Local Vascular Hemodynamic Response During and After Passive Stretching

Abstract

PURPOSE: Only few investigations focused on the peripheral hemodynamic responses to passive limb stretching (PLS), and only in the animal model. Therefore, the aim of this study was to determine in healthy humans the acute effects of PLS on limb blood flow (LBF). Our hypothesis was that peripheral hemodynamic responses would be affected by the PLS, because of the repetitive ischemia/reperfusion cycles induced by the passive muscle tension. METHODS: Twelve healthy individuals (age: 22 ± 3 yrs) underwent PLS of the knee extensors. The PLS procedure (45 s stretch/passive flexion, 15 s release/passive extension) was repeated five times. Measurements of arterial blood velocity and vessel diameter were taken in the passively stretched leg, distal to the inguinal ligament and proximal to the deep superficial femoral bifurcation by ultrasound system. RESULTS: PLS had a significant influence on peripheral hemodynamic. Specifically, LBF responses during the 1st passive flexion of PLS transitory increased with respect to baseline by ∼78% (from 495±110 to 882±121 ml/min; P<0.05). Interestingly, a second hyperemia (to 880±118 ml/min; P<0.05) was recorded during the limb passive extension after the 1st PLS. During the 2nd PLS procedure, the hyperemic response recorded during the passive flexion was markedly reduced with respect to the 1st (608±103 ml/min), while LBF recorded during the passive extension was similar to the 1st PLS (915±131 ml/min). From the 3rd PLS procedure, the hyperemic responses to PLS were negligible, while the peaks of LBF were consistently elevated. CONCLUSION: In agreement with our hypothesis, PLS significantly influenced peripheral circulation in the passively stretched knee extensors. However, the time response of these alterations in the peripheral hemodynamic suggests two different components of this phenomenon. The hyperemic response corresponding to the flexion phase of PLS may be explained by an acute release of nitric oxide derived from the mechanical stretch of the vessels. Afterwards, the response decreased progressively during the 2nd, 3rd, 4th, and 5th PLS procedures. Conversely, the constant hyperemic responses recorded during the passive extensions of PLSs were possibly caused by a reduced ischemia determined by a diminished muscle tension.