The contribution of left ventricular (LV) torsion and recoil in augmenting stroke volume during exercise is poorly understood. This study examined the effects of aging on LV torsion and recoil at rest and during sub-maximal exercise in 11 young (YU) and 9 older, untrained males (OU), and 12 age-matched older, endurance-trained males (OT) in upright and supine body positions. LV torsion increased from rest to exercise in YU in upright and supine body positions (9.9±2.3 to 13.2±5.2 degrees, p=.03, and 8.8±3.8 to 12.8±6.6 degrees, p=.02, respectively), but not in OU. LV torsion increased with exercise in the supine body position only in OT (p=.046). There were no differences in EDV or change in ESV with supine exercise across groups suggesting that once the Frank-Starling mechanism is fully recruited, the young heart, and that of older, endurance-trained subjects may augment SV by increasing LV torsion and contractility rather than contractility alone.

The contribution of left ventricular (LV) torsion and recoil in augmenting stroke volume during exercise is poorly understood. This study examined the effects of aging on LV torsion and recoil at rest and during sub-maximal exercise in 11 young (YU) and 9 older, untrained males (OU), and 12 age-matched older, endurance-trained males (OT) in upright and supine body positions. LV torsion increased from rest to exercise in YU in upright and supine body positions (9.9±2.3 to 13.2±5.2 degrees, p=.03, and 8.8±3.8 to 12.8±6.6 degrees, p=.02, respectively), but not in OU. LV torsion increased with exercise in the supine body position only in OT (p=.046). There were no differences in EDV or change in ESV with supine exercise across groups suggesting that once the Frank-Starling mechanism is fully recruited, the young heart, and that of older, endurance-trained subjects may augment SV by increasing LV torsion and contractility rather than contractility alone.