There is still controversy in the literature over the direction of change of limb vascular conductance at the onset of isometric exercise, and indeed the mechanisms underpinning such change in man (Joyner & Halliwill, 2000). We have examined lower leg vascular conductance in the passive limb before, during and after voluntary and electrically evoked isometric calf muscle contraction of the contrateral limb. With local ethics committee approval and the informed consent of 15 healthy subjects (13 males), mean age 25.0 ± 1 years, blood flow in the passive limb, by venous occlusion plethysmography, blood pressure by Finapres and heart rate from ECG, were recorded. Voluntary (VOL) or evoked (STIM) isometric contraction of the calf muscles was performed for 2 min at 30 % MVC with local circulatory occlusion. This was sustained for a further 2 min after contraction ended. In a separate series of experiments EMG was recorded from gastrocnemius and tibialis anterior muscles of the passive limb throughout the protocol. Additionally, in naòve subjects, the protocol was repeated using sham electrical stimulation at an unexpectedly low current, just insufficient to cause muscle contraction. Figure 1 shows vascular conductance in the passive limb before, during and after VOL and STIM. There was no significant difference between the experimental conditions (ANOVA, post hoc paired t test). After 10-15 s of exercise conductance had increased significantly (P < 0.05) in VOL and STIM exercise by a mean of 11.8 and 12.6 %, respectively (from 0.023 ± 0.002 to 0.0260 ± 0.003 and 0.0220 ± 0.002 to 0.0250 ± 0.003 ml min-1 (100 ml)-1 mmHg-1, respectively). Blood pressure was unchanged from rest at this time and heart rate had increased from 74 ± 3 to 82 ± 4 and from 73 ± 3 to 82 ± 4 beats min-1 in VOL and STIM, respectively, after 10 s of exercise. After the initial increase conductance fell progressively during exercise whilst blood pressure rose to reach expected values (Bull et al. 1989). During post-exercise circulatory occlusion conductance recovered towards resting levels but did not recover fully until restoration of the circulation to the exercised limb. In the EMG experiments no activity was seen in either muscle during the protocol. In the sham experiments the conductance change at the onset of stimulation replicated that seen during exercise.These data indicate that vasodilatation occurs in passive limb muscle at the onset of contralateral calf muscle exercise in man and that this response is independent of the mode of muscle activation. Progressive vaso-constriction then follows as exercise continues. Our EMG data suggest that the initial vasodilatation in the passive limb is unrelated to inadvertent muscle activation of this limb. The STIM and sham experiments suggest that neither central command nor active muscle force generation are required to induce the response. Other central mechanisms, e.g. the alerting response, remain as possible mediators of our findings.
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| Figure 1. Changes in passive lower limb vascular conductance before, during and after voluntary (squares) and electrically evoked (diamonds) contraction of the contralateral limb calf muscles. The post-exercise local circulatory occlusion phase of the experiment is indicated by PECO. |