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Updated: Apr 15, 2026

Experimental Protocol of a Three-minute, All-out Arm Crank Exercise Test in Spinal-cord Injured and Able-bodied Individuals
Published on: June 8, 2017
Lower limb conduit artery endothelial responses to acute upper limb exercise in spinal cord injured and able-bodied
Julia O Totosy de Zepetnek1, Jason S Au1, David S Ditor2
1Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada.
Abstract:
Vascular improvements in the nonactive regions during exercise are likely primarily mediated by increased shear rate (SR). Individuals with spinal cord injury (SCI) experience sublesional vascular deconditioning and could potentially benefit from upper body exercise-induced increases in lower body SR. The present study utilized a single bout of incremental arm-crank exercise to generate exercise-induced SR changes in the superficial femoral artery in an effort to evaluate the acute postexercise impact on superficial femoral artery endothelial function via flow-mediated dilation (FMD), and determine regulatory factors in the nonactive legs of individuals with and without SCI. Eight individuals with SCI and eight age, sex, and waist-circumference-matched able-bodied (AB) controls participated. Nine minutes of incremental arm-crank exercise increased superficial femoral artery anterograde SR (P = 0.02 and P < 0.01), retrograde SR (P < 0.01 and P < 0.01), and oscillatory shear index (OSI) (P < 0.001 and P < 0.001) in both SCI and AB, respectively. However, these SR alterations resulted in acute postexercise increases in FMD in the AB group only (SCI 6.0 ± 1.2% to 6.3 ± 2.7%, P = 0.74; AB 7.5 ± 1.4% to 11.2 ± 1.4%, P = 0.03). While arm exercise has many cardiovascular benefits and results in changes in SR patterns in the nonactive legs, these changes are not sufficient to induce acute changes in FMD among individuals with SCI, and therefore are less likely to stimulate exercise training-associated improvements in nonactive limb endothelial function. Understanding the role of SR patterns on FMD brings us closer to designing effective strategies to combat impaired vascular function in both healthy and clinical populations.
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