine/secondary care.

Scenario C — Patient already under specialist care, functional assessment as adjunct

Recommendation: CONSIDER as adjunct with informed consent (Conditional); do not duplicate or override specialist management.

  1. Assessment: low-burden measures (grip strength, gait speed, SPPB) to track physiological reserve and treatment tolerance; coordinate with the specialist team.
  2. Consent: clarify adjunctive role; share results with treating clinicians.
  3. Initiation: align exercise/prehabilitation with the specialist plan; avoid maximal testing where contraindicated by the underlying condition.
  4. Monitoring: integrate functional trajectory into shared reviews.
  5. Escalate/refer: any deterioration back to the responsible specialist promptly.

Scenario D — Composite biological-age scoring / molecular clocks

Recommendation: RESTRICT TO RESEARCH / registry, or offer only as explicitly experimental adjunct with consent. No robust human evidence that acting on these scores alters hard outcomes; do not base off-label therapy on them.

10. Research gaps and future directions

  • Causality vs prognosis: functional measures are proven predictors; RCTs are needed to show that assessment-guided intervention pathways improve mortality/healthspan beyond usual exercise/CGA care.
  • Midlife validation: most performance-battery mortality/disability data derive from older cohorts; thresholds and responsiveness in 40–60-year-olds (the core longevity-clinic demographic) are under-characterised (Tzemah-Shahar MAPS 2026).
  • Composite “fitness-age” indices: require standardisation, calibration, and prospective validation for individual-level prediction before clinical use.
  • Molecular–functional integration: whether epigenetic/proteomic clocks add incremental value over — or should be combined with — functional testing, and whether they change with intervention in linkage to hard endpoints, remains unresolved (Kuiper 2023; Kusters & Horvath 2025).
  • Optimal battery and re-test intervals: the minimal, highest-yield combination and clinically meaningful change thresholds are not established.
  • Where to limit practice: biological-age scoring and molecular-clock-guided decisions should ideally sit within well-designed trials or registries until outcome linkage is demonstrated.

 

Footnote


– Prognostic strength is high, causal evidence is not. Cardiorespiratory fitness (37-cohort meta-analysis, n≈2.26M; each +1-MET RR 0.89 for all-cause mortality), grip strength (UK Biobank n≈500k; PURE — stronger than SBP), and the SPPB (17-study meta-analysis, n=16,534) are robust, dose-responsive predictors. No RCT shows that acting on a test score itself alters mortality, so the document keeps measurement (prognostic) separate from intervention (exercise/CGA) and flags this explicitly.[5][8][9][10][6][7]

– Guideline anchoring. NICE-endorsed frailty thresholds (gait <0.8 m/s, TUG >12 s, PRISMA-7 >3) and the NICE caution against performance testing in acute illness are carried through. CGA is graded low–moderate certainty per Cochrane (reduces admission, no clear mortality benefit).[3][4]

– Emerging vs established is clearly demarcated. Delphi consensus supports functional measures as ageing biomarkers for research; composite “fitness-age” indices and molecular clocks are labelled research-only/experimental because individual-level prediction and intervention-responsiveness linked to hard outcomes are unproven.[1][11][12][13][14][15][16]

– Caveats. Midlife normative/threshold data are thinner than older-adult data, and surrogate-to-outcome inference is deliberately avoided. Two potentially displayable figures (grip-strength dose-response, CRF mortality curve) were available but were not essential to the reference document.[12][17]




Figure 5 Mortality Risk for the Entire Cohort According to Peak METs Achieved Kokkinos P, Faselis C, Samuel IBH, et al. Cardiorespiratory Fitness and Mortality Risk Across the Spectra of Age, Race, And Sex. Journal of the American College of Cardiology. 2022;80(6):598-609. doi:10.1016/j.jacc.2022.05.031.

 

Figure 2 Relative Mortality Risk Associated With Select Clinical Characteristics Kokkinos P, Faselis C, Samuel IBH, et al. Cardiorespiratory Fitness and Mortality Risk Across the Spectra of Age, Race, And Sex. Journal of the American College of Cardiology. 2022;80(6):598-609. doi:10.1016/j.jacc.2022.05.031.

 

Figure 1 Figure 1. Ding N, Ballew SH, Palta P, et al. Muscle Strength and Incident Cardiovascular Outcomes in Older Adults. Journal of the American College of Cardiology. 2020;75(9):1090-1092. doi:10.1016/j.jacc.2019.12.050.

 

Figure 2 Association of handgrip strength with mortality risk during follow‐up in adults 50+ years with diabetes ( n = 16 149). Andersen LL, Calatayud J, Núñez-Cortés R, Polo-López A, López-Bueno R. Graded Association of Muscle Strength With All-Cause and Cause-Specific Mortality in Older Adults With Diabetes: Prospective Cohort Study Across 28 Countries. Diabetes, Obesity & Metabolism. 2025;27(1):312-319. doi:10.1111/dom.16019.

