How are tonic and phasic cardiovascular changes related to central motor command?

We examined the influence of central motor command on heart rate, respiration, and peripheral vascular activity. Central command was enhanced or reduced using tendon vibration. Muscle tension was held constant permitting the examination of variation in central command. Experiment 1 demonstrated in 13 college-aged males an enhancement of heart rate and vascular responses to an isometric, extensor contraction when vibration of the flexor tendon was added. Experiment 2 asked whether changes in central command interacted with phasic cardiovascular changes such as stimulus-linked anticipatory cardiac deceleration. Twenty college-aged males performed either an isometric flexor or extensor contraction with or without flexor tendon vibration. As expected, vibration enhanced cardiovascular change with extensor contraction more than with flexor contraction. Relative to control contractions, however, the flexor change was not an absolute decrease in cardiovascular change. More importantly, tendon vibration failed to alter phasic cardiovascular changes. Force and central commands for force induce cardiovascular change, but this change seems independent of phasic changes induced by the anticipation and processing of environmental stimuli.

Graphical and statistical techniques for cardiac cycle time (phase) dependent changes in interbeat interval.

Cardiac cycle time effects refer to the relative lengthening or shortening of a single cardiac cycle as a function of when in the cycle brief sensorimotor events occur. These effects may provide short-latency measures of cardiac sensitivity to psychological events. Conventional representations have, however, failed to clearly separate changes in interbeat interval due to cycle time--i.e., phase dependent changes--from other types of change. This paper advocates a particular technique of plotting to solve these representation problems. Heartbeat timing is represented in real time and in the context of beats both preceding and following the event of interest. The plot, a phase-sensitive plot, conceptualizes phase-sensitive (cardiac cycle time) effects as a change in linear or higher order trend. Thus, an adaptation of trend analysis is proposed as an efficient statistical analysis that follows directly from the proposed representational technique.

Forearm, chest, and skin vascular changes during simple performance tasks.

Momentary changes in vascular variables were examined in four experiments which all induced preparation for an expected stimulus. Response requirements were minimized to permit examination of changes during stimulus presentation unconfounded with overt movement. The hypothesis examined was that vascular changes serve to maximize tissue perfusion at the time of anticipated action. Impedance plethysmographic measures of the chest and forearm were scored both for transit times and amplitude/slope indices. Similar indices were derived from photo-plethysmographic signals from the nail-bed of the thumb. The results suggested that preparatory vascular changes could be divided into an initial expectancy phase started at least 2 or 3 seconds prior to the anticipated events and a specific preparatory phase occurring just prior to and during stimulus presentation. Transit time shortening and maintained vasoconstriction characterized the initial expectancy phase when a finger movement, but not an effortful grip, was the anticipated response. Transit time lengthening and vasodilation generally characterized the specific preparation phase, but are disrupted when a signal inhibiting the response is likely to occur. Decelerative heart rate changes were positively related to the slope of the systolic rise in the chest impedance measure, suggesting that both cardiac and vascular changes may act together. Overall, the results were moderately supportive of the view that the heart and vasculature act together to maximize tissue perfusion at the time of anticipated action.

Weak sensory stimuli induce a phase sensitive bradycardia.

We attempted to demonstrate that significant perceptual stimuli would induce different degrees of heart rate deceleration depending on when (phase) in the cardiac cycle they occurred. Relative to previous work, we concurrently examined a number of factors that might alter the amplitude of such a cardiac cycle time effect. Stimulus intensity and presence or absence of a speeded response were manipulated. Liminal stimuli and a perceptual rather than motor set were expected to maximize any cardiac cycle time effect. Respiratory phase, length of average interbeat interval, and number of trials were also investigated. Twenty-four college aged, male volunteers were randomly separated into equal groups receiving instructions either to judge which of two weak visual stimuli occurred or to execute a speeded, discriminative response to the stimuli. Discriminative stimuli were presented at either 0, 150, 250, 350, or 500 ms after the R-wave of the electrocardiogram. Stimuli were presented with an intensity that had yielded either 63% or 90% correct detections in a prior psychophysical assessment. A phase dependent deceleration occurred after both intensities of stimuli. Poststimulus deceleration was greater for stimuli in early to mid cycle as suggested by earlier work. As expected, this result was clear when the stimuli were presented during the expiratory phase of respiration. Neither perceptual/motor set nor stimulus intensity altered the phase sensitive deceleration. Thus, phase sensitive deceleration was confirmed using demanding sensory stimuli and an improved representational technique.

Response inhibition initiates cardiac deceleration: evidence from a sensory-motor compatibility paradigm.

Two experiments tested the hypothesis that response selection processes alter the timing of the shift between anticipatory cardiac deceleration and acceleratory recovery. Experiment 1 compared changes in cardiac interbeat interval induced by the manipulation of sensory-motor compatibility in a four choice reaction time task. A direct spatial mapping between a linear array of light-emitting diodes (LEDs) was compared to randomly assigned, indirect (non-compatible) mappings. Experiment 2 repeated these two tasks and added a two choice condition with direct spatial mapping, a task frequently employed to examine heart rate deceleration. Fifteen college aged males participated in Experiment 1; 18 college aged males participated in Experiment 2. In both experiments anticipatory cardiac deceleration either reached a plateau or shifted to acceleration by the interbeat interval in which the stimulus occurred. In contrast to previous reports, a secondary deceleration, rather than cardiac acceleration, often followed the stimulus. The secondary deceleration was greater with non-compatible mapping, slow response speeds, and short intertrial intervals. The findings suggested that the motoric inhibition required during response selection induces a phasic cardiac deceleration.

On the shift from anticipatory heart rate deceleration to acceleratory recovery: revisiting the role of response factors.

The influence of inducing motor responses of low and high force at different times in the cardiac cycle was examined. A handgrip response was used which allowed the separation of response initiation from response completion. Based on earlier work, we expected initiation, rather than completion, to initiate poststimulus cardiac acceleration. We also thought that preparation for a high force response might alter preparatory changes of interbeat interval differently from preparation for a low force response. Fifteen college-aged male subjects performed a warned reaction time task in which a visual stimulus signalled a handgrip requiring either a high or a low force to close. NoGo trials in which an inhibit signal was presented occurred on 12% of the trials. Stimuli occurred either on the R-wave of the electrocardiogram or 300 ms later. Reaction speed was varied in different trial blocks by rewarding response times of 200 ms (+/- 50 ms), 300 ms, or 400 ms. Results based on the timing of response initiation were essentially identical to those based on the timing of response completion. High force relative to low force was associated with both earlier response initiation and earlier cardiac acceleration. Force did not alter preparatory cardiac deceleration. Force and response speed did, however, alter the level of heart rate after response occurrence. Thus, response initiation (or an earlier response process) appears to induce a cardiac acceleration whose level is influenced by the speed and force of the motor response.