Effect of interference current on forearm vascular resistance in asymptomatic humans.

An interference current (IC) is produced when two independent alternating currents of slightly different frequencies intersect. Because the sinusoidal outputs of the two circuits are out of phase, they alternately summate and cancel, resulting in an amplitude-modulated current with a beat frequency equal to the difference between the two carrier frequencies.[1]

Interference current therapy is used clinically for pain control, primarily as an alternative to the more traditional forms of transcutaneous electrical nerve stimulation (TENS).[1,2] In this regard, IC has certain advantages over traditional TENS. Higher maximum total current can be delivered to the tissues, and greater penetration is possible because of the very short pulse durations associated with IC.[1] Because IC is amplitude modulated, there is also no accommodation of the stimulated nerve fibers.[3]

In addition to having pain-relieving properties, IC therapy has been reported to cause regional vasodilation in patients with peripheral vascular disease.[4-6] The proposed mechanism of this circulatory effect is physical blockade of sympathetic vasoconstrictor nerve fibers.[2,4-6] This hypothesis, however, has not been tested systematically. The goal of this study, therefore, was to determine whether transcutaneous application of IC causes attenuation of sympathetic vasomotor outflow to the upper extremity. Accordingly, we measured forearm blood flow (venous occlusion plethysmography), systemic arterial pressure, heart rate, and hand skin temperature during applications of IC over the left stellate ganglion in asymptomatic human volunteers.

Method

Subjects

Five asymptomatic subjects (one male, four female), ranging in age from 21 to 44 years (X[bar]=33, SD=12), were recruited to participate in this study. None of the subjects reported a history of cardiovascular, neurologic, or musculoskeletal disease, and none were taking medication at the time of study. Informed consent was obtained from all subjects prior to participation.

General Procedures

Subjects were studied in the supine position. To ensure a hemodynamic steady state, subjects were asked to refrain from ingestion of food and caffeine for at least 2 hours prior to study. Room temperature was maintained at 24[degrees]C (SD=1[degrees]C). All subjects were allowed to rest quietly in the laboratory for at least 20 minutes before the start of the stimulation protocols. Heart rate was measured from electrocardiograms. Continuous beat-by-beat determinations of arterial pressure were made by photoelectric plethysmography. Measurements obtained with the plethysmograph(*) correlate well with intra-arterial measurements.[7] Skin temperature was measured using a thermistor probe([dagger]) placed on the volar surface of each subject's left hand. The probe was calibrated in a beaker of water using a mercury thermometer before and after each data collection period and was found to be accurate within [+ or -]0.2[degrees]C. Because respiratory maneuvers are known to affect peripheral blood flow,[8] subjects were instructed to maintain a stable breathing pattern throughout the data collection period. A stable breathing pattern was defined as the absence of sustained changes in the rate or depth of breathing. Respiration was monitored using a strain gauge pneumograph to ensure compliance with this instruction. The plethysmographic, arterial pressure, electrocardiographic, and respiration tracings were recorded continuously on paper([double dagger]) and on videotape.([sections])([parallel]) Skin temperature values were recorded manually at 1-minute intervals.

Measurement of Limb Blood Flow

Blood flow in the left forearm was measured by venous occlusion plethysmography. Details concerning the methods, rationale, and assumptions for venous occlusion plethysmography have been published previously.[9,10] The subject's arm was elevated above the level of the right atrium to ensure adequate drainage of the forearm veins between measurements. Blood flow measurements were obtained every 20 seconds by inflation of a collecting cuff positioned above the elbow to 40 mm Hg for four to five cardiac cycles. The coefficient of variation for steady-state blood flow measurements obtained in this manner was [+ or-]8%, indicating that this measurement was highly reproducible in these five subjects. Sixty-second averages of blood flow measurements were used in computation of results. Forearm vascular resistance (in arbitrary units) was calculated as mean arterial pressure (one third pulse pressure plus diastolic pressure, in millimeters of mercury) divided by forearm blood flow (in milliliters per 100 milliliters of tissue per minute).[11]

