A novel mechanism underlying low orthostatic tolerance in endurance athletes: blunted left ventricular untwisting

Introduction Endurance athletes have been reported to exhibit reduced orthostatic tolerance, a phenomenon potentially linked to "athlete’s heart." However, the precise underlying mechanisms remain unclear. Left ventricular (LV) twist and untwist contribute to efficient ejection and filling, respectively, and have been shown to be augmented during orthostatic stress. It is hypothesized that a blunted response in LV twist and untwist may play a crucial role in the diminished orthostatic tolerance observed in endurance athletes. Purpose The objective of this study was to elucidate differences in LV twist and untwisting motion between endurance athletes and non-athletes during presyncope induced by lower body negative pressure (LBNP) using three-dimensional(3D) echocardiography. Methods A total of 12 male endurance athletes(EA; age: 23±8 years, height: 172.5±4.5 cm, weight: 58.1±5.2 kg, mean±SD) and 12 male non-athletes(NA; 25±5 years, 169.7±6.0 cm, 67.4±8.5 kg) underwent 3D echocardiographic assessment during graded LBNP until presyncope. Orthostatic tolerance was quantified using the cumulative stress index (CSI), calculated as the summation of the product of negative pressure and duration at each LBNP level. LV twist and peak untwisting rate were analyzed in relation to both absolute and relative LBNP loads. Data from the absolute LBNP load were compared up to the LBNP stage reached by all participants. Relative LBNP loads were employed to standardize inter-individual differences in orthostatic tolerance. Results CSI was significantly lower in EA compared to NA (p<0.05). When analyzed based on absolute LBNP, neither LV twist nor peak untwisting rate exhibited significant changes up to -50 mmHg, with no differences observed between the groups. However, when analyzed in relation to relative LBNP loads, NA demonstrated a significant increase in LV twist (Baseline: 15.2±5.1, LBNP1/2max: 14.5±5.4, LBNPpre-max: 20.9±7.7 degrees, p<0.05, ANOVA) and peak untwisting rate (-138±42, -164±50, -245±88 degrees/sec, p<0.05) at LBNPpre-max. In contrast, EA exhibited no significant changes in LV twist (12.9±5.0, 16.0±4.5, 16.8±6.5 degrees, p=0.14) and only a modest increase in peak untwisting rate (-125±41, -127±37, -161±51 degrees/sec, p=0.03). A between-group comparison revealed a significantly higher peak untwisting rate at LBNPpre-max in non-athletes (p<0.05). Conclusion The present study demonstrates that non-athletes exhibit an augmented LV twist and untwisting response to increasing LBNP load, which may serve as a compensatory mechanism to maintain stroke volume during central hypovolemia induced by orthostasis. In contrast, endurance athletes do not exhibit a similar augmentation of LV twist and untwist, suggesting impaired left ventricular torsional dynamics in response to orthostatic stress. These findings indicate that blunted LV untwisting may constitute a key mechanism underlying the reduced orthostatic tolerance observed in endurance athletes.