Exercise training prevents decline in stroke volume during exercise in young healthy subjects

Stroke volume (SV) increases above the resting level during exercise and then declines at higher intensities of exercise in sedentary subjects. The purpose of this study was to determine whether an attenuation of the decline in SV at higher exercise intensities contributes to the increase in maximal cardiac output (Q̇max) that occurs in response to endurance training. We studied six men and six women, 25 ± 1 (SE) yr old, before and after 12 wk of endurance training (3 days/wk running for 40 min, 3 days/wk interval training). Cardiac output was measured at rest and during exercise at 50 and 100% of maximal O₂ uptake (V̇O(2 max)) by the C₂H₂-rebreathing method. V̇O(2 max) was increased by 19% (from 2.7 ± 0.2 to 3.2 ± 0.3 l/min, P < 0.001) in response to the training program. Q̇max was increased by 12% (from 18.1 ± 1 to 20.2 ± 1 l/min, P < 0.01), SV at maximal exercise was increased by 16% (from 97 ± 6 to 113 ± 8 ml/beat, P < 0.001) and maximal heart rate was decreased by 3% (from 185 ± 2 to 180 ± 2 beats/min, P < 0.01) after training. The calculated arteriovenous O₂ content difference at maximal exercise was increased by 7% (14.4 ± 0.4 to 15.4 ± 0.4 ml O₂/100 ml blood) after training. Before training, SV at V̇O(2 max) was 9% lower than during exercise at 50% V̇O(2 max) (P < 0.05). In contrast, after training, the decline in SV between 50 and 100% V̇O(2 max) was only 2% (P = NS). Furthermore, SV was significantly higher (P < 0.01) at 50% V̇O(2 max) after training than it was before. Left ventricular hypertrophy was evident, as determined by two-dimensional echocardiography at the completion of training. The results indicate that in young healthy subjects the training-induced increase in Q̇max is due in part to attenuation of the decrease in SV as exercise intensity is increased.