AHA Scientific Sessions 2026 Abstract · Nov 2, 2026
Higher Coronary Wall Shear Stress is Linked to Lower Peak Exercise Hemodynamic Responses During Prolonged Aerobic Exercise in Masters Athletes
By Tayon K, Carlisle A, Taylor BJ et al.
Background: Despite the cardioprotective effects of habitual exercise, master athletes (MA) demonstrate a paradoxically higher prevalence of coronary artery disease (CAD) compared to age-matched non-athletes, at approximately twice the rate. Coronary wall shear stress (WSS), the tangential force exerted by flowing blood on the endothelium, has a complex role in CAD development. Low WSS promotes plaque formation, but high WSS may injure endothelium and destabilize plaque. Acute aerobic exercise (AE) transiently increases coronary WSS, and chronic training is associated with higher resting WSS primarily due to higher antegrade coronary flow from increased vasodilatory capacity. The relationships between the hemodynamic effects of prolonged AE, coronary WSS and CAD remain unclear. Methods: Twelve MAs completed 90-minutes of submaximal AE. Heart rate (HR) was measured beat-by-beat; systolic (SBP) and diastolic (DBP) blood pressure were measured every 10 min with rate-pressure product (RPP) calculated. Within one year of AE, all participants underwent coronary CTA for assessment of mean coronary WSS during simulated hyperemia using computational fluid dynamics (Heartflow Inc.) and quantification of coronary artery calcium (CAC). Subjects on antihypertensive medication or with >50% left main or >70% left anterior descending (LAD), left circumflex (LCx) or right coronary artery (RCA) stenosis were excluded. Associations between mean WSS and AE hemodynamics were assessed using simple linear regression; the association between CAC scores and mean subject-level WSS was assessed using Spearman rank correlation. Results: Of the 12 participants (59 ± 9 years; 58% female; 347 ± 158 min/week of moderate to heavy AE), five had hyperlipidemia and eight had CAD, including four with minimal (<25%) and four with mild (25-49%) coronary stenosis. Mean CAC score was 24 AU (median 0; IQR 75; range 0-256). During AE, mean ± SD (range) HR was 138 ± 21 beats/minute (108-177), SBP was 150 ± 19 mmHg (121-176), DBP was 69 ± 12 mmHg (53-82), RPP was 20,992 ± 4,519 units (13,043-28,728), and MAP was 96 ± 12 mmHg (76-113). Subject-level mean WSS was 7.6 ± 3.0 Pa (range: 4.47-16.2; normal 1-16 Pa). Higher mean WSS was associated with lower peak RPP (R2 = 0.505; p = 0.01) and lower peak SBP (R2 = 0.426; p = 0.02) but not peak HR (R2 = 0.296; p = 0.067). Higher mean WSS was associated with lower peak RPP in the LCx (R2 = 0.555; p = 0.005), LAD (R2 = 0.434; p = 0.02), and RCA (R2 = 0.389; p = 0.03) (Figure 1). CAC score was not associated with mean subject-level WSS (r = 0.093; p = 0.77). Conclusion: In MAs, higher mean coronary WSS was associated with lower peak RPP during prolonged AE but not CAC score. While these findings should be interpreted in the context of a small sample size, they suggest that coronary shear patterns in MA relate more closely to exercise hemodynamics and coronary vasodilatory capacity than to calcific plaque burden.