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

February 2, 2026

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

Key Result

Excess cardiac activation increased cardiac output by 32.7% and exercising leg blood flow by 7% at exercise onset compared to control, with no change in leg vasodilation.

Key Points

The study investigates whether excess cardiac activation increases cardiovascular flow at the onset of exercise.
Conducted trials with 30 participants performing unilateral knee exercises.
Measured central and peripheral hemodynamics continuously using photoplethysmography and Doppler ultrasound.
Implemented occlusion of one leg to isolate the effects of cardiac activation.
ECA resulted in a greater heart rate increase compared to control (35.3 vs. 24.5 beats/min).
Cardiac output significantly increased with ECA (4.62 vs. 3.48 L/min).
Mean arterial pressure also rose more during ECA (11.9 vs. 5.5 mmHg).
Exercising leg blood flow was higher with ECA (2594.3 vs. 2425.1 mL/min).

Structured PICO

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

P

Population

30 participants (14 female)

I

Intervention

Excess cardiac activation (ECA) accomplished by initiating exercise with both the right leg and the occluded left leg (each at 50% one-legged WR PEAK)

C

Comparator

Normal cardiovascular adjustment at the onset of single leg exercise (control; CON) consisting of 30s of right-legged knee extension/flexion exercise at 50% one-legged WR PEAK

O

Outcome

Central (finger photoplethysmography) and peripheral (Doppler ultrasound) hemodynamics measured continuously, including changes in heart rate, cardiac output (Q̇), stroke volume, mean arterial pressure, total vascular conductance, exercising leg blood flow, and leg vascular conductancesurrogate

Excess exercise-induced cardiac activation can independently create a greater increase in cardiac output and exercising leg perfusion at exercise onset without changing exercising leg vasodilation magnitude.

Main Result

Absolute Event Rate: 0% vs 0%

Abstract

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.

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