We have previously reported an increase in vascular conductance of the contralateral lower limb at the onset of voluntary and stimulated isometric calf exercise (Fisher & White, 2001), but the mechanisms underpinning this change remain unclear. In dynamic exercise a similar phenomenon has been attributed to a muscle pump-induced increase in venous return and consequent sympathetic withdrawal (Joyner et al. 2001). However, this mechanism cannot explain our previous observation as (1) local circulatory arrest preceded exercise and (2) in itself this did not alter vascular conductance. The present study sought to investigate whether there are central circulatory changes at the onset of voluntary and electrically evoked isometric calf exercise that could explain our observations.
With local ethics committee approval, 13 healthy subjects (11 males), mean age (± S.E.M.) 24.1 ± 1.4 years, undertook 2 min of seated isometric plantar flexion at 30 % MVC performed either voluntarily (VOL) or electrically evoked (STIM). Circulatory occlusion commenced just prior to exercise and was sustained for 2 min after exercise. Heart rate (HR) (Cardiorater) and blood pressure (MAP) (Finapress) were recorded on a beat-to-beat basis. Indices of central haemodynamics were measured using impedance cardiography (Minnesota Impedance Cardiograph, Model 304B) with a tetrapolar band electrode configuration (Instruments for Medicine, Inc.). Stroke volume (SV) was estimated using the Kubicek formula (Kubicek et al. 1974) and cardiac output (CO) taken as the product of SV and HR. All exercise values are presented as 15 s ensemble average changes from rest. Statistical analysis was performed using repeated measures ANOVA (P < 0.05) and post-hoc paired t tests.
Table 1 shows resting HR, MAP, SV and CO values and the average changes produced by VOL and STIM over the first 15 s of exercise. SV and CO showed no significant change from resting values during either exercise protocol. During VOL but not STIM, MAP increased from resting levels and was significantly higher than STIM at this time. HR increased significantly from resting in VOL and less markedly in STIM though statistically there was no significant difference between these responses.
These data show that central haemodynamic changes are minimal at the onset of VOL and STIM. Therefore it is clear that subjects are unlikely to have inadvertently caused an increase in venous return e.g. by abdominal fixation. Thus the initiation of sympathetic withdrawal (Joyner et al. 2001) is unlikely to explain the transient increase in vascular conductance observed in the contralateral lower limb during both voluntary and stimulated isometric exercise (Fisher & White, 2001). This provides further support for a local vasodilator effect in this limb that is mediated by central pathways in response to both voluntary and stimulated exercise.
This work was supported by BHF PG/99148.
All procedures accord with current local guidelines and the Declaration of Helsinki.