The primary findings in this study were that CSAvein decreased from baseline during static elbow flexion alone, although CSAvein during static elbow flexion with tendon vibration did not change, and that BFvein did not change significantly during static exercise with or without tendon vibration. These results suggest that a reduction in central command during static exercise with tendon vibration may attenuate the superficial venous vessel response of the resting limb during sustained static arm exercise.
Superficial venous vessel response may be controlled by both the sympathetic nervous system [1, 4, 6, 29] and changes in venous pressure related to alterations in blood flow and blood volume [30, 31]. In our study, BFvein did not change throughout the protocol during EX and EX + VIB (Figure 2E). In addition, Δdeoxy-Hb in the resting forearm did not change from baseline with static elbow flexion during both EX and EX + VIB (Figure 3D). Because the change in oxy-Hb and deoxy-Hb is used to evaluate blood volume in arterial and venous vascular beds, respectively [32, 33], it is speculated that the venous blood volume in the resting forearm was unchanged during static elbow flexion. In our study, therefore, the decrease in CSAvein with exercise during EX may have been caused by sympathetic nervous system control. On the other hand, the difference in CSAvein between EX and EX + VIB during the recovery period might have been influenced by the change in venous blood volume but not by the sympathetic nervous system, because Δdeoxy-Hb of the resting forearm was also different between the two conditions (Figure 3D).
The concept of central command has been classically defined as a feed-forward control. Feed-forward characterization may be largely based on the immediate cardiovascular response to onset (or even anticipation) of exercise. In addition to feed-forward control, there is evidence that the effects of central command on cardiovascular responses are closely related to the intensity or perceived effort of the exercise [34, 35]. Central command is there also proposed to be capable of functioning as feedback control, in which somatosensory signals arising from the working muscles may provide a feedback signal capable of influencing central command via alterations of perception of effort or effort sense [19, 20]. The experimental model in our study might reflect central command that is defined as feedback control rather than feed-forward control, because the changes in HR and MAP, which are indexes of the cardiovascular response, were significantly lower during 96 to 120 seconds of exercise in EX + VIB than in EX (Figure 2A,B). These results are in agreement with those of previous studies [14, 25, 26]. In addition, the magnitude of the central command response has been assessed using an individual’s perception of effort sense during exercise, independent of force production [15, 34]. Although the relationship between central command and RPE has not been clearly defined, the RPE scale  has been widely used to assess the level of central command. In the present study, RPE immediately after exercise was lower in EX + VIB than in EX, indicating that central command, which is defined as feedback control, might be lower in EX + VIB than in EX. Thus, related to the central command response that is defined as feedback control, CSAvein was also smaller in EX than in EX + VIB during the latter half of the exercise. In addition, activation of the central command at the onset of static elbow flexion exercise in the present study, which indicated the feed-forward control, may have been too small to cause venoconstriction. If activation of central command at the onset of static elbow flexion exercise was enough to cause venoconstriction, the decrease in CSAvein had to be obtained at the onset of exercise in both EX and EX + VIB.
Vibration is a powerful stimulus for primary muscle spindle afferents when applied to the biceps tendon during static exercise. When the biceps brachii was contracting, activation of its muscle spindle primary afferents provided reflex activation, which in turn aided voluntary tension development compared with contraction only of the biceps brachii. The afferent input of decreased voluntary tension during exercise with tendon vibration might thus cause interactions between perception of effort and central command, such that the activation of central command might alter .
The increase in sympathetic nervous system activity during exercise is caused not only by central command but also by the reflex neural mechanism that is activated by exercise (muscle mechanoreflex and muscle metaboreflex) [9–11, 13, 16]. Muscle-exerted tension during static elbow flexion did not differ between EX and EX + VIB (Figure 1), showing that the degree of activation of muscle mechanoreflex may be similar under both conditions. In addition, Δdeoxy-Hb concentration of the exercising upper arm was similar between EX and EX + VIB (Figure 3B). Because deoxy-Hb of exercising muscle is the index for oxygen consumption [36, 37], the level of an exercise-induced metabolite accumulation during EX was expected to be equal to that found during EX + VIB, suggesting that the degree of activation of the muscle metaboreflex might not differ between EX and EX + VIB. In the present study, therefore, it is likely that the difference in CSAvein during static exercise between EX and EX + VIB might not be due to the differences in activation of the reflex neural mechanism under different conditions.
Although the specific regions of the brain involved in exercise-related responses remain speculative, the following theory can be considered. Animal studies suggest that subthalamic regions are capable of generating both motor and cardiovascular responses . In human studies, possible sites and neurocircuitry involving the insular cortex, sensorimotor cortex, anterior cingulate gyrus, medial prefrontal region and thalamic regions [18, 39–43], and the periaqueductal gray [44, 45], have been suggested. In addition, a recent hypothesis concerning the neural circuit responsible for generating central command is as follows: cerebral cortical output is not an essential component for the generation of central command but does seem to require a process that triggers activity in neural circuit(s) in the caudal brain to generate central command, and the region from the caudal diencephalon to the rostral mesencephalon plays an important role in the generation of central command , because in the decerebrate animal study the renal sympathetic nerve activity and HR abruptly increased in association with the start of locomotion , and spontaneous motor activity and the associated cardiovascular response were lost after decerebration at the midcollicular level .
Stewart and colleagues reported that venoconstriction during static exercise, which occurs not only in the splanchnic area but also in the resting extremities, may contribute to an increase in venous return to the heart to increase cardiac output . Taking into account previous studies, including our own, venoconstriction via central command might play a significant role in hemodynamics during exercise. However, because the relationship between venous return and venoconstriction is not obvious, further investigation is required.
Several limitations should be considered when interpreting our results. First, due to the large compliance of veins, volume (that is, CSAvein) is dependent on the venous pressure level – but we did not measure venous pressure. As mentioned above, however, BFvein and Δdeoxy-Hb (an index of venous blood volume) of the resting forearm did not change from baseline during both EX and EX + VIB (Figures 2E and 3D). We therefore believe that the effect of venous pressure-dependent control was scarcely observed during exercise in this study. Second, we did not account for the menstrual cycle in female subjects. However, because EX and EX + VIB were carried out in same day, this effect may be negligible in our study.