Interference Current

A two-circuit IC generator([sharp]) with a variable beat frequency of 90 to 100 Hz was used to produce a scanning interference field. The carrier frequencies in the two circuits (4,000 and 4,090-4,100 Hz) and the sinusoidal nature of the stimulator outputs were confirmed by use of an oscilloscope. A nonconductive pad with two fabric-covered electrodes from each circuit (oriented diagonally) was placed on the left anterolateral surface of the subject's neck at the level of the transverse process of the seventh cervical vertebra. Electrode placement over the stellate ganglion was confirmed by observing elevation of the shoulder and ipsilateral cervical rotation at stimulation intensities above the motor threshold.[6] Because all sympathetic outflow to the upper extremity passes through the stellate ganglion, we reasoned that this electrode placement would maximize potential IC-related changes in blood flow.

Experimental Protocols

Protocol 1: interference current application. Forearm blood flow, arterial pressure, skin temperature measured on the volar aspect of the hand, respiratory movements, and electrocardiographic activity were recorded until at least 5 minutes of stable baseline measurements were obtained. Measurements were continued during a 10-minute application of IC at a stimulation intensity that produced a comfortable, sustained contraction of the trapezius and sternocleidomastoid muscles and during a 5-minute poststimulation recovery period.

Protocol 2: interference current application during lower-body suction. To assess the effects of IC under conditions of heightened sympathetic nervous system activity, we repeated the IC stimulation during application of negative pressure to the lower body. This intervention increases sympathetic outflow to the skeletal muscle vascular bed through baroreflex mechanisms.[12,13] In this protocol, the subject's lower body, up to the level of the iliac crests, was enclosed in an airtight box. After at least 5 minutes of stable baseline measurements were obtained, the lower body was exposed to subatmospheric pressure (-10 mm Hg) by application of a vacuum source to the box. After 3 minutes of lower-body suction, IC was applied for 10 minutes as in protocol 1. After the IC treatment, lower-body suction was maintained for 3 minutes, followed by a 5-minute recovery period.

Protocol 3; reactive hyperemia test. To assess the ability of our subjects to respond to a vasodilator stimulus, we measured the peak blood flow following the termination of 5 minutes of vascular occlusion. After at least 5 minutes of stable forearm blood flow and arterial pressure measurements had been obtained, a blood pressure cuff placed around each subject's left arm was inflated to 160 mm Hg (a suprasystolic level in all subjects) for 5 minutes. After the release of vascular occlusion, 5 minutes of recovery measurements were made.

Data Analysis

Friedman's two-way analysis of variance by ranks[14] was used to compare group mean values for the variables of interest in the baseline period, the 10th minute of IC, and the 5th minute of the recovery period. For the lower-body suction protocol, Friedman's two-way analysis of variance by ranks was used to compare group mean values for the variables of interest in the baseline period, the 3rd minute of lower-body suction alone, the 10th minute of lower-body suction combined with IC, and the 5th minute of the recovery period. When the omnibus tests were statistically significant, the minimum difference for all pairwise contrasts was determined as described by Friedman.[15] For the reactive hyperemia protocol, Wilcoxon signed-ranks tests[16] were used to compare the baseline values with the maximal forearm blood flow and minimal vascular resistance values observed following reestablishment of flow upon release of the occlusion. All values were considered significant at P<.05.

Results

Protocol 1: Interference Current Application

Interference current had no statistically significant effect on forearm blood flow or vascular resistance (Tab. 1, Figs. 1 and 2). Nevertheless, small IC-induced decreases in forearm blood flow and increases in forearm vascular resistance occurred in four of the five subjects studied (both P=.09) (Fig. 3). Interference current did not affect heart rate or rhythm, arterial pressure, or hand skin temperature (Tab. 1). No signs of sympathetic blockade (ie, Horner's syndrome, warming of the hand, nasal congestion) were observed in any of the subjects.

