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. Thirty participants (14 females) performed 30 s of right-legged knee extension/flexion exercise at 50% of one-legged WR<sub>PEAK</sub> 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<sub>PEAK</sub>) 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 versus CON (Δ heart rate; 35.3 ± 8.4 vs. 24.5 ± 8.7 beats/min, <i>P</i> < 0.0001), which elevated ΔQ̇ (4.62 ± 1.62 vs. 3.48 ± 1.51 L/min, <i>P</i> < 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, <i>P</i> < 0.0001) via ΔQ̇, as Δ total vascular conductance was also greater during ECA (36.6 ± 18.3 vs. 31.3 ± 15.1 mL/min/mmHg, <i>P</i> = 0.0120). Δ exercising leg blood flow (LBF; 2,594.3 ± 639.6 vs. 2,425.1 ± 550.9 mL/min, <i>P</i> = 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.<b>NEW & NOTEWORTHY</b> Whether increasing cardiac activation above normal can increase cardiovascular circuit blood flow above normal at exercise onset in humans remained unclear. We found that excess exercise-induced cardiac activation created a greater increase in cardiac output via greater heart rate increases. Furthermore, exercising leg perfusion also increased to a greater extent due to elevated arterial blood pressure created by greater cardiac output. In conclusion, increased cardiac activation can improve cardiovascular circuit flow responses at exercise onset.

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Journal
Journal of Applied Physiology
Published
2026-01-30
DOI
https://doi.org/10.1152/japplphysiol.00111.2025
Primary Topic
Heart Rate Variability and Autonomic Control
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article
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article

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

Michael E. Tschakovsky, Stuart P. S. Mladen, Abigail K. Zedic, Stacey P.A. Forbes
Journal of Applied Physiology
Heart Rate Variability and Autonomic Control
article

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

Michael E. Tschakovsky, Stuart P. S. Mladen, Abigail K. Zedic, Stacey P.A. Forbes
article en

Abstract

We tested the hypothesis that excess cardiac activation (ECA) generates increased cardiovascular circuit flow at the onset of exercise. Thirty participants (14 females) performed 30 s of right-legged knee extension/flexion exercise at 50% of one-legged WR<sub>PEAK</sub> 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<sub>PEAK</sub>) 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 versus CON (Δ heart rate; 35.3 ± 8.4 vs. 24.5 ± 8.7 beats/min, <i>P</i> < 0.0001), which elevated ΔQ̇ (4.62 ± 1.62 vs. 3.48 ± 1.51 L/min, <i>P</i> < 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, <i>P</i> < 0.0001) via ΔQ̇, as Δ total vascular conductance was also greater during ECA (36.6 ± 18.3 vs. 31.3 ± 15.1 mL/min/mmHg, <i>P</i> = 0.0120). Δ exercising leg blood flow (LBF; 2,594.3 ± 639.6 vs. 2,425.1 ± 550.9 mL/min, <i>P</i> = 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.<b>NEW & NOTEWORTHY</b> Whether increasing cardiac activation above normal can increase cardiovascular circuit blood flow above normal at exercise onset in humans remained unclear. We found that excess exercise-induced cardiac activation created a greater increase in cardiac output via greater heart rate increases. Furthermore, exercising leg perfusion also increased to a greater extent due to elevated arterial blood pressure created by greater cardiac output. In conclusion, increased cardiac activation can improve cardiovascular circuit flow responses at exercise onset.

Journal of Applied PhysiologyVol. 140(3)
Queen's University (CA)
Good health and well-being
Openalex Percentile: Top 72%
Heart Rate Variability and Autonomic Control
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