Vascular compliance and viscoelasticity regulate human skeletal muscle blood flow at exercise onset

At exercise onset, large and rapid rises in skeletal muscle blood flow are facilitated by reductions in vascular resistance. However, a focus on steady-state vascular resistance overlooks the contribution of vascular mechanical properties that regulate pulsatile blood flow. Therefore, this study tested the hypothesis that compliance and viscoelasticity of the skeletal muscle vascular bed regulate blood flow responses at exercise onset. We measured beat-by-beat brachial artery blood flow (Doppler ultrasound), brachial arterial blood pressure (Finometer), and heart rate (ECG) during a 2-minute supine baseline condition and for 2-minutes after a 2-second isometric handgrip exercise (IHG, handgrip dynamometer) in 16 healthy individuals (8 females, 23 ± 2 years). This protocol was repeated for IHGs performed at 20%, 40%, 60%, and 80% of maximal voluntary contraction (MVC). Vascular compliance, viscoelasticity, and resistance were calculated using a four-element modified Windkessel model. The mean ± standard deviation of maximal percent (%) change relative to baseline are reported. Two-tailed paired t-tests were performed. IHG elicited rises in blood flow (20%: Δ 166 ± 135%, 40%: Δ 272 ± 139%, 60%: Δ 341 ± 158%, 80%: Δ 397 ± 206%, all P < 0.01) and reductions in vascular resistance (20%: Δ -59 ± 12%, 40%: Δ -71 ± 11%, 60%: Δ -77 ± 8%, 80%: Δ -80 ± 7%, all P < 0.001). IHG-mediated rises in blood flow were associated with increases in vascular compliance (20%: Δ 55 ± 44%, 40%: Δ 64 ± 60%, 60%: Δ 48 ± 33%, 80%: Δ 85 ± 69%, all P < 0.01) and increases in viscoelasticity (20%: Δ 76 ± 34%, 40%: Δ 95 ± 40%, 60%: Δ 127 ± 68%, 80%: Δ 148 ± 83%, all P < 0.0001). IHG also reduced mean arterial pressure (20%: Δ -8 ± 4%, 40%: Δ -10 ± 8%, 60%: Δ -8 ± 3%, 80%: Δ -10 ± 5%, all P < 0.001). No changes were observed for heart rate (all P > 0.2). These data suggest that increases in vascular compliance and viscoelasticity regulate blood flow responses at the onset of physical exercise in humans. This work was supported by the Match of Minds Research Award by Brock University, and Natural Sciences and Engineering Research Council of Canada (NSERC). This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

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Journal
Physiology
Published
2025-05-01
DOI
https://doi.org/10.1152/physiol.2025.40.s1.0331
Primary Topic
Cardiovascular and exercise physiology
Type
article
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article

Vascular compliance and viscoelasticity regulate human skeletal muscle blood flow at exercise onset

Deborah D. O’Leary, Stephen A. Klassen, Cameron Lynn, Felicia Bouaban et al.
2 links
Physiology
Cardiovascular and exercise physiology
article

Vascular compliance and viscoelasticity regulate human skeletal muscle blood flow at exercise onset

Deborah D. O’Leary, Stephen A. Klassen, Cameron Lynn, Felicia Bouaban, Shamae Quinquito
article en

Abstract

At exercise onset, large and rapid rises in skeletal muscle blood flow are facilitated by reductions in vascular resistance. However, a focus on steady-state vascular resistance overlooks the contribution of vascular mechanical properties that regulate pulsatile blood flow. Therefore, this study tested the hypothesis that compliance and viscoelasticity of the skeletal muscle vascular bed regulate blood flow responses at exercise onset. We measured beat-by-beat brachial artery blood flow (Doppler ultrasound), brachial arterial blood pressure (Finometer), and heart rate (ECG) during a 2-minute supine baseline condition and for 2-minutes after a 2-second isometric handgrip exercise (IHG, handgrip dynamometer) in 16 healthy individuals (8 females, 23 ± 2 years). This protocol was repeated for IHGs performed at 20%, 40%, 60%, and 80% of maximal voluntary contraction (MVC). Vascular compliance, viscoelasticity, and resistance were calculated using a four-element modified Windkessel model. The mean ± standard deviation of maximal percent (%) change relative to baseline are reported. Two-tailed paired t-tests were performed. IHG elicited rises in blood flow (20%: Δ 166 ± 135%, 40%: Δ 272 ± 139%, 60%: Δ 341 ± 158%, 80%: Δ 397 ± 206%, all P < 0.01) and reductions in vascular resistance (20%: Δ -59 ± 12%, 40%: Δ -71 ± 11%, 60%: Δ -77 ± 8%, 80%: Δ -80 ± 7%, all P < 0.001). IHG-mediated rises in blood flow were associated with increases in vascular compliance (20%: Δ 55 ± 44%, 40%: Δ 64 ± 60%, 60%: Δ 48 ± 33%, 80%: Δ 85 ± 69%, all P < 0.01) and increases in viscoelasticity (20%: Δ 76 ± 34%, 40%: Δ 95 ± 40%, 60%: Δ 127 ± 68%, 80%: Δ 148 ± 83%, all P < 0.0001). IHG also reduced mean arterial pressure (20%: Δ -8 ± 4%, 40%: Δ -10 ± 8%, 60%: Δ -8 ± 3%, 80%: Δ -10 ± 5%, all P < 0.001). No changes were observed for heart rate (all P > 0.2). These data suggest that increases in vascular compliance and viscoelasticity regulate blood flow responses at the onset of physical exercise in humans. This work was supported by the Match of Minds Research Award by Brock University, and Natural Sciences and Engineering Research Council of Canada (NSERC). This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

PhysiologyVol. 40(S1)
Brock University (CA)
Openalex Percentile: Top 77%
Cardiovascular and exercise physiology
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