Protocol 2: Interference Current Application During Lower-Body Suction

Application of a nonhypotensive level of lower-body suction (-10 mm Hg) caused the expected decrease in forearm blood flow and the expected increase in vascular resistance (Tab. 2, Figs. 4 and 5). Concomitant application of IC produced no further effect on the forearm circulation. Likewise, there was no effect of IC on heart rate or arterial pressure. Hand skin temperature was decreased relative to the baseline measurement at the 10th minute of lower body-suction combined with IC (Tab. 2). Consistent responses were observed in all subjects.

Protocol 3: Reactive Hyperemia Test

Following the release of 5 minutes of vascular occlusion, forearm blood flow increased markedly (X[bar]=4.7[SD=1.3] to 17.0 [SD=11.2] mL/100 mL/min, P<.05) and forearm vascular resistance decreased (X[bar]=19.2 [SD=3.0] to 6.9 [SD=3.2] units, P<.05). These findings were consistent in the five subjects studied.

Discussion

Several reports suggest that trunscutaneous stimulation with IC over dorsal roots, sympathetic ganglia, and peripheral nerves can increase blood flow to the extremities.[4-6] The proposed mechanism for this circulatory effect is physical blockade of sympathetic vasoconstrictor fibers[2,4-6]; however, this theory has not been well investigated. For this reason, we measured forearm blood flow, systemic arterial pressure, and hand skin temperature during IC applied over the stellate ganglion using recommended stimulation settings.[6] The findings of our study indicate that transcutaneous application of IC over the stellate ganglion does not produce forearm vasodilation in asymptomatic humans.

Previous descriptions of the vasodilatory effect of IC were based on clinical experiences in patients with peripheral vascular disease,[4-6] some of whom may have had elevated sympathetic nervous system activity. We therefore considered the possibility that our inability to detect an effect of IC on forearm vascular resistance in asymptomatic subjects could be explained by their relatively low baseline levels of sympathetic nerve activity. We doubt that this possibility can explain our negative findings, however, because when we raised sympathetic vasoconstrictor outflow with lower-body suction, we remained unable to detect IC-induced vasodilation. In contrast, forearm vascular resistance tended to increase during application of IC in our subjects. This small increase in vascular resistance, although not statistically significant, was observed in four of the five subjects. Reflex activation of sympathetic vasoconstrictor outflow elicited by IC-induced sustained contraction of the trapezius and sternocleidomastoid muscles is a possible explanation for this finding.[17]

Dissimilar methods of vascular assessment could possibly explain the discrepancy between our findings and those of other investigators. Previous reports of the vasodilatory effects of IC have relied on digital photoelectric plethysmography[6] and assessment of pulse wave velocity.4 Both techniques are difficult to quantify, and neither technique assesses blood flow in the entire limb.[18-20] We used venous occlusion plethysmography, a quantitative method for measurement of whole limb blood flow.[9] This noninvasive technique has been validated previously using both direct and electromagnetic blood flow determinations.[21,22] We found the technique to be very reproducible (coefficient of variation, <10%).

Because baseline values for forearm vascular resistance in our subjects were lower than those previously published,[23-25] we considered the possibility that vasodilation was already maximal in our asymptomatic subjects who were resting quietly in a warm room (24[degrees]C). If so, it would have been impossible for IC to produce a further decrease in forearm vascular resistance. To rule out this possibility and also the possibility of a nonspecific inability to respond to vasodilatory stimuli in our subjects, we assessed their responses to 5 minutes of complete vascular occlusion, an intervention that causes metabolically mediated vasodilation. We observed the expected marked decrease in vascular resistance following release of the occlusion in all subjects. Therefore, we believe it unlikely that our negative findings can be attributed to a "floor effect" or to a nonspecific failure of vasodilator mechanisms.

The 10-minute treatment time may have limited our ability to detect IC-induced vasodilation. We chose to apply IC for 10 minutes because in a previous case report,[6] an increase in digital pulse volume was observed after 8 minutes of treatment. The proposed explanation for this finding was physical blockade of sympathetic vasoconstrictor neurons.6 We hypothesize that if IC could produce such an inhibitory effect, the time course would be very rapid (ie, a fraction of a second, not minutes).

