REF-599 · Svensson, Heinemeier, Couppé, Kjaer & Magnusson, 2016 · Journal of Applied Physiology, · Paper · PubMed
Aging tendon turns over slowly and accumulates cross-links/glycation
It adapts and heals slower than muscle; loading helps maintain it, but masters must progress tendon load gradually to avoid tendinopathy
Key Findings
Adult tendon core collagen has very slow or absent turnover after maturity (persuasive evidence); large changes early in life are maturation, not aging.
With aging, in vitro data show reduced cell-proliferation potential and fewer stem/progenitor-like cells; glycation-derived cross-links increase substantially; tendon fibril diameter, collagen content and whole-tendon size are largely unchanged; mechanically, modulus and strength fall.
With exercise, tendon cells produce growth factors; there is some support for loading-induced collagen synthesis in humans, likely at the periphery rather than the core; fibril diameter largely unaffected, some whole-tendon hypertrophy possible.
Resistance training can increase tendon stiffness and modulus and may reduce glycation — exercise tends to counteract the effects of aging.
Inference, not tested: because core turnover is near-absent and cell capacity falls with age, tendon adaptation and repair lag the muscular/metabolic gains from a stimulus, raising overuse/tendinopathy risk when load is added quickly in older athletes.
Lifelong endurance runners (15 master athletes, 64 ± 4 y) had 21% lower patellar-tendon AGE cross-link density (pentosidine) than old untrained men and a larger patellar-tendon cross-sectional area that lowered tendon stress at a given load; tendon stiffness and Young's modulus showed no age or training effect (Couppé 2014, DOI 10.1007/s11357-014-9665-9) — full text, checked 2026-09-28 (PMC4150896).
Practical Application
Aging tendon loses modulus and strength and accumulates glycation cross-links while its core collagen barely turns over, but resistance training can raise stiffness and modulus and may reduce glycation (Svensson 2016 review) — for masters athletes, keep loading the tendons rather than sparing them, and progress the load rather than the muscle.
Inference, not tested: ramp tendon-loading slowly in masters — when muscle feels ready, tendon may not be; progress high-strain work (plyos, hard hills/sprints, heavy lifting) more gradually than in the young.
Not from this paper; the base's own practice: favor heavy slow resistance / isometrics as the tendon-friendly form of the resistance training the review supports; introduce plyometrics cautiously; use a longer progressive warm-up before high-strain work; expect longer healing timelines and keep training consistent across the years.
Limitations
Mechanistic review, not a masters intervention trial — optimal loading dose/progression undefined; human tendon-turnover data limited; lifelong-athlete data carry survivorship bias.
The abstract gives no numbers (no turnover rates, no modulus values, no dose); everything quantitative in practice comes from elsewhere.
How this entry was checked and changed
Why this level
C
Content correction 2026-09-27
"longer, progressive warm-ups (20+ min)" -> number deleted; not in the abstract; warm-up advice relabelled as the base's own practice.
"tendon adaptation lags ... raising tendinopathy risk when load is added quickly" and "ramp slowly" -> relabelled inference; the abstract describes slow core turnover, reduced cell capacity, lower modulus/strength and the counteracting effect of resistance training, not a loading-rate result.
Couppé 2014 lifelong-runner line -> labelled full text; not in this abstract. Added the abstract's own points: fibril diameter/collagen content/tendon size unchanged with age, modulus and strength reduced, early-life changes are maturation.
Cross-reference pointed at an entry whose content does not match the label (checked against the cited entry); repointed or relabelled.
2026-09-28: lines labelled "full text; not checked" read against the open-access full text of the cited Couppé 2014 paper (PMC4150896; the line cites that paper, not this review): 0 confirmed, 1 corrected ("better tendon quality" -> 21% lower pentosidine, larger tendon CSA/lower stress, no stiffness/modulus difference), 0 removed.
Full text (checked 2026-10-12)
14C bomb-pulse data indicated that at least the core of the healthy human Achilles tendon is formed during the first 17 years of life, with extremely limited turnover after this point (full text).
In cells from human Achilles tendon, the number of colony-forming units decreased with aging (28 ± 5 vs. 63 ± 14 years), with lower proliferation and reduced migration of stem/progenitor cells from the aged tendon (full text).
Young and old men of similar activity levels displayed similar tendon cross-sectional areas; the authors conclude that unlike muscle there is no loss of tendon tissue with increasing age (full text).
The only major and consistent compositional change with age is the accumulation of AGE cross-links, which accumulate more in low-turnover tissues such as tendon than in skeletal muscle or skin (full text).
A longitudinal study found that 9 mo of running in previously sedentary persons did not alter the mechanical properties or size of the Achilles tendon despite cardiovascular improvements (full text).
Resistance-training studies, mostly of limited duration (12–14 wk), report increased tendon stiffness and modulus with a modest hypertrophy, with considerable variation in the response (full text).
Athletes with a 22% side-to-side difference in leg strength from habitual asymmetric loading had 36% greater patellar tendon stiffness and 20% greater cross-sectional area on the stronger side, with no significant difference in modulus (full text).
Exercise-related reductions in tendon AGE content are more likely due to formation of new nonglycated collagen than removal of AGEs from existing collagen, and loading-induced growth likely occurs at the tendon periphery (full text).