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J Physiol Volume 546, Number 1, 315-323, January 1, 2003 DOI: 10.1113/jphysiol.2002.031476
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J Physiol (2003), 546.1, pp. 315-323
© Copyright 2002 D 2003 The Physiological Society
DOI: 10.1113/jphysiol.2002.031476

The time course and direction of lower limb vascular conductance changes during voluntary and electrically evoked isometric exercise of the contralateral calf muscle in man

James P. Fisher and Michael J. White

School of Sport and Exercise Sciences, University of Birmingham, Edgebaston, Birmingham B15 2TT, UK

This study aimed to clarify the direction and timing of the change of non-active lower limb vascular conductance at the onset of contralateral limb isometric exercise and to examine the mechanisms controlling this change. Fifteen human subjects performed 2 min of electrically evoked (Stim) or voluntary (Vol) ischaemic isometric calf plantar flexor exercise at 30 % maximum voluntary contraction (MVC). Blood pressure (BP) and heart rate were continuously recorded and blood flow in the non-active contralateral lower limb was recorded at 15 s intervals. In subsets of subjects the presence of inadvertent muscle contraction was monitored by calf muscle EMG and the effects of the sensation of electrical stimulation without muscle contraction (sham) were investigated. After 10-15 s conductance had increased significantly (P < 0.05) in Vol and Stim by a mean of 15 and 12 %, respectively, whilst BP was unchanged. Following this initial increase conductance decreased progressively during Stim and Vol whilst blood pressure rose. No EMG activity was seen during either protocol. In the sham stimulation experiments where no contraction was evoked the conductance change at the onset of stimulation replicated that seen during Stim exercise. Increases in conductance were independent of central command and muscle force generation, were not activated in anticipation of exercise but could be activated secondarily to peripheral sensations associated with expected exercise. The explanation for our results might involve sympathetic withdrawal related to mental stress; however, a central pathway, which directly activates a vasodilator mechanism in passive calf muscle, remains a possibility.



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