We considered the possibility that a Type 11 error led to our acceptance of the null hypothesis. Although we studied only five subjects, they responded consistently to IC. We did not see evidence of IC-induced vasodilation in any subject. In contrast, four of the five subjects demonstrated a small, directionally opposite response vasoconstriction), indicating that the IC-induced blockade of sympathetic fibers in the stellate ganglion, if present, was not able to overcome the reflex vasoconstriction produced by static muscle contraction. Decreases in forearm vascular resistance have been demonstrated with as few as five subjects when chemical blockade of the stellate ganglion was induced with lidocaine.[23] In our study, we estimate the likelihood of a Type II error to be small.

Two recent investigations of the circulatory effects of IC failed to demonstrate increases in either blood flow velocity[26] or skin temperature[27] in asymptomatic subjects, Our observations confirm and extend these findings by demonstrating that forearm vascular resistance, a more direct indicator of vasodilation than either blood flow velocity or skin temperature, was unaffected by application of IC.

Conclusions

Our findings indicate that IC applied over the stellate ganglion does not cause forearm vasodilation in asymptomatic individuals. These findings call into question the theory that IC is capable of blocking sympathetic vasoconstrictor impulses in peripheral nerves.

Acknowledgments

We thank Dr William Reddan of the Department of Preventive Medicine, University of Wisconsin-Madison, for the use of the telethermometer. We also appreciate the secretarial assistance of Ms Pat Mecum.

(*) Finapres model 2300 blood pressure monitor, Ohmeda, 3030 Ohmeda Dr, Madison, WI 53707. ([dagger]) Model 46TUC temperature monitor, YSI Inc, 1725 Brannum Ln, Yellow Springs, OH 45387. ([double dagger]) Model TA4000 physiologic recorder, Gould Inc, 3631 Perkins Ave, Cleveland, OH 44114. ([sections]) Model 3000A PCM recording adaptor, AR Vetter Co, Box 143, Rebersburg, PA 16872. ([parallel]) Model HR-D860U videocassette recorder, JVC Company of America, 41 Slater Dr, Elmwood Park, NJ 07407. ([sharp]) Endodyne 4 stimulator, ELMED Inc, 60 W Fay Ave, Addison, IL 60101.

