Cardiac size-exercise coupling in Paralympic athletes with spinal cord injury: the role of lesion level.

Spinal cord injury (SCI) alters autonomic cardiovascular regulation and may limit the translation of cardiac structural adaptation into aerobic performance. Whether spinal cord neurological level modifies cardiac size-exercise coupling in elite athletes remains under investigation. We enrolled 178 Paralympic athletes with SCI (33% high SCI, above T6). Athletes underwent transthoracic echocardiography and cardiopulmonary exercise testing. SCI level was analyzed as the main predictor of cardiac structure and exercise performance. Multivariable linear regression models were adjusted for age, sex, and body weight, with additional sensitivity analyses including sport category. Mediation analyses evaluated the role of indexed left ventricular end-diastolic volume (LVEDV/BSA), and interaction models tested effect modification of the LVEDV-VO₂max relationship by SCI level. Athletes with low SCI exhibited larger LVEDV/BSA (60.6 ± 14.7 vs. 51.9 ± 11.9 mL\m², p < 0.0001) and higher VO₂ max (31.0 ± 9.4 vs. 21.0 ± 9.3 mL\kg\min, p < 0.0001) than those with high SCI. In adjusted models, high SCI independently predicted lower VO₂max (β=-8.88, 95% CI - 11.71 to - 6.05, p < 0.0001) and O₂ pulse (β=-3.38, 95% CI - 5.07 to - 1.70, p = 0.0002), persisting after adjustment for sport category (VO₂: β=-6.64, p = 0.001; O₂ pulse: β=-1.87, p = 0.004). LVEDV/BSA partially mediated the association between SCI level and VO₂ max (β = 0.323 per mL\m², p = 0.0002). A significant SCI×LVEDV/BSA interaction (β=-1.229, 95% CI - 2.548 to - 1.090, p = 0.002) indicated attenuation of cardiac size-exercise coupling in high SCI. Level of spinal cord lesion independently influences cardiac remodeling and aerobic performance and modifies how cardiac size translates into functional capacity. High-level SCI is associated with a lesion-dependent uncoupling of cardiac structure and exercise performance.