Voluntary control of pulse transmission time to the ear.

Two experiments invoh-ing voluntary control of pulse transmission time (PTT) to the ear were performed. In Experiment I (within-subject, 3 sessions), U male subjects attempting to control PTf with feedback showed significant bidirectional PTf changes in the target directions accompanied by parallel changes in pre-ejection period (PEP). There was no evidence ofconcomitant changes in respiration rate or general somatic activity. PTf control deteriorated across sessions. In Experiment II (between-subjects, 3 sessions), 10 male subjects attempting to decrease PTT with feedback produced significant rrr decreases accompanied by PEP decrea~s. There was marginal evidence of increases in respiration rate but no changes in general somatic activity in this condition. Five subjects attempting to increase PTT with feedback and 5 subjects attempting bidirectional PTf control without feedback showed no significant changes in PTT or PEP. The results from tmse experiments indicate that subjects demonstrate a modest degree of control over PTT to the ear when provided with feedback. This control of PTT is accompanied by parallel changes in PEP butis relatively free of somatic and respiratory concomitance. DESCRIPTORS: Pulse transmission time, Pre-ejection period, Voluntary control, Biofeedback. This report describes two experiments which examined characteristics of voluntary control of pulse transmission time (PTT) to the ear. Previous work with feedback of PTT has utilized the interval between the R-wave of the electrocardiogram and the upstroke of the radial pulse wave (e.g. Steptoe, 1976,1977, 1978). PTT to any peripheral pulse site encompasses both an intracardiac component, essentially equal to pre-ejection period (PEP), and an arterial componenc-The PEP component is related to cardiac contractility and reflects beta-adrenergic cardiac influences (Ahmed, Levinson, Schwartz, & Ettinger, 1972; Newlin & Levenson, 1979); while the arterial component is related to arterial distensibility and mean arterial blood pressure (Gribbin, Steptoe, & Sleight, 1976). Recent research in our laboratory (Newlin, 1979; Address requests for reprints to: Robert W. Levenson, Department of Psychology. Indiana University. Bloomington. IN 47405. New lin & Levenson, 1979) indicates that changes in PTT to the finger with biofeedback are a function of changes in both the PEP and the arterial component of PTT, rather than changes in the arterial component alone. These findings are seen as arguing against interpretation of changes in PTT as simply reflecting changes in mean arterial pressure (e.g. Steptoe, 1976, 1977). Obrist, Light, McCubbin, Hutcheson, and Hoffer (1979) have provided some confirmation of the relationship between PIT and mean arterial pressure, but interpret this as a secondary effect of changes in cardiac contractility acting to alter systolic blood pressure. The present research is intended to provide additional information concerning the PEP and arterial components of PTT change with biofeedback. In these experiments, PTT to the ear rather than the finger is utilized to reduce the arterial component and thus increase the relative contribution of PEP. To the extent that voluntary control of PTT is a function of changes in PEP (and thus presumably of