References

  1. An Expert Consensus Statement on Biomarkers of Aging for Use in Intervention Studies. Perri G, French C, Agostinis-Sobrinho C, et al. The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences. 2025;80(5):glae297. doi:10.1093/gerona/glae297.
  2. Integrating Biological Aging Into Clinical Practice: A Review and Path Forward for Precision Longevity Medicine. Tuminello S, Anika R, Turner W, et al. GeroScience. 2026;:10.1007/s11357-026-02484-5. doi:10.1007/s11357-026-02484-5.
  3. Frailty and the Endocrine System. Clegg A, Hassan-Smith Z. The Lancet. Diabetes & Endocrinology. 2018;6(9):743-752. doi:10.1016/S2213-8587(18)30110-4.
  4. Comprehensive Geriatric Assessment for Community-Dwelling, High-Risk, Frail, Older People. Briggs R, McDonough A, Ellis G, et al. The Cochrane Database of Systematic Reviews. 2022;5:CD012705. doi:10.1002/14651858.CD012705.pub2.
  5. Objectively Assessed Cardiorespiratory Fitness and All-Cause Mortality Risk: An Updated Meta-Analysis of 37 Cohort Studies Involving 2,258,029 Participants. Laukkanen JA, Isiozor NM, Kunutsor SK. Mayo Clinic Proceedings. 2022;97(6):1054-1073. doi:10.1016/j.mayocp.2022.02.029.
  6. Cardiorespiratory Fitness Is a Strong and Consistent Predictor of Morbidity and Mortality Among Adults: An Overview of Meta-Analyses Representing Over 20.9 Million Observations From 199 Unique Cohort Studies. Lang JJ, Prince SA, Merucci K, et al. British Journal of Sports Medicine. 2024;58(10):556-566. doi:10.1136/bjsports-2023-107849.
  7. Thresholds of Handgrip Strength for All-Cause, Cancer, and Cardiovascular Mortality: A Systematic Review With Dose-Response Meta-Analysis. López-Bueno R, Andersen LL, Koyanagi A, et al. Ageing Research Reviews. 2022;82:101778. doi:10.1016/j.arr.2022.101778.
  8. Associations of Grip Strength With Cardiovascular, Respiratory, and Cancer Outcomes and All Cause Mortality: Prospective Cohort Study of Half a Million UK Biobank Participants. Celis-Morales CA, Welsh P, Lyall DM, et al. BMJ (Clinical Research Ed.). 2018;361:k1651. doi:10.1136/bmj.k1651.
  9. Prognostic Value of Grip Strength: Findings From the Prospective Urban Rural Epidemiology (PURE) Study. Leong DP, Teo KK, Rangarajan S, et al. Lancet (London, England). 2015;386(9990):266-73. doi:10.1016/S0140-6736(14)62000-6.
  10. Short Physical Performance Battery and All-Cause Mortality: Systematic Review and Meta-Analysis. Pavasini R, Guralnik J, Brown JC, et al. BMC Medicine. 2016;14(1):215. doi:10.1186/s12916-016-0763-7.
  11. A Novel Estimate of Biological Aging by Multiple Fitness Tests Is Associated With Risk Scores for Age-Related Diseases. Manca A, Fiorito G, Morrone M, et al. Frontiers in Physiology. 2023;14:1164943. doi:10.3389/fphys.2023.1164943.
  12. Midlife Aging and Performance Study (MAPS): Evaluating Biological Aging Through a Physical Capacity Battery. Tzemah-Shahar R, Shapiro I, Kodesh E, et al. GeroScience. 2026;48(2):2851-2861. doi:10.1007/s11357-025-01803-6.
  13. Epigenetic Clocks and EpiScore for Preventive Medicine: Risk Stratification and Intervention Models for Age-Related Diseases. Yamada H. Journal of Clinical Medicine. 2025;14(10):3604. doi:10.3390/jcm14103604.
  14. Quantification of Epigenetic Aging in Public Health. Kusters CDJ, Horvath S. Annual Review of Public Health. 2025;46(1):91-110. doi:10.1146/annurev-publhealth-060222-015657.
  15. Geroscience. Kritchevsky SB, Cummings SR. JAMA. 2025;334(12):1094-1102. doi:10.1001/jama.2025.11289.
  16. Biological Versus Chronological Aging: JACC Focus Seminar. Hamczyk MR, Nevado RM, Barettino A, Fuster V, Andrés V. Journal of the American College of Cardiology. 2020;75(8):919-930. doi:10.1016/j.jacc.2019.11.062.
  17. Reference Values for Gait Speed, Five-Times-Sit-to-Stand Test, Balance, and Handgrip Strength: Analysis of Data From the English Longitudinal Study of Ageing. Grgic J, Wazny VK, Kirk B, Poon ET, Valenzuela PL. GeroScience. 2026;:10.1007/s11357-026-02163-5. doi:10.1007/s11357-026-02163-5.
  18. Cardiorespiratory Fitness and Mortality Risk Across the Spectra of Age, Race, And Sex. Kokkinos P, Faselis C, Samuel IBH, et al. Journal of the American College of Cardiology. 2022;80(6):598-609. doi:10.1016/j.jacc.2022.05.031.
  19. Muscle Strength and Incident Cardiovascular Outcomes in Older Adults. Ding N, Ballew SH, Palta P, et al. Journal of the American College of Cardiology. 2020;75(9):1090-1092. doi:10.1016/j.jacc.2019.12.050.
  20. Graded association of muscle strength with all‐cause and cause‐specific mortality in older adults with diabetes: Prospective cohort study across 28 countries. Andersen LL, Calatayud J, Núñez-Cortés R, Polo-López A, López-Bueno R. Diabetes, Obesity & Metabolism. 2025;27(1):312-319. doi:10.1111/dom.16019.