Does excess exercise-induced cardiac activation at exercise onset independently generate increases in cardiovascular circuit flow?

We tested the hypothesis that excess cardiac activation (ECA) generates increased cardiovascular circuit flow at the onset of exercise. 30 participants (14 female) performed 30s of right-legged knee extension/flexion exercise at 50% one-legged WR PEAK to assess the normal cardiovascular adjustment at the onset of single leg exercise (control; CON). ECA in isolation was accomplished in separate trials by initiating exercise with both the right leg and the occluded left leg (each at 50% one-legged WR PEAK ) to generate additional muscle mass activation of autonomic cardiac control without allowing the exercising left leg circulation to add to the cardiovascular circuit. Central (finger photoplethysmography) and peripheral (Doppler ultrasound) hemodynamics were measured continuously. ECA increased cardiac activation vs. CON (Δ heart rate; 35.3 ±8.4 vs. 24.5 ±8.7 beats/min, P < 0.0001), which elevated Δ Q̇ (4.62 ±1.62 vs. 3.48 ±1.51 L/min, P < 0.001) as Δ stroke volume was not different between conditions. ECA increased Δ mean arterial pressure (11.9 ±5.8 vs. 5.5 ±5.6 mmHg, P < 0.0001) via Δ Q̇ as Δ total vascular conductance was also greater during ECA (36.6 ±18.3 vs. 31.3 ±15.1 mL/min/mmHg, P = 0.0120). Δ exercising leg blood flow (LBF; 2594.3 ±639.6 vs. 2425.1 ±550.9 mL/min, P = 0.0179) but not Δ leg vascular conductance was greater in ECA vs. CON. These findings demonstrate that excess exercise-induced cardiac activation can create a greater increase in Q̇ and exercising leg perfusion at exercise onset without a change in exercising leg vasodilation magnitude during sub-maximal knee flexion/extension exercise.