Single passive leg movement-induced hyperemia: a simple vascular function assessment without a chronotropic response.
Passive leg movement (PLM)-induced hyperemia is a novel approach to assess vascular function, with a potential clinical role. However, in some instances, the varying chronotropic response induced by PLM has been proposed to be a potentially confounding factor. Therefore, we simplified and modified the PLM model to require just a single PLM (sPLM), an approach that may evoke a peripheral hemodynamic response, allowing a vascular function assessment, but at the same time minimizing central responses. To both characterize and assess the utility of sPLM, in 12 healthy subjects, we measured heart rate (HR), stroke volume, cardiac output (CO), mean arterial pressure (MAP), leg blood flow (LBF), and calculated leg vascular conductance (LVC) during both standard PLM, consisting of passive knee flexion and extension performed at 1 Hz for 60 s, and sPLM, consisting of only a single passive knee flexion and extension over 1 s. During PLM, MAP transiently decreased (5 ± 1 mmHg), whereas both HR and CO increased from baseline (6.0 ± 1.1 beats/min, and 0.8 ± 0.01 l/min, respectively). Following sPLM, MAP fell similarly (5 ± 2 mmHg; P = 0.8), but neither HR nor CO responses were identifiable. The peak LBF and LVC response was similar for PLM (993 ± 189 ml/min; 11.9 ± 1.5 ml·min-1·mmHg-1, respectively) and sPLM (878 ± 119 ml/min; 10.9 ± 1.6 ml·min-1·mmHg-1, respectively). Thus sPLM represents a variant of the PLM approach to assess vascular function that is more easily performed and evokes a peripheral stimulus that induces a significant hyperemia, but does not generate a potentially confounding, chronotropic response, which may make sPLM more useful clinically.



Using the single passive leg movement (PLM) technique, a variant of the vascular function assessment PLM, we have identified a novel peripheral vascular assessment method that is more easily performed than PLM, which, by not evoking potentially confounding central hemodynamic responses, may be more useful clinically.
Department of Internal Medicine, Division of Geriatrics, University of Utah, Salt Lake City, Utah; massimo.venturelli@univr.it.|Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Verona, Italy.
Massimo
0000-0002-2469-8787
M
Venturelli
Department of Internal Medicine, Division of Geriatrics, University of Utah, Salt Lake City, Utah.
Gwenael
G
Layec
Department of Internal Medicine, Division of Geriatrics, University of Utah, Salt Lake City, Utah.|Geriatric Research, Education, and Clinical Center, George E. Whalen Veterans Affairs Medical Center, Salt Lake City, Utah; and.
Joel
J
Trinity
Department of Exercise and Sport Science, University of Utah, Salt Lake City, Utah.
Corey R
CR
Hart
Department of Exercise and Sport Science, University of Utah, Salt Lake City, Utah.
Ryan M
RM
Broxterman
Department of Internal Medicine, Division of Geriatrics, University of Utah, Salt Lake City, Utah.|Geriatric Research, Education, and Clinical Center, George E. Whalen Veterans Affairs Medical Center, Salt Lake City, Utah; and.|Department of Exercise and Sport Science, University of Utah, Salt Lake City, Utah.
Russell S
RS
Richardson
D000328:Adult; D062186:Arterial Pressure / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology; D006339:Heart Rate / Q000502:physiology; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D006940:Hyperemia / Q000503:physiopathology*; D007717:Knee / Q000098:blood supply / Q000502:physiology; D007866:Leg / Q000098:blood supply / Q000502:physiology*; D008297:Male; D009068:Movement / Q000502:physiology*; D012039:Regional Blood Flow / Q000502:physiology; D013318:Stroke Volume / Q000502:physiology
cardiovascular disease assessment; endothelial function; flow-mediated dilation