Serial left ventricular adaptations in world-class professional cyclists: implications for disease screening and follow-up
Participants
n=286 professional cyclists (group A): 148 rode the 1995 Tour de France (A1), 138 the 1998 Tour (A2), 37 rode both and were examined twice (group B)
Controls: n=52 matched sedentary volunteers (group C)
Method: echocardiography; purpose = long-term LV adaptation in very-high-level endurance athletes, with an eye to detecting hypertrophic (HCM) or dilated (DCM) cardiomyopathy in a group at particularly high risk of sudden cardiac death
Protocol
Echocardiographic comparison of professional cyclists with matched sedentary volunteers (from the abstract): 148 cyclists from the 1995 Tour de France, 138 from the 1998 race, and 52 sedentary controls.
Serial subgroup: 37 cyclists who rode both races were examined twice.
Measures: diastolic left ventricular diameter (LVID), maximal wall thickness (WT), left ventricular ejection fraction (LVEF).
Key Results (from the abstract)
| Parameter | Cyclists A (n=286) | A1 1995 (n=148) | A2 1998 (n=138) | Sedentary C (n=52) |
|---|---|---|---|---|
| LV end-diastolic diameter (LVID, mm) | 60.1 ± 3.9 | 59.2 ± 3.8 | 61.0 ± 3.9 | 49.0 ± 4.3 |
| Maximal wall thickness (WT, mm) | 11.1 ± 1.3 | 11.6 ± 1.3 | 10.6 ± 1.1 | 8.6 ± 1.0 |
A vs C and A1 vs A2: p < 0.0001 for both parameters.
LV dilation: 147 of 286 cyclists (51.4%) had LVID > 60 mm; 17 of those 147 (11.6%) also had a below-normal LV ejection fraction (< 52%) — a picture "compatible with the diagnosis of DCM".
Wall thickness: exceeded 13 mm in 25 athletes (8.7%), always < 15 mm, and 23 of those 25 also had LVID > 55 mm — thick walls essentially never occurred without dilation (< 1%), which eliminates HCM.
Serial change (group B, 1995 → 1998): LVID increased 58.3 ± 4.8 → 60.3 ± 4.2 mm (p < 0.001) and WT decreased 11.8 ± 1.2 → 10.8 ± 1.2 mm (p < 0.001) — further dilation with wall thinning over three years of professional racing.
Arithmetic on the above: cyclists' LVID is ~11 mm (~23%) larger and WT ~2.5 mm (~29%) thicker than sedentary controls.
Interpretation (the authors'): world-class cyclists show marked LV dilation, in over half of them beyond 60 mm; wall thickening is modest, never ≥ 15 mm and scarce without dilation, so HCM is excluded — but the combination of dilation with reduced ejection fraction in 11.6% of dilated hearts overlaps the diagnostic picture of DCM, and serial examinations showed the dilation progressing with wall thinning.
The conclusion is about screening and follow-up, not reassurance: these findings "might have important implications for screening in athletes".
Mechanism (what the paper supports)
Eccentric remodelling from chronic volume load: large end-diastolic diameter with only modest wall thickening, i.e. the chamber grows more than the wall — the athlete's-heart pattern for endurance sport.
The abstract reports no ejection fractions for the group as a whole, no cardiac output, no resting heart rate and no LV mass; values for these in earlier versions of this entry were not from this paper.
Inference, not tested here: the wall thinning seen on serial exams is consistent with continued volume-load remodelling, but the paper cannot distinguish adaptation from early pathology in the reduced-EF minority — which is exactly why it argues for follow-up.
Application
Among 286 Tour de France-level cyclists the left ventricle was markedly dilated versus 52 sedentary controls (end-diastolic diameter 60.1 ± 3.9 vs 49.0 ± 4.3 mm; wall 11.1 ± 1.3 vs 8.6 ± 1.0 mm), 51.4% had a diameter over 60 mm, 11.6% of those also had a reduced ejection fraction (< 52%) compatible with dilated cardiomyopathy, and 37 riders re-examined three years apart showed further dilation (58.3 → 60.3 mm) with wall thinning (11.8 → 10.8 mm); thick walls (≥ 15 mm) never occurred, excluding HCM (cross-sectional + serial echocardiography, Abergel 2004).
The practical message is screening, not reassurance: a very large LV in an endurance athlete is expected, but a large LV together with a reduced ejection fraction is not something to file under "athlete's heart" without cardiology follow-up.
For the base's readers: an athlete's own echo report showing LV dilation should be interpreted against athletic norms (60 mm is the median here), while any reduced EF, symptoms, palpitations or dizziness are a doctor's question, not a training one.
Wall thickness ≥ 15 mm is not an endurance adaptation in this cohort and should never be attributed to training.
Limitations
From the design as the abstract reports it: mostly cross-sectional echocardiography (cyclists vs sedentary controls), with a serial subgroup of only 37 riders; no clinical outcomes (events, confirmed diagnoses) are reported.
Echocardiography only: the dilated hearts with reduced LVEF (17 of 147) are described as "compatible with" DCM, not diagnosed.
World-class professional cyclists only (Tour de France riders); transfer to amateur athletes is not addressed.
Controls were sedentary volunteers, not athletes from other sports.
How this entry was checked and changed
Content correction 2026-09-27
Title corrected: the paper's subtitle is "implications for disease screening and follow-up", not "the ultrasonic and hemodynamic evidence".
Invented rows deleted: LV mass index 94 vs 64, EF 68 vs 66%, cardiac output 6.2 vs 5.1 L/min, resting HR 48 vs 62 bpm, "+47%". Added the abstract's per-Tour values, the 51.4% > 60 mm / 11.6% reduced-EF / 8.7% > 13 mm findings and the serial 1995→1998 changes.
Framing "physiological adaptation, NOT pathological, HEALTHY, optimal for performance" -> abstract: over half show unusual dilation, 11.6% of those with reduced EF are compatible with a DCM diagnosis, dilation progresses with wall thinning, implications for screening. HCM exclusion (WT always < 15 mm) retained as the paper states it.
Molecular mechanisms (sarcomeres, angiogenesis, IGF-1) deleted; Sport "cycling, strength" -> cycling.
Cross-reference labels pointed at the wrong entry or named the wrong author (checked against each cited entry's byline); repointed to the entry the label describes, or removed where the base holds no such paper.
2026-09-28: added Protocol and Limitations from the abstract (Europe PMC PMID 15234423).