References

[1] Kloth LC. Electrotherapeutic alternatives for treatment of pain. In: Gersch MR, ed. Electrotherapy in Rehabilitation. Philadelphia, Pa: FA Davis Co; 1992:197-217. [2] DeDomenico G. Pain relief with interferential therapy. Australian Journal of physiotherapy. 1982;28:14-18. [3] Kloth LC. Interference current. In: Nelson RM, Currier DP, eds. Clinical Electrotherapy. East Norwalk, Conn: Appleton & Lange; 1991:221-26o. [4] Nikolova-Troeva L. Die moderen elektrobehandlungsmethoden in der therapie der endarteriitis obliterans. Therapie der Gegenwart. 1968;107:190-198. [5] Nikolova L. Surgical conditions. In: Treatment With Interferential Current. Edinburgh, Scotland: Churchill Livingstone; 1987:95-181. [6] Schoeler H. Physikalische grenzstrangblockade. Tecknik in der Medizin. 1972;1:16-18. [7] Parati G, Casadei R, Gropelli A, et al. Comparison of finger and intra-arterial blood pressure monitoring at rest and during laboratory testing. Hypertension. 1989;13:647-655. [8] Roddie IC, Shepherd JT, Whelan RF. Reflex changes in human skeletal muscle blood flow associated with intrathoracic pressure changes. Circ Res. 1958;6:232-238. [9] Whitney RJ. The measurement of volume changes in human limbs. J Physiol. 1953; 121:1-27. [10] Indergand HJ, Morgan BJ. Effects of high-frequency transcutaneous electrical nerve stimulation on limb blood flow in healthy humans. Phys Ther. 1994;74:361-367. [11] Smith JJ, Kampine JP. Circulatory Physiology: The Essentials. Baltimore, Md: Williams & Wilkins; 1984:17. [12] Jacobsen TN, Morgan BJ, Scherrer U, et al. Relative contributions of cardiopulmonary and sinoaortic baroreflexes in causing sympathetic activation in the human skeletal muscle circulation during orthostatic stress. Circ Res. 1993;73:367-378. [13] Rowell LB. Human Circulation: Regulation During Physical Stress. New York, NY: Oxford University Press Inc; 1986:149. [14] Friedman M. The use of ranks to avoid the assumption of normality implicit in the analysis of variance. J Am Stat Assoc. 1937;32:675-701. [15] Friedman M. A comparison of alternative tests of significance for the problem of m rankings. Ann Math Stat. 1940; 11:86-92. [16] Wilcoxon F. Individual comparisons by ranking methods. Biometrics. 1945;1:80-83. [17] Seals DR, Chase PB, Taylor JA. Autonomic mediation of the pressor responses to isometric exercise in humans. J Appl Physiol. 1988;64:2190-2196. [18] Roberts VC. Measurement of major vessel flow in the assessment of peripheral vascular function. In: Mathie RT, ed. Blood Flow Measurement in Man. Tunbridge Wells, England: Castle House Publications Ltd; 1982:171-186. [19] Hainsworth R. The measurement of blood flow. In: Linden RJ, ed. Techniques in the Life Sciences, Volume P3/I. County Clare, Ireland: Elsevier Scientific Publishers Ltd; 1983; P303:1-24. [20] Girling M, Mott GT, Harrison DH. Skin blood flow measurement. In: Mathie RT, ed. Blood Flow Measurement in Man. Tunbridge Wells, England: Castle House Publications Ltd; 1982:240-248. [21] Formel PF, Doyle JT. Rationale of venous occlusion plethysmography. Circ Res. 1957; 5:354-356. [22] Conrad MC, Green HD. Evaluation of venous of occlusion plethysmograph. J Appl Physiol. 1961;16:289-292. [23] Joyner MJ, Nauss LA, Warner MA, Warner DO. Sympathetic modulation of blood flow and 02 uptake in rhythmically contracting human forearm muscles. Am J Physiol 1992; 263:H1078-H1083. [24] Morgan BJ, DeBoer LWV, Pease MO, et al. Forearm vascular resistance increases during static exercise in heart transplant recipients. J Appl Physiol. 1991;71:2224-2230. [25] Duprez DA, Essandoh LK, Vanhoutte PM, Shepherd JT. Vascular responses in forearm and calf to contralateral static exercise. J Appl Physiol. 1989;66:669-674. [26] Bergslien O, Thoreson M, Odemark H. The effects of three electrotherapeutic methods on blood velocities in human peripheral arteries. Scand J Rehabil Med. 1988;20:29-33. [27] Nussbaum E, Rush P, Disenhaus L. The effects of interferential therapy on peripheral blood flow. Physiotherapy. 1990;76:803-807.

HJ Indergand, PT, ATC, is currently with the Physical Therapy Center of Rhinelander, 1831 N Stevens, PO Box 1272, Rhinelander, WI 54501, She was a student in the Physical Therapy Program, University of Wisconsin-Madison, at the time this research was conducted.

BJ Morgan, Phd, PT, is Assistant Professor, Physical Therapy Program, Department of Kinesiology, University of Wisconsin-Madison, Madison, WI 53706. Address correspondence to Dr Morgan at 5175 Medical Sciences Center, 1300 University Avenue, Madison, WI 53706-1532 (USA). Dr Morgan is a Parker B Francis Fellow in Pulmonary Research.

This study was approved by the Center for Health Sciences Human Subjects Committee of the University of Wisconsin-Madison. Funding was provided by a Wisconsin/Hilldale Undergraduate/ Faculty Research Fellowship.

An oral presentation of this research was made at the spring meeting of the Wisconsin Physical Therapy Association on March 18, 1994.